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373 results on '"Korber, B."'

1. Consensus and Ancestral State HIV Vaccines

Author

Nickle, David C., Jensen, Mark A., Gottlieb, Geoffrey S., Shriner, Daniel, Learn, Gerald H., Rodrigo, Allen G., Mullins, James I., Gao, F., Bhattacharya, T., Gaschen, B., Taylor, J., Moore, J. P., Novitsky, V., Yusim, K., Lang, D., Foley, B., Beddows, S., Alam, M., Haynes, B., Hahn, B. H., and Korber, B.

Published
2003

3. HIV-1 Nomenclature Proposal

Author

Robertson, D. L., Anderson, J. P., Bradac, J. A., Carr, J. K., Foley, B., Funkhouser, R. K., Gao, F., Hahn, B. H., Kalish, M. L., Kuiken, C., Learn, G. H., Leitner, T., McCutchan, F., Osmanov, S., Peeters, M., Pieniazek, D., Salminen, M., Sharp, P. M., Wolinsky, S., and Korber, B.

Published
2000

6. Spike mutation pipeline reveals the emergence of a more transmissible form of SARS-CoV-2

Author

Korber, B, Fischer, WM, Gnanakaran, S, Yoon, H, Theiler, J, Abfalterer, W, Foley, B, Giorgi, EE, Bhattacharya, T, Parker, MD, Partridge, DG, Evans, CM, Freeman, TM, de Silva, TI, LaBranche, CC, and Montefiori, DC

Subjects
Genetics, 0303 health sciences, Phylogenetic tree, 030306 microbiology, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Positive selection, Context (language use), Biology, 3. Good health, law.invention, 03 medical and health sciences, Immune system, Transmission (mechanics), law, Mutation (genetic algorithm), Spike (software development), 030304 developmental biology
Abstract

SummaryWe have developed an analysis pipeline to facilitate real-time mutation tracking in SARS-CoV-2, focusing initially on the Spike (S) protein because it mediates infection of human cells and is the target of most vaccine strategies and antibody-based therapeutics. To date we have identified thirteen mutations in Spike that are accumulating. Mutations are considered in a broader phylogenetic context, geographically, and over time, to provide an early warning system to reveal mutations that may confer selective advantages in transmission or resistance to interventions. Each one is evaluated for evidence of positive selection, and the implications of the mutation are explored through structural modeling. The mutation Spike D614G is of urgent concern; it began spreading in Europe in early February, and when introduced to new regions it rapidly becomes the dominant form. Also, we present evidence of recombination between locally circulating strains, indicative of multiple strain infections. These finding have important implications for SARS-CoV-2 transmission, pathogenesis and immune interventions.

Published
2020
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8. Tetravalent immunogen assembled from conserved regions of HIV-1 and delivered as mRNA demonstrates potent preclinical T cell immunogenicity and breadth

Author

Moyo, N.A., Wee, E., Korber, B., Bahl, K., Falcone, S., Himansu, S., Wong, A.L., Dey, A.K., Feinberg, M., and Hanke, T.

Subjects
Prevention, Composition, Genetic aspects, Health aspects, AIDS vaccines -- Composition, HIV infections -- Genetic aspects -- Prevention, Immune response -- Genetic aspects, Messenger RNA -- Health aspects, HIV infection -- Genetic aspects -- Prevention
Abstract

