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4. Establishment and cryptic transmission of Zika virus in Brazil and the Americas

Author

Faria, N. R., Quick, J., Claro, I.M., Thézé, J., de Jesus, J. G., Giovanetti, M., Kraemer, M. U. G., Hill, S. C., Black, A., da Costa, A. C., Franco, L. C., Silva, S. P., Wu, C.-H., Raghwani, J., Cauchemez, S., du Plessis, L., Verotti, M. P., de Oliveira, W. K., Carmo, E. H., Coelho, G. E., Santelli, A. C. F. S., Vinhal, L. C., Henriques, C. M., Simpson, J. T., Loose, M., Andersen, K. G., Grubaugh, N. D., Somasekar, S., Chiu, C. Y., Muñoz-Medina, J. E., Gonzalez-Bonilla, C. R., Arias, C. F., Lewis-Ximenez, L. L., Baylis, S. A., Chieppe, A. O., Aguiar, S. F., Fernandes, C. A., Lemos, P. S., Nascimento, B. L. S., Monteiro, H. A. O., Siqueira, I. C., de Queiroz, M. G., de Souza, T. R., Bezerra, J. F., Lemos, M. R., Pereira, G. F., Loudal, D., Moura, L. C., Dhalia, R., França, R. F., Magalhães, T., Marques, Jr, E. T., Jaenisch, T., Wallau, G. L., de Lima, M. C., Nascimento, V., de Cerqueira, E. M., de Lima, M. M., Mascarenhas, D. L., Neto, J. P. Moura, Levin, A. S., Tozetto-Mendoza, T. R., Fonseca, S. N., Mendes-Correa, M. C., Milagres, F. P., Segurado, A., Holmes, E. C., Rambaut, A., Bedford, T., Nunes, M. R. T., Sabino, E. C., Alcantara, L. C. J., Loman, N. J., and Pybus, O. G.

Published
2017
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5. SARS-CoV-2 evolution during treatment of chronic infection

Author

Kemp, S. A., Collier, D. A., Datir, R. P., Ferreira, I. A. T. M., Gayed, S., Jahun, A., Hosmillo, M., Rees-Spear, C., Mlcochova, P., Lumb, I. U., Roberts, D. J., Chandra, A., Temperton, N., Baker, S., Dougan, G., Hess, C., Kingston, N., Lehner, P. J., Lyons, P. A., Matheson, N. J., Owehand, W. H., Saunders, C., Summers, C., Thaventhiran, J. E. D., Toshner, M., Weekes, M. P., Bucke, A., Calder, J., Canna, L., Domingo, J., Elmer, A., Fuller, S., Harris, J., Hewitt, S., Kennet, J., Jose, S., Kourampa, J., Meadows, A., O'Brien, C., Price, J., Publico, C., Rastall, R., Ribeiro, C., Rowlands, J., Ruffolo, V., Tordesillas, H., Bullman, B., Dunmore, B. J., Fawke, S., Graf, S., Hodgson, J., Huang, C., Hunter, K., Jones, E., Legchenko, E., Matara, C., Martin, J., Mescia, F., O'Donnell, C., Pointon, L., Pond, N., Shih, J., Sutcliffe, R., Tilly, T., Treacy, C., Tong, Z., Wood, J., Wylot, M., Bergamaschi, L., Betancourt, A., Bower, G., Cossetti, C., De Sa, A., Epping, M., Gleadall, N., Grenfell, R., Hinch, A., Huhn, O., Jackson, S., Jarvis, I., Lewis, D., Marsden, J., Nice, F., Okecha, G., Omarjee, O., Perera, M., Richoz, N., Romashova, V., Yarkoni, N. S., Sharma, R., Stefanucci, L., Stephens, J., Strezlecki, M., Turner, L., De Bie, E. M. D. D., Bunclark, K., Josipovic, M., Mackay, M., Rossi, S., Selvan, M., Spencer, S., Yong, C., Ansaripour, A., Michael, A., Mwaura, L., Patterson, C., Polwarth, G., Polgarova, P., di Stefano, G., Fahey, C., Michel, R., Bong, S. -H., Coudert, J. D., Holmes, E., Allison, J., Butcher, H., Caputo, D., Clapham-Riley, D., Dewhurst, E., Furlong, A., Graves, B., Gray, J., Ivers, T., Kasanicki, M., Le Gresley, E., Linger, R., Meloy, S., Muldoon, F., Ovington, N., Papadia, S., Phelan, I., Stark, H., Stirrups, K. E., Townsend, P., Walker, N., Webster, J., Robson, S. C., Loman, N. J., Connor, T. R., Golubchik, T., Martinez Nunez, R. T., Ludden, C., Corden, S., Johnston, I., Bonsall, D., Smith, C. P., Awan, A. R., Bucca, G., Estee Torok, M., Saeed, K., Prieto, J. A., Jackson, D. K., Hamilton, W. L., Snell, L. B., Moore, C., Harrison, E. M., Goncalves, S., Fairley, D. J., Loose, M. W., Watkins, J., Livett, R., Moses, S., Amato, R., Nicholls, S., Bull, M., Smith, D. L., Barrett, J., Aanensen, D. M., Curran, M. D., Parmar, S., Aggarwal, D., Shepherd, J. G., Parker, M. D., Glaysher, S., Bashton, M., Underwood, A. P., Pacchiarini, N., Loveson, K. F., Carabelli, A. M., Templeton, K. E., Langford, C. F., Sillitoe, J., de Silva, T. I., Wang, D., Kwiatkowski, D., Rambaut, A., O'Grady, J., Cottrell, S., Holden, M. T. G., Thomson, E. C., Osman, H., Andersson, M., Chauhan, A. J., Hassan-Ibrahim, M. O., Lawniczak, M., Alderton, A., Chand, M., Constantinidou, C., Unnikrishnan, M., Darby, A. C., Hiscox, J. A., Paterson, S., Martincorena, I., Robertson, D. L., Volz, E. M., Page, A. J., Pybus, O. G., Bassett, A. R., Ariani, C. V., Spencer Chapman, M. H., K. K., Li, Shah, R. N., Jesudason, N. G., Taha, Y., Mchugh, M. P., Dewar, R., Jahun, A. S., Mcmurray, C., Pandey, S., Mckenna, J. P., Nelson, A., Young, G. R., Mccann, C. M., Elliott, S., Lowe, H., Temperton, B., Roy, S., Price, A., Rey, S., Wyles, M., Rooke, S., Shaaban, S., de Cesare, M., Letchford, L., Silveira, S., Pelosi, E., Wilson-Davies, E., O'Toole, A., Hesketh, A. R., Stark, R., du Plessis, L., Ruis, C., Adams, H., Bourgeois, Y., Michell, S. L., Gramatopoulos, D., Edgeworth, J., Breuer, J., Todd, J. A., Fraser, C., Buck, D., John, M., Kay, G. L., Palmer, S., Peacock, S. J., Heyburn, D., Weldon, D., Robinson, E., Mcnally, A., Muir, P., Vipond, I. B., Boyes, J., Sivaprakasam, V., Salluja, T., Dervisevic, S., Meader, E. J., Park, N. R., Oliver, K., Jeffries, A. R., Ott, S., da Silva Filipe, A., Simpson, D. A., Williams, C., Masoli, J. A. H., Knight, B. A., Jones, C. R., Koshy, C., Ash, A., Casey, A., Bosworth, A., Ratcliffe, L., Xu-McCrae, L., Pymont, H. M., Hutchings, S., Berry, L., Jones, K., Halstead, F., Davis, T., Holmes, C., Iturriza-Gomara, M., Lucaci, A. O., Randell, P. A., Cox, A., Madona, P., Harris, K. A., Brown, J. R., Mahungu, T. W., Irish-Tavares, D., Haque, T., Hart, J., Witele, E., Fenton, M. L., Liggett, S., Graham, C., Swindells, E., Collins, J., Eltringham, G., Campbell, S., Mcclure, P. C., Clark, G., Sloan, T. J., Jones, C., Lynch, J., Warne, B., Leonard, S., Durham, J., Williams, T., Haldenby, S. T., Storey, N., Alikhan, N. -F., Holmes, N., Carlile, M., Perry, M., Craine, N., Lyons, R. A., Beckett, A. H., Goudarzi, S., Fearn, C., Cook, K., Dent, H., Paul, H., Davies, R., Blane, B., Girgis, S. T., Beale, M. A., Bellis, K. L., Dorman, M. J., Drury, E., Kane, L., Kay, S., Mcguigan, S., Nelson, R., Prestwood, L., Rajatileka, S., Batra, R., Williams, R. J., Kristiansen, M., Green, A., Justice, A., Mahanama, A. I. K., Samaraweera, B., Hadjirin, N. F., Quick, J., Poplawski, R., Kermack, L. M., Reynolds, N., Hall, G., Chaudhry, Y., Pinckert, M. L., Georgana, I., Moll, R. J., Thornton, A., Myers, R., Stockton, J., Williams, C. A., Yew, W. C., Trotter, A. J., Trebes, A., MacIntyre-Cockett, G., Birchley, A., Adams, A., Plimmer, A., Gatica-Wilcox, B., Mckerr, C., Hilvers, E., Jones, H., Asad, H., Coombes, J., Evans, J. M., Fina, L., Gilbert, L., Graham, L., Cronin, M., Kumziene-Summerhayes, S., Taylor, S., Jones, S., Groves, D. C., Zhang, P., Gallis, M., Louka, S. F., Starinskij, I., Jackson, C., Gourtovaia, M., Tonkin-Hill, G., Lewis, K., Tovar-Corona, J. M., James, K., Baxter, L., Alam, M. T., Orton, R. J., Hughes, J., Vattipally, S., Ragonnet-Cronin, M., Nascimento, F. F., Jorgensen, D., Boyd, O., Geidelberg, L., Zarebski, A. E., Raghwani, J., Kraemer, M. U. G., Southgate, J., Lindsey, B. B., Freeman, T. M., Keatley, J. -P., Singer, J. B., de Oliveira Martins, L., Yeats, C. A., Abudahab, K., Taylor, B. E. W., Menegazzo, M., Danesh, J., Hogsden, W., Eldirdiri, S., Kenyon, A., Mason, J., Robinson, T. I., Holmes, A., Hartley, J. A., Curran, T., Mather, A. E., Shankar, G., Jones, R., Howe, R., Morgan, S., Wastenge, E., Chapman, M. R., Mookerjee, S., Stanley, R., Smith, W., Peto, T., Eyre, D., Crook, D., Vernet, G., Kitchen, C., Gulliver, H., Merrick, I., Guest, M., Munn, R., Bradley, D. T., Wyatt, T., Beaver, C., Foulser, L., Churcher, C. M., Brooks, E., Smith, K. S., Galai, K., Mcmanus, G. M., Bolt, F., Coll, F., Meadows, L., Attwood, S. W., Davies, A., De Lacy, E., Downing, F., Edwards, S., Scarlett, G. P., Jeremiah, S., Smith, N., Leek, D., Sridhar, S., Forrest, S., Cormie, C., Gill, H. K., Dias, J., Higginson, E. E., Maes, M., Young, J., Wantoch, M., Jamrozy, D., Lo, S., Patel, M., Hill, V., Bewshea, C. M., Ellard, S., Auckland, C., Harrison, I., Bishop, C., Chalker, V., Richter, A., Beggs, A., Best, A., Percival, B., Mirza, J., Megram, O., Mayhew, M., Crawford, L., Ashcroft, F., Moles-Garcia, E., Cumley, N., Hopes, R., Asamaphan, P., Niebel, M. O., Gunson, R. N., Bradley, A., Maclean, A., Mollett, G., Blacow, R., Bird, P., Helmer, T., Fallon, K., Tang, J., Hale, A. D., Macfarlane-Smith, L. R., Harper, K. L., Carden, H., Machin, N. W., Jackson, K. A., Ahmad, S. S. Y., George, R. P., Turtle, L., O'Toole, E., Watts, J., Breen, C., Cowell, A., Alcolea-Medina, A., Charalampous, T., Patel, A., Levett, L. J., Heaney, J., Rowan, A., Taylor, G. P., Shah, D., Atkinson, L., Lee, J. C. D., Westhorpe, A. P., Jannoo, R., Lowe, H. L., Karamani, A., Ensell, L., Chatterton, W., Pusok, M., Dadrah, A., Symmonds, A., Sluga, G., Molnar, Z., Baker, P., Bonner, S., Essex, S., Barton, E., Padgett, D., Scott, G., Greenaway, J., Payne, B. A. I., Burton-Fanning, S., Waugh, S., Raviprakash, V., Sheriff, N., Blakey, V., Williams, L. -A., Moore, J., Stonehouse, S., Smith, L., Davidson, R. K., Bedford, L., Coupland, L., Wright, V., Chappell, J. G., Tsoleridis, T., Ball, J., Khakh, M., Fleming, V. M., Lister, M. M., Howson-Wells, H. C., Boswell, T., Joseph, A., Willingham, I., Duckworth, N., Walsh, S., Wise, E., Moore, N., Mori, M., Cortes, N., Kidd, S., Williams, R., Gifford, L., Bicknell, K., Wyllie, S., Lloyd, A., Impey, R., Malone, C. S., Cogger, B. J., Levene, N., Monaghan, L., Keeley, A. J., Partridge, D. G., Raza, M., Evans, C., Johnson, K., Abnizova, I., Aigrain, L., Ali, M., Allen, L., Anderson, R., Ariani, C., Austin-Guest, S., Bala, S., Bassett, A., Battleday, K., Beal, J., Beale, M., Bellany, S., Bellerby, T., Bellis, K., Berger, D., Berriman, M., Betteridge, E., Bevan, P., Binley, S., Bishop, J., Blackburn, K., Bonfield, J., Boughton, N., Bowker, S., Brendler-Spaeth, T., Bronner, I., Brooklyn, T., Buddenborg, S. K., Bush, R., Caetano, C., Cagan, A., Carter, N., Cartwright, J., Monteiro, T. C., Chapman, L., Chillingworth, T. -J., Clapham, P., Clark, R., Clarke, A., Clarke, C., Cole, D., Cook, E., Coppola, M., Cornell, L., Cornwell, C., Corton, C., Crackett, A., Cranage, A., Craven, H., Craw, S., Crawford, M., Cutts, T., Dabrowska, M., Davies, M., Dawson, J., Day, C., Densem, A., Dibling, T., Dockree, C., Dodd, D., Dogga, S., Dougherty, M., Dove, A., Drummond, L., Dudek, M., Durrant, L., Easthope, E., Eckert, S., Ellis, P., Farr, B., Fenton, M., Ferrero, M., Flack, N., Fordham, H., Forsythe, G., Francis, M., Fraser, A., Freeman, A., Galvin, A., Garcia-Casado, M., Gedny, A., Girgis, S., Glover, J., Goodwin, S., Gould, O., Gray, A., Gray, E., Griffiths, C., Gu, Y., Guerin, F., Hamilton, W., Hanks, H., Harrison, E., Harrott, A., Harry, E., Harvison, J., Heath, P., Hernandez-Koutoucheva, A., Hobbs, R., Holland, D., Holmes, S., Hornett, G., Hough, N., Huckle, L., Hughes-Hallet, L., Hunter, A., Inglis, S., Iqbal, S., Jackson, A., Jackson, D., Verdejo, C. J., Jones, M., Kallepally, K., Kay, K., Keatley, J., Keith, A., King, A., Kitchin, L., Kleanthous, M., Klimekova, M., Korlevic, P., Krasheninnkova, K., Lane, G., Langford, C., Laverack, A., Law, K., Lensing, S., Lewis-Wade, A., Liddle, J., Lin, Q., Lindsay, S., Linsdell, S., Long, R., Lovell, J., Mack, J., Maddison, M., Makunin, A., Mamun, I., Mansfield, J., Marriott, N., Martin, M., Mayho, M., Mccarthy, S., Mcclintock, J., Mchugh, S., Mcminn, L., Meadows, C., Mobley, E., Moll, R., Morra, M., Morrow, L., Murie, K., Nash, S., Nathwani, C., Naydenova, P., Neaverson, A., Nerou, E., Nicholson, J., Nimz, T., Noell, G. G., O'Meara, S., Ohan, V., Olney, C., Ormond, D., Oszlanczi, A., Pang, Y. F., Pardubska, B., Park, N., Parmar, A., Patel, G., Payne, M., Peacock, S., Petersen, A., Plowman, D., Preston, T., Puethe, C., Quail, M., Rajan, D., Rance, R., Rawlings, S., Redshaw, N., Reynolds, J., Reynolds, M., Rice, S., Richardson, M., Roberts, C., Robinson, K., Robinson, M., Robinson, D., Rogers, H., Rojo, E. M., Roopra, D., Rose, M., Rudd, L., Sadri, R., Salmon, N., Saul, D., Schwach, F., Scott, C., Seekings, P., Shirley, L., Simms, A., Sinnott, M., Sivadasan, S., Siwek, B., Sizer, D., Skeldon, K., Skelton, J., Slater-Tunstill, J., Sloper, L., Smerdon, N., Smith, C., Smith, J., Smith, K., Smith, M., Smith, S., Smith, T., Sneade, L., Soria, C. D., Sousa, C., Souster, E., Sparkes, A., Spencer-Chapman, M., Squares, J., Steed, C., Stickland, T., Still, I., Stratton, M., Strickland, M., Swann, A., Swiatkowska, A., Sycamore, N., Swift, E., Symons, E., Szluha, S., Taluy, E., Tao, N., Taylor, K., Thompson, S., Thompson, M., Thomson, M., Thomson, N., Thurston, S., Toombs, D., Topping, B., Tovar-Corona, J., Ungureanu, D., Uphill, J., Urbanova, J., Jansen Van, P., Vancollie, V., Voak, P., Walker, D., Walker, M., Waller, M., Ward, G., Weatherhogg, C., Webb, N., Wells, A., Wells, E., Westwood, L., Whipp, T., Whiteley, T., Whitton, G., Whitwham, A., Widaa, S., Williams, M., Wilson, M., Wright, S., Farr, B. W., Quail, M. A., Thurston, S. A. J., Bronner, I. F., Redshaw, N. M., Lensing, S. V., Balcazar, C. E., Gallagher, M. D., Williamson, K. A., Stanton, T. D., Michelsen, M. L., Warwick-Dugdale, J., Manley, R., Farbos, A., Harrison, J. W., Sambles, C. M., Studholme, D. J., Lackenby, A., Mbisa, T., Platt, S., Miah, S., Bibby, D., Manso, C., Hubb, J., Dabrera, G., Ramsay, M., Bradshaw, D., Schaefer, U., Groves, N., Gallagher, E., Lee, D., Williams, D., Ellaby, N., Hartman, H., Manesis, N., Patel, V., Ledesma, J., Twohig, K. A., Allara, E., Pearson, C., Cheng, J. K. J., Bridgewater, H. E., Frost, L. R., Taylor-Joyce, G., Brown, P. E., Tong, L., Broos, A., Mair, D., Nichols, J., Carmichael, S. N., Smollett, K. L., Nomikou, K., Aranday-Cortes, E., Johnson, N., Nickbakhsh, S., Vamos, E. E., Hughes, M., Rainbow, L., Eccles, R., Nelson, C., Whitehead, M., Gregory, R., Gemmell, M., Wierzbicki, C., Webster, H. J., Fisher, C. L., Signell, A. W., Betancor, G., Wilson, H. D., Nebbia, G., Flaviani, F., Cerda, A. C., Merrill, T. V., Wilson, R. E., Cotic, M., Bayzid, N., Thompson, T., Acheson, E., Rushton, S., O'Brien, S., Baker, D. J., Rudder, S., Aydin, A., Sang, F., Debebe, J., Francois, S., Vasylyeva, T. I., Zamudio, M. E., Gutierrez, B., Marchbank, A., Maksimovic, J., Spellman, K., Mccluggage, K., Morgan, M., Beer, R., Afifi, S., Workman, T., Fuller, W., Bresner, C., Angyal, A., Green, L. R., Parsons, P. J., Tucker, R. M., Brown, R., Whiteley, M., Rowe, W., Siveroni, I., Le-Viet, T., Gaskin, A., Johnson, R., Sharrocks, K., Blane, E., Modis, Y., Leigh, K. E., Briggs, J. A. G., van Gils, M. J., Smith, K. G. C., Bradley, J. R., Doffinger, R., Ceron-Gutierrez, L., Barcenas-Morales, G., Pollock, D. D., Goldstein, R. A., Smielewska, A., Skittrall, J. P., Gouliouris, T., Goodfellow, I. G., Gkrania-Klotsas, E., Illingworth, C. J. R., Mccoy, L. E., Gupta, R. K., Medical Microbiology and Infection Prevention, AII - Infectious diseases, Collier, Dami A [0000-0001-5446-4423], Jahun, Aminu [0000-0002-4585-1701], Temperton, Nigel [0000-0002-7978-3815], Modis, Yorgo [0000-0002-6084-0429], Briggs, John AG [0000-0003-3990-6910], Goldstein, Richard A [0000-0001-5148-4672], Skittrall, Jordan P [0000-0002-8228-3758], Gkrania-Klotsas, Effrossyni [0000-0002-0930-8330], McCoy, Laura E [0000-0001-9503-7946], Gupta, Ravindra K [0000-0001-9751-1808], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Male, Time Factors, viruses, Passive, Antibodies, Viral, CITIID-NIHR BioResource COVID-19 Collaboration, 2.1 Biological and endogenous factors, Viral, Aetiology, Neutralizing, Lung, Phylogeny, neutralising antibodies, Infectivity, education.field_of_study, Genome, Multidisciplinary, Alanine, biology, High-Throughput Nucleotide Sequencing, Viral Load, Spike Glycoprotein, Virus Shedding, Adenosine Monophosphate, Aged, Antibodies, Neutralizing, COVID-19, Chronic Disease, Genome, Viral, Humans, Immune Evasion, Immune Tolerance, Immunization, Passive, Immunosuppression Therapy, Mutagenesis, Mutant Proteins, Mutation, SARS-CoV-2, Spike Glycoprotein, Coronavirus, Evolution, Molecular, Infectious Diseases, Pneumonia & Influenza, Antibody, Infection, Viral load, Biotechnology, Evolution, General Science & Technology, antibody escape, Convalescent plasma, 030106 microbiology, Population, evasion, Antibodies, Virus, Article, Vaccine Related, resistance, 03 medical and health sciences, Immune system, COVID-19 Genomics UK (COG-UK) Consortium, Biodefense, Genetics, Viral shedding, education, COVID-19 Serotherapy, QR355, Prevention, Wild type, Molecular, Pneumonia, Virology, COVID-19 Drug Treatment, Coronavirus, Emerging Infectious Diseases, Good Health and Well Being, 030104 developmental biology, biology.protein, Immunization, immune suppression, mutation
Abstract

The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is critical for virus infection through the engagement of the human ACE2 protein1 and is a major antibody target. Here we show that chronic infection with SARS-CoV-2 leads to viral evolution and reduced sensitivity to neutralizing antibodies in an immunosuppressed individual treated with convalescent plasma, by generating whole-genome ultra-deep sequences for 23 time points that span 101 days and using in vitro techniques to characterize the mutations revealed by sequencing. There was little change in the overall structure of the viral population after two courses of remdesivir during the first 57 days. However, after convalescent plasma therapy, we observed large, dynamic shifts in the viral population, with the emergence of a dominant viral strain that contained a substitution (D796H) in the S2 subunit and a deletion (ΔH69/ΔV70) in the S1 N-terminal domain of the spike protein. As passively transferred serum antibodies diminished, viruses with the escape genotype were reduced in frequency, before returning during a final, unsuccessful course of convalescent plasma treatment. In vitro, the spike double mutant bearing both ΔH69/ΔV70 and D796H conferred modestly decreased sensitivity to convalescent plasma, while maintaining infectivity levels that were similar to the wild-type virus.The spike substitution mutant D796H appeared to be the main contributor to the decreased susceptibility to neutralizing antibodies, but this mutation resulted in an infectivity defect. The spike deletion mutant ΔH69/ΔV70 had a twofold higher level of infectivity than wild-type SARS-CoV-2, possibly compensating for the reduced infectivity of the D796H mutation. These data reveal strong selection on SARS-CoV-2 during convalescent plasma therapy, which is associated with the emergence of viral variants that show evidence of reduced susceptibility to neutralizing antibodies in immunosuppressed individuals.