OA12.03 N.A. Moyo (1); E. Wee (1); B. Korber (2); K. Bahl (3); S. Falcone (3); S. Himansu (3); A.L. Wong (4); A.K. Dey (4); M. Feinberg (4) and T. [...], Background: A vaccine will likely be one of the key tools for ending the HIV-1/AIDS epidemic by preventing HIV-1 spread within unin-fected populations and achieving a cure for people living with HIV-1. The currently prevailing view of the vaccine field is to introduce protective antibodies, nevertheless, an effective vaccine may need to harness protective T cells. We postulated that focusing a T-cell response on the most vulnerable regions of the HIV-1 proteome while maximizing a perfect match between the vaccine and circulating viruses will control HIV-1 replication. Here, we exploit the mRNA lipid nanoparticle (LNP) platform by designing tetravalent immunogens to assess induction of T-cell responses in a pre-clinical model. Methods: Two Gag and four Pol protein regions of the HIV-1 proteome were selected for their high conservation among the HIV-1 Group M isolates and inclusion of beneficial regions. These were computed into two complementing mosaics, which together achieved over 80% match of potential 9-mer T-cell epitopes over most of the six HIVconsvX regions. Here, using a novel epigraph algorithm, two versions of the same six regions were sequentially designed to cover additional common variants of potential 9-mer epitopes and make further improvements over the previous vaccine in matching the global HIV-1 isolates. These two mosaics and 2 epigraphs were converted into mRNA and the fully synthetic tetravalent mRNAs, collectively called HIVconsvM, were encapsulated into LNPs. Results: In a mouse model, intramuscular injection of the LNP-encapsulated mRNA induced high frequencies of T cells, which recognized seven out of seven examined H-[2.sup.d] class I-restricted epitopes in most animals. This combination of mRNA and tetravalent immunogens induced potent, broad and polyfunctional T-cell responses. There was an overall trend of a direct correlation between the magnitude of vaccine responses and valency of the vaccine cocktail both for individual epitopes and the overall 'global' response. Conclusions: Our data show a great potency of this vaccine platform for induction of T-cell responses and support evaluation of the HIV-consvM mRNA LNPs in humans, the species in which HIV-1 evolved and for which further vaccine optimizations and response analyses will be the most relevant.

Published
2021
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13. Search for the Origin of HIV and AIDS

Author

Hooper, Edward, Korber, B., Bhattacharya, T., Theiler, J., Gupta, R., Lapedes, A., Hahn, B., Gao, F., Muldoon, M., Wolinsky, S., Plotkin, Stanley A., and Koprowski, Hilary

Published
2000

15. A new classification for HIV-1

Author

Berger, E. A., Doms, R. W., Fenyo, E.-M., Korber, B. T. M., Littman, D. R., Moore, J. P., Sattentau, Q. J., Schuitemaker, H., Sodroski, J., and Weiss, R. A.

Published
1998

16. Protecting HIV databases

Author

Korber, B. T. M., Learn, G., Mullins, J. I., Hahn, B. H., Wolinsky, S., Briant, L., Puel, J., Wade, C. M., Brown, A. J. Leigh, and Guyader, M.

Published
1995

19. Duration of ruptured membranes and vertical transmission of HIV-1: a meta-analysis from 15 prospective cohort studies