Published
2021

9. Sensitivity of SARS-CoV-2 B.1.1.7 to mRNA vaccine-elicited antibodies

Author

Collier, D. A., De Marco, A., Ferreira, I. A. T. M., Meng, B., Datir, R. P., Walls, A. C., Kemp, S. A., Bassi, J., Pinto, D., Silacci-Fregni, C., Bianchi, S., Tortorici, M. A., Bowen, J., Culap, K., Jaconi, S., Cameroni, E., Snell, G., Pizzuto, M. S., Pellanda, A. F., Garzoni, C., Riva, A., Baker, S., Dougan, G., Hess, C., Kingston, N., Lehner, P. J., Lyons, P. A., Matheson, N. J., Owehand, W. H., Saunders, C., Summers, C., Thaventhiran, J. E. D., Toshner, M., Weekes, M. P., Bucke, A., Calder, J., Canna, L., Domingo, J., Elmer, A., Fuller, S., Harris, J., Hewitt, S., Kennet, J., Jose, S., Kourampa, J., Meadows, A., O'Brien, C., Price, J., Publico, C., Rastall, R., Ribeiro, C., Rowlands, J., Ruffolo, V., Tordesillas, H., Bullman, B., Dunmore, B. J., Fawke, S., Graf, S., Hodgson, J., Huang, C., Hunter, K., Jones, E., Legchenko, E., Matara, C., Martin, J., Mescia, F., O'Donnell, C., Pointon, L., Pond, N., Shih, J., Sutcliffe, R., Tilly, T., Treacy, C., Tong, Z., Wood, J., Wylot, M., Bergamaschi, L., Betancourt, A., Bower, G., Cossetti, C., De Sa, A., Epping, M., Grenfell, R., Hinch, A., Huhn, O., Jackson, S., Jarvis, I., Lewis, D., Marsden, J., Nice, F., Okecha, G., Omarjee, O., Perera, M., Richoz, N., Romashova, V., Yarkoni, N. S., Sharma, R., Stefanucci, L., Stephens, J., Strezlecki, M., Turner, L., De Bie, E. M. D. D., Bunclark, K., Josipovic, M., Mackay, M., Rossi, S., Selvan, M., Spencer, S., Yong, C., Ansaripour, A., Michael, A., Mwaura, L., Patterson, C., Polwarth, G., Polgarova, P., di Stefano, G., Fahey, C., Michel, R., Bong, S. -H., Coudert, J. 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P., Pacchiarini, N., Loveson, K. F., Carabelli, A. M., Templeton, K. E., Langford, C. F., Sillitoe, J., de Silva, T. I., Wang, D., Kwiatkowski, D., Rambaut, A., O'Grady, J., Cottrell, S., Holden, M. T. G., Thomson, E. C., Osman, H., Andersson, M., Chauhan, A. J., Hassan-Ibrahim, M. O., Lawniczak, M., Alderton, A., Chand, M., Constantinidou, C., Unnikrishnan, M., Darby, A. C., Hiscox, J. A., Paterson, S., Martincorena, I., Robertson, D. L., Volz, E. M., Page, A. J., Pybus, O. G., Bassett, A. R., Ariani, C. V., Spencer Chapman, M. H., K. K., Li, Shah, R. N., Jesudason, N. G., Taha, Y., Mchugh, M. P., Dewar, R., Jahun, A. S., Mcmurray, C., Pandey, S., Mckenna, J. P., Nelson, A., Young, G. R., Mccann, C. M., Elliott, S., Lowe, H., Temperton, B., Roy, S., Price, A., Rey, S., Wyles, M., Rooke, S., Shaaban, S., de Cesare, M., Letchford, L., Silveira, S., Pelosi, E., Wilson-Davies, E., Hosmillo, M., O'Toole, A., Hesketh, A. R., Stark, R., du Plessis, L., Ruis, C., Adams, H., Bourgeois, Y., Michell, S. L., Gramatopoulos, D., Edgeworth, J., Breuer, J., Todd, J. A., Fraser, C., Buck, D., John, M., Kay, G. L., Palmer, S., Peacock, S. J., Heyburn, D., Weldon, D., Robinson, E., Mcnally, A., Muir, P., Vipond, I. B., Boyes, J., Sivaprakasam, V., Salluja, T., Dervisevic, S., Meader, E. J., Park, N. R., Oliver, K., Jeffries, A. R., Ott, S., da Silva Filipe, A., Simpson, D. A., Williams, C., Masoli, J. A. H., Knight, B. A., Jones, C. R., Koshy, C., Ash, A., Casey, A., Bosworth, A., Ratcliffe, L., Xu-McCrae, L., Pymont, H. M., Hutchings, S., Berry, L., Jones, K., Halstead, F., Davis, T., Holmes, C., Iturriza-Gomara, M., Lucaci, A. O., Randell, P. A., Cox, A., Madona, P., Harris, K. A., Brown, J. R., Mahungu, T. W., Irish-Tavares, D., Haque, T., Hart, J., Witele, E., Fenton, M. L., Liggett, S., Graham, C., Swindells, E., Collins, J., Eltringham, G., Campbell, S., Mcclure, P. C., Clark, G., Sloan, T. J., Jones, C., Lynch, J., Warne, B., Leonard, S., Durham, J., Williams, T., Haldenby, S. T., Storey, N., Alikhan, N. -F., Holmes, N., Carlile, M., Perry, M., Craine, N., Lyons, R. A., Beckett, A. H., Goudarzi, S., Fearn, C., Cook, K., Dent, H., Paul, H., Davies, R., Blane, B., Girgis, S. T., Beale, M. A., Bellis, K. L., Dorman, M. J., Drury, E., Kane, L., Kay, S., Mcguigan, S., Nelson, R., Prestwood, L., Rajatileka, S., Batra, R., Williams, R. J., Kristiansen, M., Green, A., Justice, A., Mahanama, A. I. K., Samaraweera, B., Hadjirin, N. F., Quick, J., Poplawski, R., Kermack, L. M., Reynolds, N., Hall, G., Chaudhry, Y., Pinckert, M. L., Georgana, I., Moll, R. J., Thornton, A., Myers, R., Stockton, J., Williams, C. A., Yew, W. C., Trotter, A. J., Trebes, A., MacIntyre-Cockett, G., Birchley, A., Adams, A., Plimmer, A., Gatica-Wilcox, B., Mckerr, C., Hilvers, E., Jones, H., Asad, H., Coombes, J., Evans, J. M., Fina, L., Gilbert, L., Graham, L., Cronin, M., Kumziene-Summerhayes, S., Taylor, S., Jones, S., Groves, D. C., Zhang, P., Gallis, M., Louka, S. F., Starinskij, I., Jackson, C., Gourtovaia, M., Tonkin-Hill, G., Lewis, K., Tovar-Corona, J. M., James, K., Baxter, L., Alam, M. T., Orton, R. J., Hughes, J., Vattipally, S., Ragonnet-Cronin, M., Nascimento, F. F., Jorgensen, D., Boyd, O., Geidelberg, L., Zarebski, A. E., Raghwani, J., Kraemer, M. U. G., Southgate, J., Lindsey, B. B., Freeman, T. M., Keatley, J. -P., Singer, J. B., de Oliveira Martins, L., Yeats, C. A., Abudahab, K., Taylor, B. E. W., Menegazzo, M., Danesh, J., Hogsden, W., Eldirdiri, S., Kenyon, A., Mason, J., Robinson, T. I., Holmes, A., Hartley, J. A., Curran, T., Mather, A. E., Shankar, G., Jones, R., Howe, R., Morgan, S., Wastenge, E., Chapman, M. R., Mookerjee, S., Stanley, R., Smith, W., Peto, T., Eyre, D., Crook, D., Vernet, G., Kitchen, C., Gulliver, H., Merrick, I., Guest, M., Munn, R., Bradley, D. T., Wyatt, T., Beaver, C., Foulser, L., Churcher, C. M., Brooks, E., Smith, K. S., Galai, K., Mcmanus, G. M., Bolt, F., Coll, F., Meadows, L., Attwood, S. W., Davies, A., De Lacy, E., Downing, F., Edwards, S., Scarlett, G. P., Jeremiah, S., Smith, N., Leek, D., Sridhar, S., Forrest, S., Cormie, C., Gill, H. K., Dias, J., Higginson, E. E., Maes, M., Young, J., Wantoch, M., Jamrozy, D., Lo, S., Patel, M., Hill, V., Bewshea, C. M., Ellard, S., Auckland, C., Harrison, I., Bishop, C., Chalker, V., Richter, A., Beggs, A., Best, A., Percival, B., Mirza, J., Megram, O., Mayhew, M., Crawford, L., Ashcroft, F., Moles-Garcia, E., Cumley, N., Hopes, R., Asamaphan, P., Niebel, M. O., Gunson, R. N., Bradley, A., Maclean, A., Mollett, G., Blacow, R., Bird, P., Helmer, T., Fallon, K., Tang, J., Hale, A. D., Macfarlane-Smith, L. R., Harper, K. L., Carden, H., Machin, N. W., Jackson, K. A., Ahmad, S. S. Y., George, R. P., Turtle, L., O'Toole, E., Watts, J., Breen, C., Cowell, A., Alcolea-Medina, A., Charalampous, T., Patel, A., Levett, L. J., Heaney, J., Rowan, A., Taylor, G. P., Shah, D., Atkinson, L., Lee, J. C. D., Westhorpe, A. P., Jannoo, R., Lowe, H. L., Karamani, A., Ensell, L., Chatterton, W., Pusok, M., Dadrah, A., Symmonds, A., Sluga, G., Molnar, Z., Baker, P., Bonner, S., Essex, S., Barton, E., Padgett, D., Scott, G., Greenaway, J., Payne, B. A. I., Burton-Fanning, S., Waugh, S., Raviprakash, V., Sheriff, N., Blakey, V., Williams, L. -A., Moore, J., Stonehouse, S., Smith, L., Davidson, R. K., Bedford, L., Coupland, L., Wright, V., Chappell, J. G., Tsoleridis, T., Ball, J., Khakh, M., Fleming, V. M., Lister, M. M., Howson-Wells, H. C., Boswell, T., Joseph, A., Willingham, I., Duckworth, N., Walsh, S., Wise, E., Moore, N., Mori, M., Cortes, N., Kidd, S., Williams, R., Gifford, L., Bicknell, K., Wyllie, S., Lloyd, A., Impey, R., Malone, C. S., Cogger, B. J., Levene, N., Monaghan, L., Keeley, A. J., Partridge, D. G., Raza, M., Evans, C., Johnson, K., Betteridge, E., Farr, B. W., Goodwin, S., Quail, M. A., Scott, C., Shirley, L., Thurston, S. A. J., Rajan, D., Bronner, I. F., Aigrain, L., Redshaw, N. M., Lensing, S. V., Mccarthy, S., Makunin, A., Balcazar, C. E., Gallagher, M. D., Williamson, K. A., Stanton, T. D., Michelsen, M. L., Warwick-Dugdale, J., Manley, R., Farbos, A., Harrison, J. W., Sambles, C. M., Studholme, D. J., Lackenby, A., Mbisa, T., Platt, S., Miah, S., Bibby, D., Manso, C., Hubb, J., Dabrera, G., Ramsay, M., Bradshaw, D., Schaefer, U., Groves, N., Gallagher, E., Lee, D., Williams, D., Ellaby, N., Hartman, H., Manesis, N., Patel, V., Ledesma, J., Twohig, K. A., Allara, E., Pearson, C., Cheng, J. K. J., Bridgewater, H. E., Frost, L. R., Taylor-Joyce, G., Brown, P. E., Tong, L., Broos, A., Mair, D., Nichols, J., Carmichael, S. N., Smollett, K. L., Nomikou, K., Aranday-Cortes, E., Johnson, N., Nickbakhsh, S., Vamos, E. E., Hughes, M., Rainbow, L., Eccles, R., Nelson, C., Whitehead, M., Gregory, R., Gemmell, M., Wierzbicki, C., Webster, H. J., Fisher, C. L., Signell, A. W., Betancor, G., Wilson, H. D., Nebbia, G., Flaviani, F., Cerda, A. C., Merrill, T. V., Wilson, R. E., Cotic, M., Bayzid, N., Thompson, T., Acheson, E., Rushton, S., O'Brien, S., Baker, D. J., Rudder, S., Aydin, A., Sang, F., Debebe, J., Francois, S., Vasylyeva, T. I., Zamudio, M. E., Gutierrez, B., Marchbank, A., Maksimovic, J., Spellman, K., Mccluggage, K., Morgan, M., Beer, R., Afifi, S., Workman, T., Fuller, W., Bresner, C., Angyal, A., Green, L. R., Parsons, P. J., Tucker, R. M., Brown, R., Whiteley, M., Bonfield, J., Puethe, C., Whitwham, A., Liddle, J., Rowe, W., Siveroni, I., Le-Viet, T., Gaskin, A., Johnson, R., Abnizova, I., Ali, M., Allen, L., Anderson, R., Ariani, C., Austin-Guest, S., Bala, S., Bassett, A., Battleday, K., Beal, J., Beale, M., Bellany, S., Bellerby, T., Bellis, K., Berger, D., Berriman, M., Bevan, P., Binley, S., Bishop, J., Blackburn, K., Boughton, N., Bowker, S., Brendler-Spaeth, T., Bronner, I., Brooklyn, T., Buddenborg, S. K., Bush, R., Caetano, C., Cagan, A., Carter, N., Cartwright, J., Monteiro, T. C., Chapman, L., Chillingworth, T. -J., Clapham, P., Clark, R., Clarke, A., Clarke, C., Cole, D., Cook, E., Coppola, M., Cornell, L., Cornwell, C., Corton, C., Crackett, A., Cranage, A., Craven, H., Craw, S., Crawford, M., Cutts, T., Dabrowska, M., Davies, M., Dawson, J., Day, C., Densem, A., Dibling, T., Dockree, C., Dodd, D., Dogga, S., Dougherty, M., Dove, A., Drummond, L., Dudek, M., Durrant, L., Easthope, E., Eckert, S., Ellis, P., Farr, B., Fenton, M., Ferrero, M., Flack, N., Fordham, H., Forsythe, G., Francis, M., Fraser, A., Freeman, A., Galvin, A., Garcia-Casado, M., Gedny, A., Girgis, S., Glover, J., Gould, O., Gray, A., Gray, E., Griffiths, C., Gu, Y., Guerin, F., Hamilton, W., Hanks, H., Harrison, E., Harrott, A., Harry, E., Harvison, J., Heath, P., Hernandez-Koutoucheva, A., Hobbs, R., Holland, D., Holmes, S., Hornett, G., Hough, N., Huckle, L., Hughes-Hallet, L., Hunter, A., Inglis, S., Iqbal, S., Jackson, A., Jackson, D., Verdejo, C. J., Jones, M., Kallepally, K., Kay, K., Keatley, J., Keith, A., King, A., Kitchin, L., Kleanthous, M., Klimekova, M., Korlevic, P., Krasheninnkova, K., Lane, G., Langford, C., Laverack, A., Law, K., Lensing, S., Lewis-Wade, A., Lin, Q., Lindsay, S., Linsdell, S., Long, R., Lovell, J., Mack, J., Maddison, M., Mamun, I., Mansfield, J., Marriott, N., Martin, M., Mayho, M., Mcclintock, J., Mchugh, S., Mcminn, L., Meadows, C., Mobley, E., Moll, R., Morra, M., Morrow, L., Murie, K., Nash, S., Nathwani, C., Naydenova, P., Neaverson, A., Nerou, E., Nicholson, J., Nimz, T., Noell, G. G., O'Meara, S., Ohan, V., Olney, C., Ormond, D., Oszlanczi, A., Pang, Y. F., Pardubska, B., Park, N., Parmar, A., Patel, G., Payne, M., Peacock, S., Petersen, A., Plowman, D., Preston, T., Quail, M., Rance, R., Rawlings, S., Redshaw, N., Reynolds, J., Reynolds, M., Rice, S., Richardson, M., Roberts, C., Robinson, K., Robinson, M., Robinson, D., Rogers, H., Rojo, E. 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W., Lanzavecchia, A., Piccoli, L., Doffinger, R., Wills, M., Veesler, D., Corti, D., and Gupta, R. K.

Subjects
0301 basic medicine, Male, Models, Molecular, Passive, Antibodies, Viral, Neutralization, 0302 clinical medicine, Models, Monoclonal, 80 and over, Viral, Neutralizing antibody, Neutralizing, Aged, 80 and over, Vaccines, Vaccines, Synthetic, Multidisciplinary, biology, Antibodies, Monoclonal, C500, Middle Aged, C700, Spike Glycoprotein, Vaccination, Spike Glycoprotein, Coronavirus, Female, Angiotensin-Converting Enzyme 2, Antibody, Aged, Antibodies, Neutralizing, COVID-19, COVID-19 Vaccines, HEK293 Cells, Humans, Immune Evasion, Immunization, Passive, Mutation, Neutralization Tests, SARS-CoV-2, medicine.drug_class, B100, Monoclonal antibody, Antibodies, Virus, 03 medical and health sciences, Immune system, medicine, COVID-19 Serotherapy, QR355, Synthetic, Molecular, Virology, Coronavirus, 030104 developmental biology, Immunization, biology.protein, 030217 neurology & neurosurgery
Abstract

Transmission of SARS-CoV-2 is uncontrolled in many parts of the world; control is compounded in some areas by the higher transmission potential of the B.1.1.7 variant1, which has now been reported in 94 countries. It is unclear whether the response of the virus to vaccines against SARS-CoV-2 on the basis of the prototypic strain will be affected by the mutations found in B.1.1.7. Here we assess the immune responses of individuals after vaccination with the mRNA-based vaccine BNT162b22. We measured neutralizing antibody responses after the first and second immunizations using pseudoviruses that expressed the wild-type spike protein or a mutated spike protein that contained the eight amino acid changes found in the B.1.1.7 variant. The sera from individuals who received the vaccine exhibited a broad range of neutralizing titres against the wild-type pseudoviruses that were modestly reduced against the B.1.1.7 variant. This reduction was also evident in sera from some patients who had recovered from COVID-19. Decreased neutralization of the B.1.1.7 variant was also observed for monoclonal antibodies that target the N-terminal domain (9 out of 10) and the receptor-binding motif (5 out of 31), but not for monoclonal antibodies that recognize the receptor-binding domain that bind outside the receptor-binding motif. Introduction of the mutation that encodes the E484K substitution in the B.1.1.7 background to reflect a newly emerged variant of concern (VOC 202102/02) led to a more-substantial loss of neutralizing activity by vaccine-elicited antibodies and monoclonal antibodies (19 out of 31) compared with the loss of neutralizing activity conferred by the mutations in B.1.1.7 alone. The emergence of the E484K substitution in a B.1.1.7 background represents a threat to the efficacy of the BNT162b2 vaccine.

Published
2021

10. The effect of human mobility and control measures on the COVID-19 epidemic in China

Author

Kraemer, M U G, Yang, C-H, Gutierrez, B, Wu, C-H, Klein, B, Pigott, D M, du Plessis, L, Faria, N R, Li, R, Hanage, W P, Brownstein, J S, Layan, M, Vespignani, A, Tian, H, Dye, C, Pybus, O G, and Scarpino, S V

Abstract

The ongoing COVID-19 outbreak expanded rapidly throughout China. Major behavioral, clinical, and state interventions have been undertaken to mitigate the epidemic and prevent the persistence of the virus in human populations in China and worldwide. It remains unclear how these unprecedented interventions, including travel restrictions, affected COVID-19 spread in China. We use real-time mobility data from Wuhan and detailed case data including travel history to elucidate the role of case importation on transmission in cities across China and ascertain the impact of control measures. Early on, the spatial distribution of COVID-19 cases in China was explained well by human mobility data. Following the implementation of control measures, this correlation dropped and growth rates became negative in most locations, although shifts in the demographics of reported cases were still indicative of local chains of transmission outside Wuhan. This study shows that the drastic control measures implemented in China substantially mitigated the spread of COVID-19.

Published
2020

11. An integrated national scale SARS-CoV-2 genomic surveillance network

Author

Aanensen, DM, Abudahab, K, Adams, A, Afifi, S, Alam, MT, Alderton, A, Alikhan, N-F, Allan, J, Almsaud, M, Alrezaihi, A, Alruwaili, M, Amato, R, Andersson, M, Angyal, A, Aranday-Cortes, E, Ariani, C, Armstrong, SD, Asamaphan, P, Attwood, S, Aydin, A, Badhan, A, Baker, D, Baker, P, Balcazar, CE, Ball, J, Barton, AE, Bashton, M, Baxter, L, Beale, M, Beaver, C, Beckett, A, Beer, R, Beggs, A, Bell, A, Bellis, KL, Bentley, EG, Berriman, M, Betteridge, E, Bibby, D, Bicknell, K, Birchley, A, Black, G, Blane, B, Bloomfield, S, Bolt, F, Bonsall, DG, Bosworth, A, Bourgeois, Y, Boyd, O, Bradshaw, D, Breuer, J, Bridgewater, H, Brooks, T, Broos, A, Brown, JR, Brown, RL, Brunker, K, Bucca, G, Buck, D, Bull, M, Butcher, E, Caddy, SL, Caller, LG, Cambell, S, Carlile, M, Carmichael, S, Carrilero, L, Castellano, S, Chaloner, J, Chand, M, Chapman, MR, Chappell, J, Charles, I, Chauhan, AJ, Chawla, A, Cheng, E, Churcher, CM, Clark, G, Clark, JJ, Collins, J, Colquhoun, R, Connor, TR, Constantinidou, C, Coombes, J, Corden, S, Cottrell, S, Cowell, A, Curran, MD, Curran, T, Dabrera, G, Danesh, J, Darby, AC, De Cesare, M, Martins, LDO, De Silva, TI, Debebe, B, Dervisevic, S, Dewar, RA, Dia, M, Dorman, M, Dougan, G, Dover, L, Downing, F, Drury, E, Du Plessis, L, Dyal, PL, Eccles, R, Edwards, S, Ellaby, N, Elliott, S, Eltringham, G, Elumogo, N, Essex, S, Evans, CM, Evans, J, Nascimento, FF, Fairley, DJ, Farr, B, Feltwell, T, Ferguson, N, Filipe, ADS, Findlay, J, Forrest, LM, Forrest, S, Foulser, L, Francois, S, Fraser, C, Frost, L, Gallagher, E, Gallagher, MD, Garcia-Dorival, I, Gaskin, A, Gatica-Wilcox, B, Gavriil, A, Geidelberg, L, Gemmell, M, Gerada, A, Gifford, L, Gilbert, L, Gilmore, P, Gilroy, R, Girgis, S, Glaysher, S, Golubchik, T, Goncalves, S, Goodfellow, I, Goodwin, S, Graham, C, Graham, L, Grammatopoulos, D, Green, A, Green, LR, Greenaway, J, Gregory, R, Groves, DC, Groves, N, Guest, M, Gunson, R, Haldenby, S, Hall, G, Hamilton, WL, Han, X, Harris, KA, Harrison, EM, Hartley, C, Herrera, C, Hesketh, A, Heyburn, D, Hill, V, Hiscox, JA, Holden, M, Holmes, A, Holmes, N, Holt, GS, Hopes, R, Hosmillo, M, Houldcroft, CJ, Howson-Wells, H, Hubb, J, Hughe, J, Hughes, M, Hutchings, S, Impey, R, Iturriza-Gomara, M, Jackson, A, Jackson, B, Jackson, DK, Jahun, AS, James, K, Jamrozy, D, Jeffries, A, Jesudason, N, John, M, Johnson, J, Johnson, KJ, Johnson, N, Johnston, I, Jones, B, Jones, R, Jones, S, Jorgensen, D, Kane, L, Kay, GL, Kay, S, Keatley, J-P, Keeley, AJ, Khakh, M, Khokhar, FA, Kitchen, C, Knight, B, Kolyva, A, Kraemer, M, Kristiansen, M, Kumziene-Summerhayes, S, Kwiatkowski, D, Lackenby, A, Langford, C, Lawniczak, M, Thanh, L-V, Lee, D, Letchford, L, Li, K, Li, L, Liggett, S, Lindsey, BB, Livett, R, Lloyd, A, Lo, S, Lockhart, M, Loh, J, Loman, NJ, Loose, M, Lucaci, A, Ludden, C, Luu, L, Lyons, RA, MacIntyre-Cockett, G, MacLean, A, Mair, D, Maksimovic, J, Manley, R, Manso, C, Manson, J, Martincorena, I, Masoli, J, Mather, AE, Mbisa, T, McCluggage, K, McClure, P, McCrone, JT, McDonald, S, McHugh, MP, McKenna, JM, McMinn, L, McMurray, C, Meadows, L, Menegazzo, M, Meredith, LW, Merrick, I, Mestek-Boukhibar, L, Miah, S, Michell, S, Michelsen, ML, Molnar, Z, Moore, C, Moore, N, Morgan, M, Morgan, S, Muddyman, D, Muir, DA, Muir, P, Myers, R, Nastouli, E, Naydenova, P, Nelson, A, Nelson, C, Nelson, R, Nicholls, S, Nichols, J, Niebel, M, Niola, P, Nomikou, K, O'Grady, J, O'Toole, AN, O'Toole, E, Olateju, C, Orton, RJ, Osman, H, Ott, S, Pacchiarini, N, Padgett, D, Page, AJ, Palmer, S, Panchbhaya, YN, Pandey, S, Park, N, Parker, MD, Parkhill, J, Parr, YA, Parsons, PJ, Partridge, DG, Patel, M, Patterson, S, Payne, B, Peacock, SJ, Penrice-Randal, R, Perry, M, Platt, S, Poplawski, R, Prakash, R, Prestwood, L, Price, A, Price, JR, Puethe, C, Pybus, O, Pymont, H, Quail, M, Quick, J, Raghwani, J, Ragonnet-Cronin, M, Rahman, S, Rainbow, L, Rajatileka, S, Rambaut, A, Ramsay, M, Randell, PA, Randle, NP, Raviprakash, V, Raza, M, Silva, PR, Rey, S, Richter, A, Robertson, DL, Robinson, TI, Robson, SC, Rooke, S, Rowan, A, Rowe, W, Roy, S, Rudder, S, Ruis, C, Sang, F, Scarlett, G, Schaefer, U, Scott, C, Scott, G, Sethi, D, Shaaban, S, Shah, R, Sharma, P, Shawli, GT, Shepherd, J, Sherriff, N, Shirley, L, Sillitoe, J, Simpson, DA, Singer, JB, Siveroni, I, Smith, C, Smith, CP, Smith, DL, Smith, N, Smith, W, Smith-Palmer, A, Smollett, K, Southgate, J, Spellman, K, Spencer-Chapman, M, Sridhar, S, Stanley, R, Stark, R, Stewart, JP, Stockton, J, Stuart, C, Studholme, D, Swainston, N, Swindells, E, Taha, Y, Tariq, MA, Taylor, B, Taylor, GP, Taylor, S, Taylor-Joyce, G, Tedim, AP, Temperton, B, Templeton, KE, Thomson, EC, Thomson, NM, Thornton, A, Thurston, S, Todd, J, Tong, L, Tonkin-Hill, G, Torok, ME, Trebes, A, Trotter, AJ, Tsoleridis, T, Tucker, RM, Tutill, HJ, Underwood, A, Unnikrishnan, M, Vamos, E, Vasylyeva, T, Vattipally, S, Victoria, A, Vipond, B, Volz, EM, Wain, J, Wang, D, Warwick-Dugdale, J, Wastnedge, E, Watkins, J, Watts, J, Webber, M, Weeks, S, Weldon, D, Whitehead, M, Williams, CA, Williams, C, Williams, D, Williams, R, Williams, TC, Wise, E, Wright, V, Wyles, MD, Wyllie, S, Yakovleva, A, Yasir, M, Yeats, C, Yew, WC, Young, GR, Yu, X, and Zarebski, A

Subjects
Microbiology (medical), Scale (ratio), SARS-CoV-2, viruses, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), COVID-19, COVID-19 Genomics UK (COG-UK) consortiumcontact@cogconsortium.uk, C500, Genome, Viral, Genomics, Biology, C700, Microbiology, Article, Infectious Diseases, Virology, Humans, Cartography
Abstract

The Coronavirus Disease 2019 (COVID-19) Genomics UK Consortium (COG-UK) was launched in March, 2020, with £20 million support from UK Research and Innovation, the UK Department of Health and Social Care, and Wellcome Trust. The goal of this consortium is to sequence severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) for up to 230 000 patients, health-care workers, and other essential workers in the UK with COVID-19, which will help to enable the tracking of SARS-CoV-2 transmission, identify viral mutations, and integrate with health data to assess how the viral genome interacts with cofactors and consequences of COVID-19.

Published
2020

12. Emergence of the Zika virus Asian lineage in Angola: an outbreak investigation

Author

Hill, SC, Vasconcelos, J, Neto, Z, Jandondo, D, Ze-Ze, L, Aguiar, RS, Xavier, J, Theze, J, Mirandela, M, Candido, AL, Vaz, F, Dos Santos, S, Wu, C-H, Kraemer, MU, Melo, A, Schamber-Reis, BLF, de Azevedo, GS, Tanuri, A, Higa, LM, Clemente, C, Da Silva, S, da Silva Candido, D, Claro, IM, Quibuco, D, Domingos, C, Pocongo, B, Watts, AG, Khan, K, Alcantra, LC, Sabino, EC, Lackritz, E, Pybus, O, Alves, M-J, Afonso, J, and Faria, N

Abstract

BackgroundZika virus infections and suspected microcephaly cases have been reported in Angola since late 2016, but no data are available about the origins, epidemiology, and diversity of the virus. We aimed to investigate the emergence and circulation of Zika virus in Angola.MethodsDiagnostic samples collected by the Angolan Ministry of Health as part of routine arboviral surveillance were tested by real-time reverse transcription PCR by the Instituto Nacional de Investigação em Saúde (Ministry of Health, Luanda, Angola). To identify further samples positive for Zika virus and appropriate for genomic sequencing, we also tested samples from a 2017 study of people with HIV in Luanda. Portable sequencing was used to generate Angolan Zika virus genome sequences from three people positive for Zika virus infection by real-time reverse transcription PCR, including one neonate with microcephaly. Genetic and mobility data were analysed to investigate the date of introduction and geographical origin of Zika virus in Angola. Brain CT and MRI, and serological assays were done on a child with microcephaly to confirm microcephaly and assess previous Zika virus infection.FindingsSerum samples from 54 people with suspected acute Zika virus infection, 76 infants with suspected microcephaly, 24 mothers of infants with suspected microcephaly, 336 patients with suspected dengue virus or chikungunya virus infection, and 349 samples from the HIV study were tested by real-time reverse transcription PCR. Four cases identified between December, 2016, and June, 2017, tested positive for Zika virus. Analyses of viral genomic and human mobility data suggest that Zika virus was probably introduced to Angola from Brazil between July, 2015, and June, 2016. This introduction probably initiated local circulation of Zika virus in Angola that continued until at least June, 2017. The infant with microcephaly in whom CT and MRI were done had brain abnormalities consistent with congenital Zika syndrome and serological evidence for Zika virus infection.InterpretationOur analyses show that autochthonous transmission of the Asian lineage of Zika virus has taken place in Africa. Zika virus surveillance and surveillance of associated cases of microcephaly throughout the continent is crucial.FundingRoyal Society, Wellcome Trust, Global Challenges Research Fund (UK Research and Innovation), Africa Oxford, John Fell Fund, Oxford Martin School, European Research Council, Departamento de Ciência e Tecnologia/Ministério da Saúde/National Council for Scientific and Technological Development, and Ministério da Educação/Coordenação de Aperfeicoamento de Pessoal de Nível Superior.

Published
2019

13. Genomic Surveillance of Yellow Fever Virus Epidemic Waves in São Paulo, Brazil, 2017 – 2018

Author

de Souza, R. P., Hill, S. C., Thézé, J., Claro, I., Aguiar, R. S., Dellicour, S., Abade, L., Santos, F. C. P., Cunha, M. S., Nogueira, J. S., Salles, F. C. S., Rocco, I. M., Maeda, A. Y., Vasami, F. G. S., du Plessis, L., Silveira, P. P., Giovanetti, M., de Goes, J., Quick, J., Fernandes, N. C. C. A., Guerra, J. M., Réssio, R. A., Cirqueira, C. S., Iglezias, S. D., Delgado, J.D., Macedo, F. L. L., Timenetsky, M. C. S. T., de Paula, R., Spinola, R., Deus, J.T., Mucci, L.F., Tubaki, R.M., Menezes, R.M.T., Ramos, P.L., Abreu, A. L., Cruz, L. N., Loman, N., Bispo, A., Pybus, O. G., Alcantara, L. C. J., Sabino, E. C., and Faria, N. R.

Subjects
parasitic diseases
Abstract

São Paulo (SP), a densely populated state in southeast Brazil that contains one of the world’s largest urban regions, has experienced its largest yellow fever virus (YFV) outbreak in decades. Surveillance in non-human primates (NHP) is important in order to detect YFV early during an epidemic or epizootic, to quantify the magnitude of the outbreak in NHP, and to evaluate the risk of YFV spillover infection in human populations. To better understand the genetic diversity and spatial distribution of YFV during the current outbreak in southeast Brazil, we generated 46 new virus genomes from YFV positive cases identified in 18 different municipalities in SP, mostly sampled from non-human primates between April 2017 and February 2018. Our data show that most NHP cases in São Paulo state were likely caused by the introduction of a single YFV lineage from Minas Gerais to São Paulo. Phylogenetic and phylogeographic analyses of these data indicate that YFV spread southwards from Minas Gerais into São Paulo state at a typical rate of

Published
2019
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14. The Changing Epidemiological Profile of HIV-1 Subtype B Epidemic in Ukraine

Author

Vasylyeva, TI, Liulchuk, M, Du Plessis, L, Fearnhill, E, Zadorozhna, V, Babii, N, Scherbinska, A, Novitsky, V, Pybus, O, and Faria, NMRP

Subjects
Male, Geography, Epidemiology, Genetic Variation, Bayes Theorem, HIV Infections, Molecular epidemiology, HIV-1, BFSU, Ukraine, People who inject drugs, Humans, RNA, Viral, Female, Epidemics, Phylogeny
Abstract

While HIV-1 subtype B has caused a large epidemic in the Western world, its transmission in Ukraine remains poorly understood. We assessed the genetic diversity of HIV-1 subtype B viruses circulating in Ukraine, characterized the transmission group structure, and estimated key evolutionary and epidemiological parameters. We analyzed 120 HIV-1 subtype B pol sequences (including 46 newly generated) sampled from patients residing in 11 regions of Ukraine between 2002 and 2017. Phylogenies were estimated using maximum likelihood and Bayesian phylogenetic methods. A Bayesian molecular clock coalescent analysis was used to estimate effective population size dynamics and date the most recent common ancestors of identified clades. A phylodynamic birth–death model was used to estimate the effective reproductive number (Re) of these clades. We identified two phylogenetically distinct predominantly Ukrainian (≥75%) clades of HIV-1 subtype B. We found no significant transmission group structure for either clade, suggesting frequent mixing among transmission groups. The estimated dates of origin of both subtype B clades were around early 1970s, similar to the introduction of HIV-1 subtype A into Ukraine. Re was estimated to be 1.42 [95% highest posterior density (HPD) 1.26–1.56] for Clade 1 and 1.69 (95% HPD 1.49–1.84) for Clade 2. Evidently, the subtype B epidemic in the country is no longer concentrated in specific geographical regions or transmission groups. The study results highlight the necessity for strengthening preventive and monitoring efforts to reduce the further spread of HIV-1 subtype B., Aids Research and Human Retroviruses, 35 (2), ISSN:0889-2229, ISSN:1931-8405