Author

Bulterys, M. B., Fowler, M. G., Hanson, I. C., Lemay, M., Mayaux, M. J., Mofenson, L., Newell, M. -L., Peavy, H., Peckham, C., Read, J. S., Rother, C., Simpson, B. J., Van Dyke, R. B., Harris, D. R., Peavy, H. H., Easley, K., Khammy, A., Nugent, R. P., Mitchell, R., Owen, W., Van Dyke, R., Widmayer, S., Bardeguez, A., Hanson, C., Wiznia, A., Luzuriaga, K., Viscarello, R., Ho, D., Koup, R., Chen, I., Krogstad, P., Mullins, J., Wolinsky, S., Korber, B., Walker, B., Ammann, A., Clapp, S., Mcdonald, D., Lapointe, N., Boucher, M., Fauvel, M., Hankins, C., Samson, J., Newell, M. L., Peckham, C. S., Thorne, C. N., Giaquinto, C., Ruga, E., De Rossi, A., Truscia, D., Grosch-Worner, I., Schafer, A., Mok, J., Johnstone, F., Jiminez, J., de Alba, C., Garcia Rodriguez, M. C., Bates, I., de Josee, I., Hawkins, F., Martinez Zapico, R., Pena, J. M., Gonzalez Garcia, J., Arribas Lopez, J. R., Asensi-Botet, F., Otero, M. C., Peerez-Tamarit, D., Moya, A., Galbis, M. J., Scherpbier, H., Boer, K., Bohlin, A. B., Lindgren, S., Anzen, B., Belfrage, E., Lidin-Jansson, G., Levy, J., Barlow, P., Hainaut, M., Peltier, A., Ferrazin, A., De Maria, A., Gotta, C., Mur, A., Vinolas, M., Paya, A., Loepez-Vilchez, M. A., Coll, O., Fortuny, C., Boguna, J., Casellas Caro, M., Canet, Y., Pardi, G., Ravizza, M., Semprini, E., Castagna, C., Fiore, S., Guerra, B., Lanari, M., Bianchi, S., Bovicelli, L., Prati, E., Zanelli, S., Duse, M., Soresina, A., Scaravelli, G., Stegagno, M., De Santis, M., Muggiasca, M. L., Vigano, A., Spinillo, A., Ravagni Probizer, F., Bucceri, A., Rancilio, L., Taylor, G. P., Lyall, H., Penn, Z., Blott, M., Valerius, N. H., Martinelli, P., Buffolano, W., Tibaldi, C., Ziarati, N., Semprini, A., Della Torre, M., Parazzini, F., Dallacasa, P., Bianchi, U., Pachi, A., Mancuso, S., Villa, P., Conti, M., Principi, N., Muggiasca, M., Marchisio, P., Zara, C., Ravagni, F., Vignali, M., Rossi, G., Selvaggi, L., Greco, P., Vimercati, A., Massi, G., Innocenti, T., Fiscella, A., Sansone, M., Benedetto, C., Tadrist, B., Thevenieau, D., Gondry, J., Paulard, B., Alisy, C., Brault, D., Tordjeman, N., Mamou, J., Rozan, M., Colombani, D., Pincemaille, O., Salvetti, A., Chabanier, C., Hernandorena, X., Leroy, J., Schaal, J., Balde, P., Faucher, P., Lachassinne, E., Benoit, S., Douard, D., Hocke, C., Barjot, P., Brouard, J., Delattre, P., Stien, L., Audibert, F., Labrune, P., Vial, M., Mazy, F., Sitbon, D., Crenn-Hebert, C., Floch-Tudal, C., Akakpo, R., Daveau, C., Leblanc, A., Cesbron, P., Duval-Arnould, M., Huraux-Rendu, C., Lemerle, S., Touboul, C., Guerin, M., Maingueneau, C., Reynaud, I., Rousseau, T., Ercoil, V., Lanza, M., Denavit, M., Garnier, J., Lahsinat, K., Pia, P., Allouche, C., Nardou, M., Grall, F., May, A., Dallot, M., Lhuillier, P., Cecile, W., Mezin, R., Bech, A., Lobut, J., Algava, G., Chalvon Dermesay, A., Busuttil, R., Jacquemot, M., Bader-Meunier, B., Fridman, S., Codaccioni, X., Maxingue, F., Thomas, D., Alain, J., De Lumley, L., Tabaste, J., Bailly Salin, P., Seaume, H., Guichard, A., Kebaill, K., Roussouly, C., Botto, C., De Lanete, A., Wipff, P., Cravello, L., De Boisse, P., Leclaire, M., Michel, G., Crumiere, C., Lefevre, V., Le Lorier, B., Pauly, I., Robichez, B., Seguy, D., Delhinger, M., Rideau, F., Talon, P., Benos, P., Huret, C., Nicolas, J., Heller-Roussin, B., Saint-Leger, S., Delaporte, M., Hubert, C., De Sarcus, B., Karoubi, P., Mechinaud, F., Bertcrottiere, D., Bongain, A., Monpoux, F., De Gennes, C., Devianne, F., Nisand, I., Rousset, M., Mouchnino, G., Muray, J., Munzer, M., Quereux, C., Brossard, V., Clavier, B., Allemon, M., Rotten, D., Stephan, J., Varlet, M., Guyot, B., Narcy, P., Bardinet, F., De Caunes, F., Jeny, R., Robin, M., Raison Boulley, A., Savey, L., Berrebi, A., Tricoire, J., Borderon, J., Fignon, A., Guillot, F., Maria, B., Broyard, A., Chitrit, Y., Firtion, G., Mandelbrot, L., Lafay Pillet, M., Parat, S., Boissinot, C., Garec, N., Levine, M., Ottenwalter, A., Schaller, F., Vilmer, E., Courpotin, C., Brunner, C., Ciraru-Vigneron, N., Hatem-Gantzer, G., Fritel, X., Wallet, A., Bouille, J., Milliez, J., Bensaid