Published
2019
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15. High-resolution evolutionary analysis of within-host hepatitis C virus infection

Author

Raghwani, J, Wu, C, Ho, C, De Jong, M, Molenkamp, R, Schinkel, J, Pybus, O, Lythgoe, K, AII - Infectious diseases, and Medical Microbiology and Infection Prevention

Subjects
hepatitis C virus, Genotype, HIV Infections, Hepacivirus, Virus Replication, Antiviral Agents, molecular epidemiology, Evolution, Molecular, Major Articles and Brief Reports, viral evolution, Drug Resistance, Viral, Humans, Recombination, Genetic, Coinfection, Genetic Variation, High-Throughput Nucleotide Sequencing, population genetics, virus diseases, Hepatitis C, Chronic, Hepatitis C, recombination, phylogenetics, Genetics, Population, Viruses, HIV-1, viral replication
Abstract

Background Despite recent breakthroughs in treatment of hepatitis C virus (HCV) infection, we have limited understanding of how virus diversity generated within individuals impacts the evolution and spread of HCV variants at the population scale. Addressing this gap is important for identifying the main sources of disease transmission and evaluating the risk of drug-resistance mutations emerging and disseminating in a population. Methods We have undertaken a high-resolution analysis of HCV within-host evolution from 4 individuals coinfected with human immunodeficiency virus 1 (HIV-1). We used long-read, deep-sequenced data of full-length HCV envelope glycoprotein, longitudinally sampled from acute to chronic HCV infection to investigate the underlying viral population and evolutionary dynamics. Results We found statistical support for population structure maintaining the within-host HCV genetic diversity in 3 out of 4 individuals. We also report the first population genetic estimate of the within-host recombination rate for HCV (0.28 × 10−7 recombination/site/year), which is considerably lower than that estimated for HIV-1 and the overall nucleotide substitution rate estimated during HCV infection. Conclusions Our findings indicate that population structure and strong genetic linkage shapes within-host HCV evolutionary dynamics. These results will guide the future investigation of potential HCV drug resistance adaptation during infection, and at the population scale., Using long-read serially sampled deep-sequenced data, we undertook a robust evolutionary analysis to formally evaluate, for the first time, whether or not HCV infection exhibits a structured viral population and the within-host HCV recombination rate.

Published
2019

17. Distinct rates and patterns of spread of the major HIV-1 subtypes in Central and East Africa

Author

Faria, R. (Rui), Vidal, N. (Nicole), Lourenco, J. (José), Raghwani, J. (Jayna), Sigaloff, K.C. (Kim), Tatem, A.J. (Andy J.), Vijver, D.A.M.C. (David) van de, Pineda-Peña, A.-C. (Andrea-Clemencia), Rose, R. (Rebecca), Wallis, C.L. (Carole L.), Ahuka-Mundeke, S. (Steve), Muyembe-Tamfum, J.-J. (Jean-Jacques), Muwonga, J. (Jérémie), Suchard, M.A. (Marc), Rinke de Wit, T.F. (Tobias), Hamers, R.L. (Raph), Ndembi, N. (Nicaise), Baele, G. (Guy), Peeters, M.C. (Marian), Pybus, O. (Oliver), Lemey, P. (Philippe), Dellicour, S. (Simon), Faria, R. (Rui), Vidal, N. (Nicole), Lourenco, J. (José), Raghwani, J. (Jayna), Sigaloff, K.C. (Kim), Tatem, A.J. (Andy J.), Vijver, D.A.M.C. (David) van de, Pineda-Peña, A.-C. (Andrea-Clemencia), Rose, R. (Rebecca), Wallis, C.L. (Carole L.), Ahuka-Mundeke, S. (Steve), Muyembe-Tamfum, J.-J. (Jean-Jacques), Muwonga, J. (Jérémie), Suchard, M.A. (Marc), Rinke de Wit, T.F. (Tobias), Hamers, R.L. (Raph), Ndembi, N. (Nicaise), Baele, G. (Guy), Peeters, M.C. (Marian), Pybus, O. (Oliver), Lemey, P. (Philippe), and Dellicour, S. (Simon)

Abstract

Since the ignition of the HIV-1 group M pandemic in the beginning of the 20th century, group M lineages have spread heterogeneously throughout the world. Subtype C spread rapidly through sub-Saharan Africa and is currently the dominant HIV lineage worldwide. Yet the epidemiological and evolutionary circumstances that contributed to its epidemiological expansion remain poorly understood. Here, we analyse 346 novel pol sequences from the DRC to compare the evolutionary dynamics of the main HIV-1 lineages, subtypes A1, C and D. Our results place the origins of subtype C in the 1950s in Mbuji-Mayi, the mining city of southern DRC, while subtypes A1 and D emerged in the capital city of Kinshasa, and subtypes H and J in the less accessible port city of Matadi. Following a 15-year period of local transmission in southern DRC, we find that subtype C spread at least three-fold faster than other subtypes circulating in Central and East Africa. In conclusion, our results shed light on the origins of HIV-1 main lineages and suggest that socio-historical rather than evolutionary factors may have determined the epidemiological fate of subtype C in sub-Saharan Africa.

Published
2019
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21. Role for migratory wild birds in the global spread of avian influenza H5N8

Author

Lycett, S J, Bodewes, R, Pohlmann, A, Banks, J, Banyai, K, Boni, MF, Bouwstra, R, Breed, AC, Brown, IH, Chen, HL, Dan, A, DeLiberto, T J, Diep, N, Gilbert, M, Hill, S, Ip, H S, Ke, CW, Kida, H, Killian, M L, Koopmans, Marion, Kwon, J H, Lee, D H, Lee, YJ, Lu, L, Monne, I, Pasick, J, Pybus, O G, Rambaut, A, Robinson, T P, Sakoda, Y, Zohari, S, Song, C S, Swayne, DE, Torchetti, M K, Tsai, H J, Fouchier, Ron, Beer, M, Woolhouse, M, Kuiken, Thijs, and Virology

Subjects
0301 basic medicine, viruses, medicine.disease_cause, Poultry, Disease Outbreaks, PHYLOGEOGRAPHY, Japan, Waterfowl, Influenza A Virus, H5N8 Subtype, PHYLOGENETIC ANALYSIS, Clade, Multidisciplinary, biology, virus diseases, Virology & Molecular Biology, Europe, Phylogeography, Hemagglutinins, PBR Biodiversity and genetic variation, Reassortant Viruses, animal structures, MIGRATION, 030106 microbiology, Neuraminidase, Hemagglutinin (influenza), Epidemics/veterinary, H5N1 genetic structure, Article, Virus, Birds, 03 medical and health sciences, PBR Biodiversiteit en Genetische Variatie, Influenza, Human, Republic of Korea, medicine, Animals, Humans, Life Science, Outbreak, biology.organism_classification, Virology, Influenza A virus subtype H5N1, Virologie & Moleculaire Biologie, 030104 developmental biology, Influenza in Birds, North America, biology.protein, Animal Migration, AVIAN INFLUENZA
Abstract

Migration of influenza in wild birds Virus surveillance in wild birds could offer an early warning system that, combined with adequate farm hygiene, would lead to effective influenza control in poultry units. The Global Consortium for H5N8 and Related Influenza Viruses found that the H5 segment common to the highly pathogenic avian influenza viruses readily reassorts with other influenza viruses (see the Perspective by Russell). H5 is thus a continual source of new pathogenic variants. These data also show that the H5N8 virus that recently caused serious outbreaks in European and North American poultry farms came from migrant ducks, swans, and geese that meet at their Arctic breeding grounds. Because the virus is so infectious, culling wild birds is not an effective control measure. Science , this issue p. 213 ; see also p. 174

Published
2016

22. Reconstruction and prediction of viral disease epidemics

Author

Kraemer, M., Cummings, D., Funk, S., Reiner Jr., R., Faria, N., Pybus, O., Cauchemez, S., Harvard Medical School [Boston] (HMS), Boston Children's Hospital, University of Oxford, University of Florida [Gainesville] (UF), London School of Hygiene and Tropical Medicine (LSHTM), University of Washington [Seattle], Modélisation mathématique des maladies infectieuses - Mathematical modelling of Infectious Diseases, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Centre de Bioinformatique, Biostatistique et Biologie Intégrative (C3BI), MUGK is supported by The Branco Weiss Fellowship – Society in Science, administered by the ETH Zurich and acknowledges funding from a Training Grant from the National Institute of Child Health and Human Development (T32HD040128) and the National Library of Medicine of the National Institutes of Health (R01LM010812, R01LM011965). OGP acknowledges support from the Oxford Martin School. SC acknowledges financial support from the Investissement d'Avenir program, the Laboratoire d'Excellence Integrative Biology of Emerging Infectious Diseases program (Grant ANR-10-LABX-62-IBEID), the Models of Infectious Disease Agent Study of the National Institute of General Medical Sciences, the AXA Research Fund. NRF is supported by a Sir Henry Dale Fellowship (204311/Z/16/Z), internal GCRF grant 005073 and John Fell Fund grant 005166. SF was supported by a Wellcome Trust Senior Research Fellowship in Basic Biomedical Science (210758/Z/18/Z)., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), University of Oxford [Oxford], and Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, medicine.medical_specialty, Epidemiology, 030106 microbiology, Context (language use), Disease, Diagnostic tools, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, medicine, real-time prediction, viral epidemics, 030212 general & internal medicine, [MATH]Mathematics [math], Environmental planning, Ebola virus, Transmission (medicine), Public health, Yellow fever, medicine.disease, 3. Good health, Infectious Diseases, Geography, Viral disease, Geographic spread
Abstract

A growing number of infectious pathogens are spreading among geographic regions. Some pathogens that were previously not considered to pose a general threat to human health have emerged at regional and global scales, such as Zika and Ebola Virus Disease. Other pathogens, such as yellow fever virus, were previously thought to be under control but have recently re-emerged, causing new challenges to public health organisations. A wide array of new modelling techniques, aided by increased computing capabilities, novel diagnostic tools, and the increased speed and availability of genomic sequencing allow researchers to identify new pathogens more rapidly, assess the likelihood of geographic spread, and quantify the speed of human-to-human transmission. Despite some initial successes in predicting the spread of acute viral infections, the practicalities and sustainability of such approaches will need to be evaluated in the context of public health responses.

Published
2018
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23. Molecular evolution, diversity and adaptation of H7N9 viruses in China during 2013-2017

Author

Lu, J, Raghwani, J, Pryce, R, Bowden, T A, Thézé, J, Huang, S, Song, Y, Zou, L, Liang, L, Bai, R, Jing, Y, Zhou, P, Kang, M, Yi, L, Wu, J, Pybus, O G, and Ke, C

Abstract

The substantial increase in prevalence and emergence of antigenically divergent or highly pathogenic influenza A(H7N9) viruses during 2016–17 raises concerns about the epizootic potential of these viruses. We investigated the evolution and adaptation of H7N9 viruses by analyzing available data and newly generated virus sequences isolated in Guangdong Province, China, during 2015–2017. Phylogenetic analyses showed that circulating H7N9 viruses belong to distinct lineages with differing spatial distributions. Hemagglutination inhibition assays performed on serum samples from patients infected with these viruses identified 3 antigenic clusters for 16 strains of different virus lineages. We used ancestral sequence reconstruction to identify parallel amino acid changes on multiple separate lineages. We inferred that mutations in hemagglutinin occur primarily at sites involved in receptor recognition or antigenicity. Our results indicate that highly pathogenic strains likely emerged from viruses circulating in eastern Guangdong Province during March 2016 and are associated with a high rate of adaptive molecular evolution.

Published
2018

24. Genomic epidemiology reconstructs the introduction and spread of Zika virus in Central America and Mexico

Author

Thézé, J, Li, T, du Plessis, L, Bouquet, J, Kraemer, M, Somasekar, S, Yu, G, de Cesare, M, Balmaseda, A, Kuan, G, Harris, E, Wu, C, Ansari, A, Bowden, R, Faria, N, Yagi, S, Messenger, S, Brooks, T, Stone, M, Bloch, E, Busch, M, Munoz-Medina, J, Gonzalez-Bonilla, C, Wolinsky, S, Lopez, S, Arias, C, Bonsall, D, Chiu, C, Pybus, O, University of Oxford [Oxford], and European Research Council under the European Commission Seventh Framework Program (FP7)/European Research Council grant 614725-PATHPHYLODYN Oxford Martin School Society in Science Branco Weiss Fellowship United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD) Appeared in article as National Institute of Child Health and Human Development T32HD040128 National Library of Medicine of the NIH R01LM010812 R01LM011965 Wellcome Trust Appeared in article as Wellcome Trust Royal Society of London Appeared in article as Royal Society 204311/Z/16/Z Abbott Laboratories Appeared in article as Abbott Laboratories United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Institute of Allergy & Infectious Diseases (NIAID) Appeared in article as NIH from the National Institute of Allergy and Infectious Diseases R01AI099631 P01AI106695 U19 AI118610 R21AI129455 United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Heart Lung & Blood Institute (NHLBI) Appeared in article as NIH from the National Heart, Lung, and Blood Institute R01 HL105704 Wellcome Trust Appeared in article as Wellcome Trust core award 203141/Z/16/Z

Subjects
Adult, Immunity, Herd, Adolescent, Sequence Analysis, RNA, Zika Virus Infection, [SDV]Life Sciences [q-bio], transmission, Central America, Genome, Viral, Mosquito Vectors, Zika Virus, phylodynamics, bait capture enrichment, effective reproductive number, metagenomic sequencing, Child, Preschool, genomics, Humans, “spiked” primer enrichment, Metagenomics, Child, Mexico, Brazil, Phylogeny
Abstract

International audience; The Zika virus (ZIKV) epidemic in the Americas established ZIKV as a major public health threat and uncovered its association with severe diseases, including microcephaly. However, genetic epidemiology in some at-risk regions, particularly Central America and Mexico, remains limited. We report 61 ZIKV genomes from this region, generated using metagenomic sequencing with ZIKV-specific enrichment, and combine phylogenetic, epidemiological, and environmental data to reconstruct ZIKV transmission. These analyses revealed multiple independent ZIKV introductions to Central America and Mexico. One introduction, likely from Brazil via Honduras, led to most infections and the undetected spread of ZIKV through the region from late 2014. Multiple lines of evidence indicate biannual peaks of ZIKV transmission in the region, likely driven by varying local environmental conditions for mosquito vectors and herd immunity. The spatial and temporal heterogeneity of ZIKV transmission in Central America and Mexico challenges arbovirus surveillance and disease control measures. Thézé et al. examine the genomic epidemiology of Zika virus in Central America and Mexico. Following its likely introduction to Honduras in 2014, the virus spread undetected in the region. Genetic and epidemiological data indicate that biannual transmission peaks occurred, and could potentially be explained by local variation in mosquito abundance.

Published
2018

25. Hologenomic adaptations underlying the evolution of sanguivory in the common vampire bat.

Author

Zepeda Mendoza, M., Xiong, Z., Escalera-Zamudio, M., Runge, A., Thézé, J., Streicker, D., Frank, H., Loza-Rubio, E., Liu, S., Ryder, O., Samaniego Castruita, J., Katzourakis, A., Pacheco, G., Taboada, B., Löber, U., Pybus, O., Li, Y., Rojas-Anaya, E., Bohmann, K., Carmona Baez, A., Arias, C., Greenwood, A., Bertelsen, M., White, Nicole, Bunce, Michael, Zhang, G., Sicheritz-Pontén, T., Gilbert, M., Zepeda Mendoza, M., Xiong, Z., Escalera-Zamudio, M., Runge, A., Thézé, J., Streicker, D., Frank, H., Loza-Rubio, E., Liu, S., Ryder, O., Samaniego Castruita, J., Katzourakis, A., Pacheco, G., Taboada, B., Löber, U., Pybus, O., Li, Y., Rojas-Anaya, E., Bohmann, K., Carmona Baez, A., Arias, C., Greenwood, A., Bertelsen, M., White, Nicole, Bunce, Michael, Zhang, G., Sicheritz-Pontén, T., and Gilbert, M.

Abstract

Adaptation to specialized diets often requires modifications at both genomic and microbiome levels. We applied a hologenomic approach to the common vampire bat (Desmodus rotundus), one of the only three obligate blood-feeding (sanguivorous) mammals, to study the evolution of its complex dietary adaptation. Specifically, we assembled its high-quality reference genome (scaffold N50?=?26.9?Mb, contig N50?=?36.6?kb) and gut metagenome, and compared them against those of insectivorous, frugivorous and carnivorous bats. Our analyses showed a particular common vampire bat genomic landscape regarding integrated viral elements, a dietary and phylogenetic influence on gut microbiome taxonomic and functional profiles, and that both genetic elements harbour key traits related to the nutritional (for example, vitamin and lipid shortage) and non-nutritional (for example, nitrogen waste and osmotic homeostasis) challenges of sanguivory. These findings highlight the value of a holistic study of both the host and its microbiota when attempting to decipher adaptations underlying radical dietary lifestyles.

Published
2018

26. Defining HIV-1 transmission clusters based on sequence data: A systematic review and perspectives

Author

Pybus, O, Hassan, A, Sanders, E, Albert, J, and Esbjoernsson, J

Subjects
virus diseases
Abstract

Understanding HIV-1 transmission dynamics is relevant to both screening and intervention strategies of HIV-1 infection. Commonly, HIV-1 transmission chains are determined based on sequence similarity assessed either directly from a sequence alignment or by inferring a phylogenetic tree. This review is aimed at both non-experts interested in understanding and interpreting studies of HIV-1 transmission, and experts interested in finding the most appropriate cluster definition for a specific dataset and research question. We start by introducing the concepts and methodologies of how HIV-1 transmission clusters usually have been defined. We then present the results of a systematic review of 105 HIV-1 molecular epidemiology studies summarising the most popular methods and definitions in the literature. Finally, we offer our perspectives on how HIV-1 transmission clusters can be defined and provide some guidance based on examples from real life datasets.

Published
2017

27. Spread of Yellow Fever Virus outbreak in Angola and the Democratic Republic Congo 2015-2016: a modelling study

Author

Kraemer, M, Faria, N, Reiner, R, Golding, N, Nikolay, B, Stasse, S, Johansson, M, Salje, H, Faye, O, Wint, G, Niedrig, M, Shearer, F, Hill, S, Thompson, R, Bisanzio, D, Taveira, N, Nax, H, Pradelski, B, Nsoesie, E, Murphy, N, Bogoch, I, Khan, K, Brownstein, J, Tatem, A, de Oliveira, T, Smith, D, Sall, A, Pybus, O, Hay, S, and Cauchemez, S

Subjects
Angola, Yellow fever virus, Democratic Republic of Congo
Abstract

This is an Open Access article under the CC BY license. BACKGROUND: Since late 2015, an epidemic of yellow fever has caused more than 7334 suspected cases in Angola and the Democratic Republic of the Congo, including 393 deaths. We sought to understand the spatial spread of this outbreak to optimise the use of the limited available vaccine stock. METHODS: We jointly analysed datasets describing the epidemic of yellow fever, vector suitability, human demography, and mobility in central Africa to understand and predict the spread of yellow fever virus. We used a standard logistic model to infer the district-specific yellow fever virus infection risk during the course of the epidemic in the region. FINDINGS: The early spread of yellow fever virus was characterised by fast exponential growth (doubling time of 5-7 days) and fast spatial expansion (49 districts reported cases after only 3 months) from Luanda, the capital of Angola. Early invasion was positively correlated with high population density (Pearson's r 0·52, 95% CI 0·34-0·66). The further away locations were from Luanda, the later the date of invasion (Pearson's r 0·60, 95% CI 0·52-0·66). In a Cox model, we noted that districts with higher population densities also had higher risks of sustained transmission (the hazard ratio for cases ceasing was 0·74, 95% CI 0·13-0·92 per log-unit increase in the population size of a district). A model that captured human mobility and vector suitability successfully discriminated districts with high risk of invasion from others with a lower risk (area under the curve 0·94, 95% CI 0·92-0·97). If at the start of the epidemic, sufficient vaccines had been available to target 50 out of 313 districts in the area, our model would have correctly identified 27 (84%) of the 32 districts that were eventually affected. INTERPRETATION: Our findings show the contributions of ecological and demographic factors to the ongoing spread of the yellow fever outbreak and provide estimates of the areas that could be prioritised for vaccination, although other constraints such as vaccine supply and delivery need to be accounted for before such insights can be translated into policy. info:eu-repo/semantics/publishedVersion

Published
2017

29. Evolutionary and molecular analysis of the emergent severe fever with thrombocytopenia syndrome virus

Author

Lam, T, Liu, W, Bowden, T, Cui, N, Zhuang, L, Liu, K, Zhang, Y, Cao, W, and Pybus, O

Subjects
Phlebovirus, Phylogenetic, Infectious Diseases, Evolution, Epidemiology, Virology, Public Health, Environmental and Occupational Health, Parasitology, Tick-borne disease, Severe fever with thrombocytopenia syndrome, Nucleoprotein structure, Microbiology
Abstract

In 2009, a novel Bunyavirus, called severe fever with thrombocytopenia syndrome virus (SFTSV) was identified in the vicinity of Huaiyangshan, China. Clinical symptoms of this zoonotic virus included severe fever, thrombocytopenia, and leukocytopenia, with a mortality rate of ∼10%. By the end of 2011 the disease associated with this pathogen had been reported from eleven Chinese provinces and human-to-human transmission suspected. However, current understanding of the evolution and molecular epidemiology of SFTSV before and after its identification is limited. To address this we undertake phylogenetic, evolutionary and structural analyses of all available SFTSV genetic sequences, including a new SFTSV complete genome isolated from a patient from Henan in 2011. Our discovery of a mosaic L segment sequence, which is descended from two major circulating lineages of SFTSV in China, represents the first evidence that homologous recombination plays a role in SFTSV evolution. Selection analyses indicate that negative selection is predominant in SFTSV genes, yet differences in selective forces among genes are consistent between Phlebovirus species. Further analysis reveals structural conservation between SFTSV and Rift Valley fever virus in the residues of their nucleocapsids that are responsible for oligomerisation and RNA-binding, suggesting the viruses share similar modes of higher-order assembly. We reconstruct the epidemic history of SFTSV using molecular clock and coalescent-based methods, revealing that the extant SFTSV lineages originated 50–150 years ago, and that the viral population experienced a recent growth phase that concurs with and extends the earliest serological reports of SFTSV infection. Taken together, our combined structural and phylogenetic analyses shed light into the evolutionary behaviour of SFTSV in the context of other, better-known, pathogenic Phleboviruses.

Published
2013
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30. Virus genomes reveal factors that spread and sustained the Ebola epidemic

Author

Dudas, G. (Gytis), Carvalho, L.M. (Luiz Max), Bedford, T. (Trevor), Tatem, A.J. (Andrew J.), Baele, G. (Guy), Faria, R. (Rui), Park, D.J. (Daniel J.), Ladner, J.T. (Jason T.), Arias, A., Asogun, D. (Danny), Bielejec, F. (Filip), Caddy, S.L., Cotten, M. (Matthew), D'Ambrozio, J. (Jonathan), Dellicour, S. (Simon), Di Caro, A. (Antonino), Diclaro, J.W. (Joseph W.), Duraffour, S. (Sophie), Elmore, M.J. (Michael J.), Fakoli, L.S. (Lawrence S.), Faye, O. (Ousmane), Gilbert, M.L. (Merle L.), Gevao, S.M. (Sahr M.), Gire, S. (Stephen), Gladden-Young, A. (Adrianne), Gnirke, A. (Andreas), Goba, A. (Augustine), Grant, D.S. (Donald S.), Haagmans, B.L. (Bart), Hiscox, J.A. (Julian A.), Jah, U., Kugelman, J.R. (Jeffrey R.), Liu, D. (Di), Lu, J. (Jia), Malboeuf, C.M. (Christine M.), Mate, S. (Suzanne), Matthews, D.A. (David A.), Matranga, C.B. (Christian B.), Meredith, L.W. (Luke W.), Qu, J. (James), Quick, J. (Joshua), Pas, S.D. (Suzan), Phan, M.V.T. (My V. T.), Pollakis, G. (G.), Reusken, C.B.E.M. (Chantal), Sanchez-Lockhart, M. (Mariano), Schaffner, S.F. (Stephen F.), Schieffelin, J.S. (John S.), Sealfon, R.S. (Rachel S.), Simon-Loriere, E. (Etienne), Smits, S.L. (Saskia), Stoecker, K. (Kilian), Thorne, L. (Lucy), Tobin, E.A. (Ekaete Alice), Vandi, M.A. (Mohamed A.), Watson, S.J. (Simon J.), West, K. (Kendra), Whitmer, S. (Shannon), Wiley, M.R. (Michael R.), Winnicki, S.M. (Sarah M.), Wohl, S. (Shirlee), Wölfel, R. (Roman), Yozwiak, N.L. (Nathan L.), Andersen, K.G. (Kristian G.), Blyden, S.O. (Sylvia O.), Bolay, F. (Fatorma), Carroll, M.W. (Miles W.), Dahn, B. (Bernice), Diallo, B. (Boubacar), Formenty, P. (Pierre), Fraser, C. (Christophe), Gao, G.F. (George F.), Garry, R.F. (Robert F.), Goodfellow, I. (Ian), Günther, S. (Stephan), Happi, C.T. (Christian T.), Holmes, E.C. (Edward C.), Kargbo, B. (Brima), Keïta, S. (Sakoba), Kellam, P. (Paul), Koopmans D.V.M., M.P.G. (Marion), Kuhn, J.H. (Jens H.), Loman, N.J. (Nicholas J.), Magassouba, N. (N'Faly), Naidoo, D. (Dhamari), Nichol, S.T. (Stuart T.), Nyenswah, T. (Tolbert), Palacios, G. (Gustavo), Pybus, O. (Oliver), Sabeti, P.C. (Pardis C.), Sall, A. (Amadou), Ströher, U. (Ute), Wurie, I., Suchard, M.A. (Marc), Lemey, P. (Philippe), Rambaut, A. (Andrew), Dudas, G. (Gytis), Carvalho, L.M. (Luiz Max), Bedford, T. (Trevor), Tatem, A.J. (Andrew J.), Baele, G. (Guy), Faria, R. (Rui), Park, D.J. (Daniel J.), Ladner, J.T. (Jason T.), Arias, A., Asogun, D. (Danny), Bielejec, F. (Filip), Caddy, S.L., Cotten, M. (Matthew), D'Ambrozio, J. (Jonathan), Dellicour, S. (Simon), Di Caro, A. (Antonino), Diclaro, J.W. (Joseph W.), Duraffour, S. (Sophie), Elmore, M.J. (Michael J.), Fakoli, L.S. (Lawrence S.), Faye, O. (Ousmane), Gilbert, M.L. (Merle L.), Gevao, S.M. (Sahr M.), Gire, S. (Stephen), Gladden-Young, A. (Adrianne), Gnirke, A. (Andreas), Goba, A. (Augustine), Grant, D.S. (Donald S.), Haagmans, B.L. (Bart), Hiscox, J.A. (Julian A.), Jah, U., Kugelman, J.R. (Jeffrey R.), Liu, D. (Di), Lu, J. (Jia), Malboeuf, C.M. (Christine M.), Mate, S. (Suzanne), Matthews, D.A. (David A.), Matranga, C.B. (Christian B.), Meredith, L.W. (Luke W.), Qu, J. (James), Quick, J. (Joshua), Pas, S.D. (Suzan), Phan, M.V.T. (My V. T.), Pollakis, G. (G.), Reusken, C.B.E.M. (Chantal), Sanchez-Lockhart, M. (Mariano), Schaffner, S.F. (Stephen F.), Schieffelin, J.S. (John S.), Sealfon, R.S. (Rachel S.), Simon-Loriere, E. (Etienne), Smits, S.L. (Saskia), Stoecker, K. (Kilian), Thorne, L. (Lucy), Tobin, E.A. (Ekaete Alice), Vandi, M.A. (Mohamed A.), Watson, S.J. (Simon J.), West, K. (Kendra), Whitmer, S. (Shannon), Wiley, M.R. (Michael R.), Winnicki, S.M. (Sarah M.), Wohl, S. (Shirlee), Wölfel, R. (Roman), Yozwiak, N.L. (Nathan L.), Andersen, K.G. (Kristian G.), Blyden, S.O. (Sylvia O.), Bolay, F. (Fatorma), Carroll, M.W. (Miles W.), Dahn, B. (Bernice), Diallo, B. (Boubacar), Formenty, P. (Pierre), Fraser, C. (Christophe), Gao, G.F. (George F.), Garry, R.F. (Robert F.), Goodfellow, I. (Ian), Günther, S. (Stephan), Happi, C.T. (Christian T.), Holmes, E.C. (Edward C.), Kargbo, B. (Brima), Keïta, S. (Sakoba), Kellam, P. (Paul), Koopmans D.V.M., M.P.G. (Marion), Kuhn, J.H. (Jens H.), Loman, N.J. (Nicholas J.), Magassouba, N. (N'Faly), Naidoo, D. (Dhamari), Nichol, S.T. (Stuart T.), Nyenswah, T. (Tolbert), Palacios, G. (Gustavo), Pybus, O. (Oliver), Sabeti, P.C. (Pardis C.), Sall, A. (Amadou), Ströher, U. (Ute), Wurie, I., Suchard, M.A. (Marc), Lemey, P. (Philippe), and Rambaut, A. (Andrew)

Abstract

The 2013-2016 West African epidemic caused by the Ebola virus was of unprecedented magnitude, duration and impact. Here we reconstruct the dispersal, proliferation and decline of Ebola virus throughout the region by analysing 1,610 Ebola virus genomes, which represent over 5% of the known cases. We test the association of geography, climate and demography with viral movement among administrative regions, inferring a classic 'gravity' model, with intense dispersal between larger and closer populations. Despite attenuation of international dispersal after border closures, cross-border transmission had already sown the seeds for an international epidemic, rendering these measures ineffective at curbing the epidemic. We address why the epidemic did not spread into neighbouring countries, showing that these countries were susceptible to substantial outbreaks but at lower risk of introductions. Finally, we reveal that this large epidemic was a heterogeneous and spatially dissociated collection of transmission clusters of varying size, duration and connectivity. These insights will help to inform interventions in future epidemics.