Mrejen, D., Dermer, E., Noseda, G., Bardou, D., Cressaty, J., Francoual, C., Carlus Moncomble, C., Cohen, H., Blanche, S., Bastion, H., Benifla, J., Benkhatar, F., Berkane, N., Hervee, F., Ronzier, M., Mayaux, Mj., de Martino, M., Tovo, P. -A., Galli, L., Gabiano, C., Ferraris, G., Garetto, S., Palomba, E., Riva, C., Vierucci, A., de Luca, M., Farina, S., Fundaro, C., Genovese, O., Mereu, G., Forni, G. L., Casadei, A., Zuccotti, G. V., Riva, E., Cellini, M., Baraldi, C., Consolini, R., Palla, G., Ruggeri, M., Ciccimarra, F., Guarino, A., Osimani, P., Benaglia, G., Romano, A., De Mattia, D., Caselli, D., Boni, S., Dell'Erba, G., Bassanetti, F., Sticca, M., Timpano, C., Magnani, C., Salvatore, C., Lipreri, R., Tornaghi, R., Pinzani, R., Cecchi, M. T., Bezzi, T., Battisti, L., Bresciani, E., Castelli Gattinara, G., Nasi, C., Pellegatta, A., Mazza, A., Baldi, F., Altobelli, R., Deiana, M., Colnaghi, C., Tarallo, L., Tondo, U., Anastasio, E., Chiriaco, P. G., Ruggeri, C., Scott, G., Hutto, C., O'Sullivan, M., Malmsberry, A., Willoughby, A., Burns, D., Goedert, J., Landesman, S., Minkoff, H., Mendez, H., Holman, S., Rubinstein, A., Durako, S., Muenz, L., Goodwin, S., Bryson, Y., Dillon, M., Nielsen, K., Boyer, P., Liao, D., Keller, M., Deveikis, A., Nesheim, S., Lindsay, M., Lee, F., Nahmias, A., Sawyer, M., Vink, P., Farley, J., Alger, L., Abrams, E., Bamji, M., Lambert, G., Schoenbaum, E., Thomas, P., Weedon, J., Palumbo, P., Denny, T., Oleske, J., Bulterys, M., Simonds, R., Ethier-Ives, J., Rogers, M., Schluchter, M., Kutner, M., Kaplan, S., Kattan, M., Lipshultz, S., Mellins, R., Shearer, W., Sopko, G., Sloand, E., Wu, M., Kind, C., Nadal, D., Rudin, C., Siegrist, C. -A., Wyler, C. -A., Cheseaux, J. -J., Aebi, C., Gnehm, H., Schubiger, G., Klingler, J., Hunziker, U., Kuchler, H., Gianinazzi, M., Buhlmann, U., Biedermann, K., Lauper, U., Irion, O., Brunelli, A., Spoletini, G., Schreyer, A., Hosli, I., Saurenmann, E., Drack, G., Isenschmid, M., Poorbeik, M., Schupbach, J., Perrin, L., Erb, P., Joller, H., Kovacs, A., Stek, A., Chan, L., Khoury, M., Diaz, C., Pacheco-Acosta, E., Tuomala, R., Cooper, E., Mesthene, D., Pitt, J., Higgins, A., Moroso, G., Rich, K., Turpin, D., Cooper, N., Davenny, K., Thompson, B., Andiman, W., Simpson, J., THE INTERNATIONAL PERINATAL HIV, Group, Martinelli, Pasquale, Bulterys M.B., Fowler M.G., Hanson I.C., Lemay M., Mayaux M.J., Mofenson L., Newell M.-L., Peavy H., Peckham C., Read J.S., Rother C., Simpson B.J., Van Dyke R.B., Harris D.R., Peavy H.H., Easley K., Khammy A., Nugent R.P., Mitchell R., Owen W., Van Dyke R., Widmayer S., Bardeguez A., Hanson C., Wiznia A., Luzuriaga K., Viscarello R., Ho D., Koup R., Chen I., Krogstad P., Mullins J., Wolinsky S., Korber B., Walker B., Ammann A., Clapp S., McDonald D., Lapointe N., Boucher M., Fauvel M., Hankins C., Samson J., Newell M.L., Peckham C.S., Thorne C.N., Giaquinto C., Ruga E., De Rossi A., Truscia D., Grosch-Worner I., Schafer A., Mok J., Johnstone F., Jiminez J., de Alba C., Garcia Rodriguez M.C., Bates I., de Josee I., Hawkins F., Martinez Zapico R., Pena J.M., Gonzalez Garcia J., Arribas Lopez J.R., Asensi-Botet F., Otero M.C., Peerez-Tamarit D., Moya A., Galbis M.J., Scherpbier H., Boer K., Bohlin A.B., Lindgren S., Anzen B., Belfrage E., Lidin-Jansson G., Levy J., Barlow P., Hainaut M., Peltier A., Ferrazin A., De Maria A., Gotta C., Mur A., Vinolas M., Paya A., Loepez-Vilchez M.A., Coll O., Fortuny C., Boguna J., Casellas Caro M., Canet Y., Pardi G., Ravizza M., Semprini E., Castagna C., Fiore S., Guerra B., Lanari M., Bianchi S., Bovicelli L., Prati E., Zanelli S., Duse M., Soresina A., Scaravelli G., Stegagno M., De Santis M., Muggiasca M.L., Vigano A., Spinillo A., Ravagni Probizer F., Bucceri A., Rancilio L., Taylor G.P., Lyall H., Penn Z., Blott M., Valerius N.H., Martinelli P., Buffolano W., Tibaldi C., Ziarati N., Semprini A., Della Torre M., Parazzini F., Dallacasa P., Bianchi U., Pachi A., Mancuso S., Villa P., Conti M., Principi N., Muggiasca M., Marchisio P., Zara C., Ravagni F., Vignali M., Rossi G., Selvaggi L., Greco