Published
2017
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31. Virus genomes reveal the factors that spread and sustained the West African Ebola epidemic

Author

Dudas, G, Carvalho, LM, Bedford, T, Tatem, A, Baele, G, Faria, N, Park, D, Ladner, J, Arias, A, Asogun, D, Bielejec, F, Caddy, S, Cotten, M, Dambrozio, J, Dellicour, S, Di Caro, A, Diclaro, J, Duraffour, S, Elmore, M, Fakoli, L, Gilbert, M, Gevao, S, Gire, S, Gladden-Young, A, Gnirke, A, Goba, A, Grant, D, Haagmans, B, Hiscox, J, Jah, U, Kargbo, B, Kugelman, J, Liu, D, Lu, J, Malboeuf, C, Mate, S, Matthews, D, Matranga, C, Meredith, L, Qu, J, Quick, J, Pas, S, Phan, MVT, Poliakis, G, Reusken, C, Sanchez-Lockhart, M, Schaffner, S, Schieffelin, J, Sealfon, R, Simon-Loriere, E, Smits, S, Stoecker, K, Thorne, L, Tobin, E, Vandi, M, Watson, S, West, K, Whitmer, S, Wiley, M, Winnicki, S, Wohl, S, Wölfel, R, Yozwiak, N, Andersen, K, Blyden, S, Bolay, F, Carroll, M, Dahn, B, Diallo, B, Formenty, P, Fraser, C, Gao, G, Garry, R, Goodfellow, I, Günther, S, Happi, C, Holmes, E, Kellam, P, Koopmans, MPG, Loman, N, Magassouba, N, Naidoo, D, Nichol, S, Nyenswah, T, Palacios, G, Pybus, O, Sabeti, P, Sall, A, Sakoba, K, Ströeher, U, Wurie, I, Suchard, M, Lemey, P, Rambaut, A, and Wellcome Trust

Subjects
viruses
Abstract

Summary The 2013-2016 epidemic of Ebola virus disease in West Africa was of unprecedented magnitude, duration and impact. Extensive collaborative sequencing projects have produced a large collection of over 1600 Ebola virus genomes, representing over 5% of known cases, unmatched for any single human epidemic. In this comprehensive analysis of this entire dataset, we reconstruct in detail the history of migration, proliferation and decline of Ebola virus throughout the region. We test the association of geography, climate, administrative boundaries, demography and culture with viral movement among 56 administrative regions. Our results show that during the outbreak viral lineages moved according to a classic ‘gravity’ model, with more intense migration between larger and more proximate population centers. Notably, we find that despite a strong attenuation of international dispersal after border closures, localized cross-border transmission beforehand had already set the seeds for an international epidemic, rendering these measures relatively ineffective in curbing the epidemic. We use this empirical evidence to address why the epidemic did not spread into neighboring countries, showing that although these regions were susceptible to developing significant outbreaks, they were also at lower risk of viral introductions. Finally, viral genome sequence data uniquely reveals this large epidemic to be a heterogeneous and spatially dissociated collection of transmission clusters of varying size, duration and connectivity. These insights will help inform approaches to intervention in such epidemics in the future.

Published
2016

32. Eight novel hepatitis c virus genomes reveal the changing taxonomic structure of genotype 6

Author

Wang, H, Yuan, Z, Barnes, E, Yuan, M, Li, C, Fu, Y, Xia, X, Li, G, Newton, P, Vongsouvath, M, Klenerman, P, Pybus, O, Murphy, D, Abe, K, and Lu, L

Subjects
RNA viruses, Genotype, Hepatitis C virus, Short Communication, Molecular Sequence Data, Genome, Viral, Hepacivirus, Biology, medicine.disease_cause, Genome, 03 medical and health sciences, Phylogenetics, Virology, Genetic variation, medicine, Humans, Base sequence, Amino Acid Sequence, Peptide sequence, Phylogeny, 030304 developmental biology, Genetics, 0303 health sciences, Phylogenetic tree, Base Sequence, 030306 microbiology, Animal, Genetic Variation, Hepatitis C, 3. Good health, RNA, Viral
Abstract

Analysis of partial hepatitis C virus sequences has revealed many novel genotype 6 variants that cannot be unambiguously classified, which obscure the distinctiveness of pre-existing subtypes. To explore this uncertainty, we obtained genomes of 98.0–98.8 % full-length for eight such variants (KM35, QC273, TV257, TV476, TV533, L349, QC271 and DH027) and characterized them using phylogenetic analyses and per cent nucleotide similarities. The former four are closely related phylogenetically to subtype 6k, TV533 and L349 to subtype 6l, QC271 to subtypes 6i and 6j, and DH027 to subtypes 6m and 6n. The former six defined a high-level grouping that comprised subtypes 6k and 6l, plus related strains. The threshold between intra- and inter-subtype diversity in this group was indistinct. We propose that similar results would be seen elsewhere if more intermediate variants like QC271 and DH027 were sampled.

Published
2016

33. A standardized framework for accurate, high-throughput genotyping of recombinant and non-recombinant viral sequences

Author

Alcantara, L, Cassol, S, Libin, P, Deforche, K, Pybus, O, Van Ranst, M, Galvão-Castro, B, Vandamme, A, and de Oliveira, T

Subjects
Hepatitis B virus, Genotype, Sequence analysis, Hepacivirus, Sequence alignment, medicine.disease_cause, Virus, law.invention, 03 medical and health sciences, law, Genetics, medicine, natural sciences, Genotyping, Phylogeny, 030304 developmental biology, Recombination, Genetic, 0303 health sciences, biology, Base Sequence, 030306 microbiology, Genetic Variation, Articles, Reference Standards, biology.organism_classification, 3. Good health, Viruses, Recombinant DNA, HIV-1, Sequence Alignment, Sequence Analysis, Software
Abstract

Human immunodeficiency virus type-1 (HIV-1), hepatitis B and C and other rapidly evolving viruses are characterized by extremely high levels of genetic diversity. To facilitate diagnosis and the development of prevention and treatment strategies that efficiently target the diversity of these viruses, and other pathogens such as human T-lymphotropic virus type-1 (HTLV-1), human herpes virus type-8 (HHV8) and human papillomavirus (HPV), we developed a rapid high-throughput-genotyping system. The method involves the alignment of a query sequence with a carefully selected set of pre-defined reference strains, followed by phylogenetic analysis of multiple overlapping segments of the alignment using a sliding window. Each segment of the query sequence is assigned the genotype and sub-genotype of the reference strain with the highest bootstrap (>70%) and bootscanning (>90%) scores. Results from all windows are combined and displayed graphically using color-coded genotypes. The new Virus-Genotyping Tools provide accurate classification of recombinant and non-recombinant viruses and are currently being assessed for their diagnostic utility. They have incorporated into several HIV drug resistance algorithms including the Stanford (http://hivdb.stanford.edu) and two European databases (http://www.umcutrecht.nl/subsite/spread-programme/ and http://www.hivrdb.org.uk/) and have been successfully used to genotype a large number of sequences in these and other databases. The tools are a PHP/JAVA web application and are freely accessible on a number of servers including: http://bioafrica.mrc.ac.za/rega-genotype/html/, http://lasp.cpqgm.fiocruz.br/virus-genotype/html/, http://jose.med.kuleuven.be/genotypetool/html/.

Published
2016

34. HIV maintains an evolving and dispersed population among multiple tissues during suppressive cART with periods of rapid expansion corresponding to the onset of cancer

Author

Rose, R, Lamers, S, Nolan, D, Maidji, E, Faria, N, Pybus, O, Dollar, J, Maruniak, S, McAvoy, A, Salemi, M, Stoddart, C, Singer, E, and McGrath, M

Subjects
virus diseases
Abstract

While combined antiretroviral therapy (cART) can result in undetectable plasma viral loads, it does not eradicate HIV infection. Furthermore, HIV-infected individuals while on cART remain at an increased risk of developing serious co-morbidities, such as cancer, neurological disease, and atherosclerosis, suggesting that during cART, tissue-based HIV may contribute to such pathologies. We obtained DNA and RNA env, nef and pol sequences using single genome sequencing from post mortem tissues of three HIV+/cART+ individuals with undetectable viral load and metastatic cancer at death, and performed time-scaled Bayesian evolutionary analyses. We used a sensitive in situ hybridization technique to visualize HIV gag-pol mRNA transcripts in cerebellum and lymph node tissues from one patient. Tissue-associated virus evolved at a similar rate in cART+ and cART- patients. Phylogenetic trees were characterized by two distinct features: 1) branching patterns consistent with constant viral evolution and dispersal amongst tissues; and 2) very recently derived clades containing both DNA and RNA sequences from multiple tissues. Cancer diagnoses were temporally associated with diversification of viral lineages. Rapid expansion of virus near death corresponded to wide-spread metastasis. HIV RNA+ cells clustered in cerebellum tissue but were dispersed in lymph node tissue, mirroring the evolutionary patterns observed for that patient. Activated, infiltrating macrophages were associated with HIV-expressing cells. Our data provide evidence that tissues serve as a sanctuary for wild-type HIV during cART and suggest the importance of macrophages as an alternative reservoir and mechanism of virus spread.

Published
2016

35. First Complete Genome Sequences of Zika Virus Isolated from Febrile Patient Sera in Ecuador

Author

Márquez, S., primary, Carrera, J., additional, Pullan, S. T., additional, Lewandowski, K., additional, Paz, V., additional, Loman, N., additional, Quick, J., additional, Bonsall, D., additional, Powell, R., additional, Thézé, J., additional, Pybus, O. G., additional, Klenerman, P., additional, Eisenberg, J., additional, Coloma, J., additional, Carroll, M. W., additional, Trueba, G., additional, and Logue, C. H., additional

Published
2017
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36. Wild waterfowl migration and domestic duck density shape the epidemiology of highly pathogenic H5N8 influenza in the Republic of Korea

Author

Hill, S C, Lee, Y-J, Song, B-M, Kang, H-M, Lee, E-K, Hanna, A, Gilbert, M, Brown, I H, and Pybus, O G

Abstract

Highly pathogenic avian influenza (HPAI) viruses threaten human and animal health yet their emergence is poorly understood, partly because sampling of the HPAI Asian-origin H5N1 lineage immediately after its identification in 1996 was comparatively sparse. The discovery of a novel H5N8 virus in 2013 provides a new opportunity to investigate HPAI emergence in greater detail. Here we investigate the origin and transmission of H5N8 in the Republic of Korea, the second country to report the new strain. We reconstruct viral spread using phylogeographic methods and interpret the results in the context of ecological data on poultry density, overwintering wild bird numbers, and bird migration patterns. Our results indicate that wild waterfowl migration and domestic duck density were important to H5N8 epidemiology. Specifically, we infer that H5N8 entered the Republic of Korea via Jeonbuk province, then spread rapidly among western provinces where densities of overwintering waterfowl and domestic ducks are higher, yet rarely persisted in eastern regions. The common ancestor of H5N8 in the Republic of Korea was estimated to have arrived during the peak of inward migration of overwintering birds. Recent virus isolations likely represent re-introductions via bird migration from an as-yet unsampled reservoir. Based on the limited data from outside the Republic of Korea, our data suggest that H5N8 may have entered Europe at least twice, and Asia at least three times from this reservoir, most likely carried by wild migrating birds.

Published
2015

37. Reconstruction and prediction of viral disease epidemics.

Author

Kraemer, M. U. G., Cummings, D. A. T., Funk, S., Reiner, R. C., Faria, N. R., Pybus, O. G., and Cauchemez, S.

Abstract

A growing number of infectious pathogens are spreading among geographic regions. Some pathogens that were previously not considered to pose a general threat to human health have emerged at regional and global scales, such as Zika and Ebola Virus Disease. Other pathogens, such as yellow fever virus, were previously thought to be under control but have recently re-emerged, causing new challenges to public health organisations. A wide array of new modelling techniques, aided by increased computing capabilities, novel diagnostic tools, and the increased speed and availability of genomic sequencing allow researchers to identify new pathogens more rapidly, assess the likelihood of geographic spread, and quantify the speed of human-to-human transmission. Despite some initial successes in predicting the spread of acute viral infections, the practicalities and sustainability of such approaches will need to be evaluated in the context of public health responses. [ABSTRACT FROM AUTHOR]

Published
2019
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38. Effect of live poultry market interventions on influenza A(H7N9) virus, Guangdong, China

Author

Wu, J. (Jie), Lu, J. (Jing), Faria, R. (Rui), Zeng, X. (Xianqiao), Song, Y. (Yingchao), Zou, L. (Lirong), Yi, L. (Lina), Liang, L. (Lijun), Ni, H. (Hanzhong), Kang, M. (Min), Zhang, X. (Xin), Huang, G. (Guofeng), Zhong, H. (Haojie), Bowden, T.A. (Thomas A.), Raghwani, J. (Jayna), He, J. (Jianfeng), He, X. (Xiang), Lin, J. (Jinyan), Koopmans D.V.M., M.P.G. (Marion), Pybus, O. (Oliver), Ke, C. (Changwen), Wu, J. (Jie), Lu, J. (Jing), Faria, R. (Rui), Zeng, X. (Xianqiao), Song, Y. (Yingchao), Zou, L. (Lirong), Yi, L. (Lina), Liang, L. (Lijun), Ni, H. (Hanzhong), Kang, M. (Min), Zhang, X. (Xin), Huang, G. (Guofeng), Zhong, H. (Haojie), Bowden, T.A. (Thomas A.), Raghwani, J. (Jayna), He, J. (Jianfeng), He, X. (Xiang), Lin, J. (Jinyan), Koopmans D.V.M., M.P.G. (Marion), Pybus, O. (Oliver), and Ke, C. (Changwen)

Abstract

Since March 2013, three waves of human infection with avian influenza A(H7N9) virus have been detected in China. To investigate virus transmission within and across epidemic waves, we used surveillance data and whole-genome analysis of viruses sampled in Guangdong during 2013–2015. We observed a geographic shift of human A(H7N9) infections from the second to the third waves. Live poultry market interventions were undertaken in epicenter cities; however, spatial phylogenetic analysis indicated that the third-wave outbreaks in central Guangdong most likely resulted from local virus persistence rather than introduction from elsewhere. Although the number of clinical cases in humans declined by 35% from

Published
2016
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39. Effect of Live Poultry Market Interventions on Influenza A(H7N9) Virus, Guangdong, China

Author

Wu, J, Lu, J, Faria, NR, Zeng, XQ, Song, Y C, Zou, LR, Yi, LN, Liang, LJ, Ni, HZ, Kang, M, Zhang, Xiandong, Huang, G F, Zhong, HJ, Bowden, T A, Raghwani, J, He, JF, He, X, Lin, JY, Koopmans, Marion, Pybus, O G, Ke, CW, Wu, J, Lu, J, Faria, NR, Zeng, XQ, Song, Y C, Zou, LR, Yi, LN, Liang, LJ, Ni, HZ, Kang, M, Zhang, Xiandong, Huang, G F, Zhong, HJ, Bowden, T A, Raghwani, J, He, JF, He, X, Lin, JY, Koopmans, Marion, Pybus, O G, and Ke, CW

Published
2016

40. The early spread and epidemic ignition of HIV-1 in human populations

Author

Faria, N. R., Rambaut, A., Suchard, M. A., Baele, G., Bedford, T., Ward, M. J., Tatem, A. J., Sousa, J. D., Arinaminpathy, N., Pepin, J., Posada, D., Peeters, Martine, Pybus, O. G., and Lemey, P.