P., Vimercati A., Massi G., Innocenti T., Fiscella A., Sansone M., Benedetto C., Tadrist B., Thevenieau D., Gondry J., Paulard B., Alisy C., Brault D., Tordjeman N., Mamou J., Rozan M., Colombani D., Pincemaille O., Salvetti A., Chabanier C., Hernandorena X., Leroy J., Schaal J., Balde P., Faucher P., Lachassinne E., Benoit S., Douard D., Hocke C., Barjot P., Brouard J., Delattre P., Stien L., Audibert F., Labrune P., Vial M., Mazy F., Sitbon D., Crenn-Hebert C., Floch-Tudal C., Akakpo R., Daveau C., Leblanc A., Cesbron P., Duval-Arnould M., Huraux-Rendu C., Lemerle S., Touboul C., Guerin M., Maingueneau C., Reynaud I., Rousseau T., Ercoil V., Lanza M., Denavit M., Garnier J., Lahsinat K., Pia P., Allouche C., Nardou M., Grall F., May A., Dallot M., Lhuillier P., Cecile W., Mezin R., Bech A., Lobut J., Algava G., Chalvon Dermesay A., Busuttil R., Jacquemot M., Bader-Meunier B., Fridman S., Codaccioni X., Maxingue F., Thomas D., Alain J., De Lumley L., Tabaste J., Bailly Salin P., Seaume H., Guichard A., Kebaill K., Roussouly C., Botto C., De Lanete A., Wipff P., Cravello L., De Boisse P., Leclaire M., Michel G., Crumiere C., Lefevre V., Le Lorier B., Pauly I., Robichez B., Seguy D., Delhinger M., Rideau F., Talon P., Benos P., Huret C., Nicolas J., Heller-Roussin B., Saint-Leger S., Delaporte M., Hubert C., De Sarcus B., Karoubi P., Mechinaud F., Bertcrottiere D., Bongain A., Monpoux F., De Gennes C., Devianne F., Nisand I., Rousset M., Mouchnino G., Muray J., Munzer M., Quereux C., Brossard V., Clavier B., Allemon M., Rotten D., Stephan J., Varlet M., Guyot B., Narcy P., Bardinet F., De Caunes F., Jeny R., Robin M., Raison Boulley A., Savey L., Berrebi A., Tricoire J., Borderon J., Fignon A., Guillot F., Maria B., Broyard A., Chitrit Y., Firtion G., Mandelbrot L., Lafay Pillet M., Parat S., Boissinot C., Garec N., Levine M., Ottenwalter A., Schaller F., Vilmer E., Courpotin C., Brunner C., Ciraru-Vigneron N., Hatem-Gantzer G., Fritel X., Wallet A., Bouille J., Milliez J., Bensaid Mrejen D., Dermer E., Noseda G., Bardou D., Cressaty J., Francoual C., Carlus Moncomble C., Cohen H., Blanche S., Bastion H., Benifla J., Benkhatar F., Berkane N., Hervee F., Ronzier M., Mayaux MJ., de Martino M., Tovo P.-A., Galli L., Gabiano C., Ferraris G., Garetto S., Palomba E., Riva C., Vierucci A., de Luca M., Farina S., Fundaro C., Genovese O., Mereu G., Forni G.L., Casadei A., Zuccotti G.V., Riva E., Cellini M., Baraldi C., Consolini R., Palla G., Ruggeri M., Ciccimarra F., Guarino A., Osimani P., Benaglia G., Romano A., De Mattia D., Caselli D., Boni S., Dell'Erba G., Bassanetti F., Sticca M., Timpano C., Magnani C., Salvatore C., Lipreri R., Tornaghi R., Pinzani R., Cecchi M.T., Bezzi T., Battisti L., Bresciani E., Castelli Gattinara G., Nasi C., Pellegatta A., Mazza A., Baldi F., Altobelli R., Deiana M., Colnaghi C., Tarallo L., Tondo U., Anastasio E., Chiriaco P.G., Ruggeri C., Scott G., Hutto C., O'Sullivan M., Malmsberry A., Willoughby A., Burns D., Goedert J., Landesman S., Minkoff H., Mendez H., Holman S., Rubinstein A., Durako S., Muenz L., Goodwin S., Bryson Y., Dillon M., Nielsen K., Boyer P., Liao D., Keller M., Deveikis A., Nesheim S., Lindsay M., Lee F., Nahmias A., Sawyer M., Vink P., Farley J., Alger L., Abrams E., Bamji M., Lambert G., Schoenbaum E., Thomas P., Weedon J., Palumbo P., Denny T., Oleske J., Bulterys M., Simonds R., Ethier-Ives J., Rogers M., Schluchter M., Kutner M., Kaplan S., Kattan M., Lipshultz S., Mellins R., Shearer W., Sopko G., Sloand E., Wu M., Kind C., Nadal D., Rudin C., Siegrist C.-A., Wyler C.-A., Cheseaux J.-J., Aebi C., Gnehm H., Schubiger G., Klingler J., Hunziker U., Kuchler H., Gianinazzi M., Buhlmann U., Biedermann K., Lauper U., Irion O., Brunelli A., Spoletini G., Schreyer A., Hosli I., Saurenmann E., Drack G., Isenschmid M., Poorbeik M., Schupbach J., Perrin L., Erb P., Joller H., Kovacs A., Stek A., Chan L., Khoury M., Diaz C., Pacheco-Acosta E., Tuomala R., Cooper E., Mesthene D., Pitt J., Higgins A., Moroso G., Rich K., Turpin D., Cooper N., Davenny K., Thompson B., Andiman W., and Simpson J.