Abstract

Thirty years after the discovery of HIV-1, the early transmission, dissemination, and establishment of the virus in human populations remain unclear. Using statistical approaches applied to HIV-1 sequence data from central Africa, we show that from the 1920s Kinshasa (in what is now the Democratic Republic of Congo) was the focus of early transmission and the source of pre-1960 pandemic viruses elsewhere. Location and dating estimates were validated using the earliest HIV-1 archival sample, also from Kinshasa. The epidemic histories of HIV-1 group M and nonpandemic group O were similar until similar to 1960, after which group M underwent an epidemiological transition and outpaced regional population growth. Our results reconstruct the early dynamics of HIV-1 and emphasize the role of social changes and transport networks in the establishment of this virus in human populations.

Published
2014

41. Phylodynamics of H5N1 avian influenza virus in Indonesia

Author

Lam, T, Hon, C, Lemey, P, Pybus, O, Shi, M, Tun, H, Li, J, Jiang, J, Holmes, E, and Leung, F

Subjects
virus diseases
Abstract

Understanding how pathogens invade and become established in novel host populations is central to the ecology and evolution of infectious disease. Influenza viruses provide unique opportunities to study these processes in nature because of their rapid evolution, extensive surveillance, large data sets and propensity to jump species boundaries. H5N1 highly pathogenic avian influenza virus (HPAIV) is a major animal pathogen and public health threat. The virus is of particular importance in Indonesia, causing severe outbreaks among poultry and sporadic human infections since 2003. However, little is known about how H5N1 HPAIV emerged and established in Indonesia. To address these questions, we analysed Indonesian H5N1 HPAIV gene sequences isolated during 2003-2007. We find that the virus originated from a single introduction into East Java between November 2002 and October 2003. This invasion was characterized by an initially rapid burst of viral genetic diversity followed by a steady rate of lineage replacement and the maintenance of genetic diversity. Several antigenic sites in the haemagglutinin gene were subject to positive selection during the early phase, suggesting that host-immune-driven selection played a role in host adaptation and expansion. Phylogeographic analyses show that after the initial invasion of H5N1, genetic variants moved both eastwards and westwards across Java, possibly involving long-distance transportation by humans. The phylodynamics we uncover share similarities with other recently studied viral invasions, thereby shedding light on the ecological and evolutionary processes that determine disease emergence in a new geographical region. © 2012 Blackwell Publishing Ltd.

Published
2012

44. Ancient urbanization predicts genetic resistance to tuberculosis

Author

Barnes, I, Duda, A, Pybus, O, and Thomas, MG

Abstract

A link between urban living and disease is seen in recent and historical records, but the presence of this association in prehistory has been difficult to assess. If the transition to urban living does result in an increase in disease-based mortality, we might expect to see evidence of increased disease resistance in longer-term urbanized populations, as the result of natural selection. To test this, we determined the frequency of an allele (SLC11A1 1729 + 55del4) associated with natural resistance to intracellular pathogens such as tuberculosis and leprosy. We found a highly significantly correlation with duration of urban settlement-populations with a long history of living in towns are better adapted to resisting these infections. This correlation remains strong when we correct for autocorrelation in allele frequencies due to shared population history. Our results therefore support the interpretation that infectious disease loads became an increasingly important cause of human mortality after the advent of urbanization, highlighting the importance of population density in determining human health and the genetic structure of human populations.

Published
2011

45. New trends of HCV infection in China revealed by genetic analysis of viral sequences determined from first-time volunteer blood donors

Author

Fu, Y, Wang, Y, Xia, W, Pybus, O, Qin, W, Lu, L, and Nelson, K

Subjects
virus diseases
Abstract

Recently, we studied hepatitis C virus (HCV) sera-prevalence among 559 890 first-time volunteer blood donors in China. From randomly selected 450 anti-HCV positive donors, we detected HCV RNA in 270 donors. In this study, we amplified HCV E1 and/or NS5B sequences from 236 of these donors followed by DNA sequencing and phylogenetic analysis. The results indicate new trends of HCV infection in China. The HCV genotype distribution differed according to the donors' region of origin. Among donors from Guangdong province, we detected subtypes 6a, 1b, 3a, 3b, 2a, and 1a at frequencies of 49.7%, 31.0%, 7.6%, 5.5%, 4.1%, and 2.1%, respectively. Among donors from outside Guangdong, we detected 1b, 2a, 6a, 3b, 3a, 6e, and 6n at frequencies 57.1%, 13.2%, 11.0%, 9.9%, 4.4%, 2.2%, and 2.2%, respectively. Although we found no significant differences among regions in age or gender, subtype 6a was more common (P < 0.001) in donors from Guangdong than those from elsewhere, whilst subtypes 1b (P < 0.02) and 2a (P < 0.001) were more frequent outside Guangdong. Disregarding origins, the male/female ratio was higher for subtype 6a-infected donors (P < 0.05) than for subtype 1b donors, whilst the mean age of subtype 2a donors was 8-10 years older (P < 0.05) than that for all other subtypes. Detailed phylogenetic analysis of our sequence data provides further insight into the transmission of HCV within China, and between China and other countries. The predominance of HCV 6a among blood donors in Guangdong is striking and mandates studies into risk factors for its acquisition.

Published
2011

46. Hepatitis C virus network dynamics among people who inject drugs in Vancouver, Canada

Author

Jacka, B, Poon, A, Applegate, TL, Krajden, M, Olmstead, A, Harrigan, R, Marshall, BD, DeBeck, K, Milloy, M-J, Lamoury, F, Pybus, O, Lima, V, Magiorkinis, G, Montoya, V, Montaner, J, Joy, J, Dore, GJ, Kerr, T, Wood, E, Grebely, J, Jacka, B, Poon, A, Applegate, TL, Krajden, M, Olmstead, A, Harrigan, R, Marshall, BD, DeBeck, K, Milloy, M-J, Lamoury, F, Pybus, O, Lima, V, Magiorkinis, G, Montoya, V, Montaner, J, Joy, J, Dore, GJ, Kerr, T, Wood, E, and Grebely, J

Published
2014

47. Unifying Viral Genetics and Human Transportation Data to Predict the Global Transmission Dynamics of Human Influenza H3N2

Author

Lemey, P. (Philippe), Rambaut, A. (Andrew), Bedford, T. (Trevor), Faria, R. (Rui), Bielejec, F. (Filip), Baele, G. (Guy), Russell, C.A. (Colin), Smith, D.J. (Derek James), Pybus, O. (Oliver), Brockmann, K., Suchard, M.A. (Marc), Lemey, P. (Philippe), Rambaut, A. (Andrew), Bedford, T. (Trevor), Faria, R. (Rui), Bielejec, F. (Filip), Baele, G. (Guy), Russell, C.A. (Colin), Smith, D.J. (Derek James), Pybus, O. (Oliver), Brockmann, K., and Suchard, M.A. (Marc)

Abstract

Information on global human movement patterns is central to spatial epidemiological models used to predict the behavior of influenza and other infectious diseases. Yet it remains difficult to test which modes of dispersal drive pathogen spread at various geographic scales using standard epidemiological data alone. Evolutionary analyses of pathogen genome sequences increasingly provide insights into the spatial dynamics of influenza viruses, but to date they have largely neglected the wealth of information on human mobility, mainly because no statistical framework exists within which viral gene sequences and empirical data on host movement can be combined. Here, we address this problem by applying a phylogeographic approach to elucidate the global spread of human influenza subtype H3N2 and assess its ability to predict the spatial spread of human influenza A viruses worldwide. Using a framework that estimates the migration history of human influenza while simultaneously testing and quantifying a range of potential predictive variables of spatial spread, we show that the global dynamics of influenza H3N2 are driven by air passenger flows, whereas at more local scales spread is also determined by processes that correlate with geographic distance. Our analyses further confirm a central role

Published
2014
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48. Tracing the HIV-1 subtype B mobility in Europe: A phylogeographic approach

Author

Paraskevis, D. Pybus, O. Magiorkinis, G. Hatzakis, A. Wensing, A.M.J. van de Vijver, D.A. Albert, J. Angarano, G. Åsjö, B. Balotta, C. Boeri, E. Camacho, R. Chaix, M.-L. Coughlan, S. Costagliola, D. De Luca, A. de Mendoza, C. Derdelinckx, I. Grossman, Z. Hamouda, O. Hoepelman, I.M. Horban, A. Korn, K. Kücherer, C. Leitner, T. Loveday, C. MacRae, E. Maljovic-Berry, I. Meyer, L. Nielsen, C. Op de Coul, E.L.M. Ormaasen, V. Perrin, L. Puchhammer-Stöckl, E. Ruiz, L. Salminen, M.O. Schmit, J.-C. Schuurman, R. Soriano, V. Stanczak, J. Stanojevic, M. Struck, D. Van Laethem, K. Violin, M. Yerly, S. Zazzi, M. Boucher, C.A. Vandamme, A.-M.

Abstract

Background: The prevalence and the origin of HIV-1 subtype B, the most prevalent circulating clade among the long-term residents in Europe, have been studied extensively. However the spatial diffusion of the epidemic from the perspective of the virus has not previously been traced. Results: In the current study we inferred the migration history of HIV-1 subtype B by way of a phylogeography of viral sequences sampled from 16 European countries and Israel. Migration events were inferred from viral phylogenies by character reconstruction using parsimony. With regard to the spatial dispersal of the HIV subtype B sequences across viral phylogenies, in most of the countries in Europe the epidemic was introduced by multiple sources and subsequently spread within local networks. Poland provides an exception where most of the infections were the result of a single point introduction. According to the significant migratory pathways, we show that there are considerable differences across Europe. Specifically, Greece, Portugal, Serbia and Spain, provide sources shedding HIV-1; Austria, Belgium and Luxembourg, on the other hand, are migratory targets, while for Denmark, Germany, Italy, Israel, Norway, the Netherlands, Sweden, Switzerland and the UK we inferred significant bidirectional migration. For Poland no significant migratory pathways were inferred. Conclusion: Subtype B phylogeographies provide a new insight about the geographical distribution of viral lineages, as well as the significant pathways of virus dispersal across Europe, suggesting that intervention strategies should also address tourists, travellers and migrants. © 2009 Paraskevis et al; licensee BioMed Central Ltd.

Published
2009

49. Increasing prevalence of HIV-1 subtype A in Greece: estimating epidemic history and origin

Author

Paraskeva, D., Magiorkinis, Emmanouil, Magiorkinis, Gkikas, Sypsa, V., Paparizos, V., Lazanas, Marios, Gargalianos, Panagiotis, Antoniadou, Anastasia, Panos, G., Chrysos, Georgios, Sambatakou, H., Karafoulidou, Anastasia, Skoutelis, A., Kordossis, Theodoros, Koratzanis, Georgios, Theodoridou, M., Daikos, Georgios L., Nikolopoulos, Georgios K., Pybus, O. G., Hatzakis, A., Nikolopoulos, Georgios K.[0000-0002-3307-0246], Magiorkinis, Gkikas [0000-0002-0141-4753], Magiorkinis, Emmanouil [0000-0001-8883-7275], Gargalianos, Panagiotis [0000-0001-7070-8635], and Antoniadou, Anastasia [0000-0003-0991-9198]

Subjects
Infection risk, Adult, Male, Hiv reverse transcriptase, Multivariate analysis, Human immunodeficiency virus (HIV), HIV Infections, Major clinical study, Dna sequence, Biology, medicine.disease_cause, Article, HIV Protease, Hiv infections, Prevalence, medicine, Humans, Immunology and Allergy, Middle aged, Variation (genetics), Phylogeny, Priority journal, Greece, Phylogenetic tree, Human immunodeficiency virus, Transmission (medicine), Confidence interval, Hiv-1, Genetic Variation, Odds ratio, Middle Aged, Human immunodeficiency virus 1 infection, Hiv protease, Virology, HIV Reverse Transcriptase, Infectious Diseases, Heterosexuality, HIV-1, Female, Human, Founder effect
Abstract

Background. In North America and Europe, human immunodeficiency virus (HIV)-1 infection has typically been dominated by subtype B transmission. More recently, however, non-B subtypes have been increasingly reported in Europe. Methods. We analyzed 1158 HIV-1-infected individuals in Greece by DNA sequencing and phylogenetic analyses of protease and partial reverse-transcriptase regions. Results. We found that the prevalence of non-B subtypes has increased over time and that this significant trend can be mainly attributed to subtype A, which eventually surpassed subtype B in prevalence in 2004 (42% and 33%, respectively). Multivariate analysis revealed that the year of HIV diagnosis was independently associated with subtype A infection (odds ratio for being infected with subtype A for a 10-year increase in the time period of diagnosis, 2.09 [95% confidence interval, 1.36-3.24]; P

Published
2007

50. Molecular epidemiology: HIV-1 and HCV sequences from Libyan outbreak

Author

de Oliveira, T, Pybus, O, Rambaut, A, Salemi, M, Cassol, S, Ciccozzi, M, Rezza, G, Gattinara, G, D'Arrigo, R, Amicosante, M, Perrin, L, Colizzi, V, and Perno, Cf

Subjects
Phylogeny, Hepacivirus, Reproducibility of Results, HIV Infections, Humans, Nurses, Physicians, Libya, Child, Hepatitis C, HIV-1, Settore MED/04 - Patologia Generale, Settore MED/07 - Microbiologia e Microbiologia Clinica
Abstract

In 1998, outbreaks of human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infection were reported in children attending Al-Fateh Hospital in Benghazi, Libya. Here we use molecular phylogenetic techniques to analyse new virus sequences from these outbreaks. We find that the HIV-1 and HCV strains were already circulating and prevalent in this hospital and its environs before the arrival in March 1998 of the foreign medical staff (five Bulgarian nurses and a Palestinian doctor) who stand accused of transmitting the HIV strain to the children.

Published
2006

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