Subjects
Time Factors, Epidemiology, Infectious Disease Transmission, Prevention of perinatal transmission, Extraembryonic Membranes, Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, Cohort Studies, Pregnancy, Risk Factors, INFECTION, Vertical, Immunology and Allergy, HIV Infection, MOTHER-TO-CHILD, Pregnancy Complications, Infectious, Prospective cohort study, prevention of perinatal transmission, vertical transmission, obstetrics/gynaecology, epidemiology, Obstetrics, Transmission (medicine), Infectious, HUMAN-IMMUNODEFICIENCY-VIRUS, MOTHER-TO-CHILD, ZIDOVUDINE PROPHYLAXIS, RISK-FACTORS, TYPE-1, PREGNANCY, INFECTION, TRIAL, PREVENTION, Breast Feeding, Infectious Diseases, Meta-analysis, HUMAN-IMMUNODEFICIENCY-VIRUS, Vertical transmission, Regression Analysis, TRIAL, Female, Delivery, Obstetrics gynaecology, Human, medicine.medical_specialty, Time Factor, Ruptured membranes, Immunology, Regression Analysi, NO, ZIDOVUDINE PROPHYLAXIS, Extraembryonic Membrane, medicine, Humans, TYPE-1, business.industry, Risk Factor, Infant, Newborn, Infant, Obstetric, Delivery, Obstetric, Newborn, PREVENTION, Infectious Disease Transmission, Vertical, Pregnancy Complications, Obstetrics/gynaecology, RISK-FACTORS, Cohort Studie, business
Abstract

Objective: To test the a priori hypothesis that longer duration of ruptured membranes is associated with increased risk of vertical transmission of HIV. Design: The relationship between duration of ruptured membranes and vertical transmission of HIV was evaluated in an individual patient data meta-analysis. Methods: Eligible studies were prospective cohort studies including at least 100 mother-child pairs, from regions where HIV-infected women are counselled not to breastfeed. Analyses were restricted to vaginal deliveries and non-elective Cesarean sections; elective Cesarean section deliveries (those performed before onset of labour and before rupture of membranes) were excluded. Results: The primary analysis included 4721 deliveries with duration of ruptured membranes ≤ 24 h. After adjusting for other factors known to be associated with vertical transmission using logistic regression analysis to assess the strength of the relationship, the risk of vertical HIV transmission increased approximately 2% with an increase of 1 h in the duration of ruptured membranes [adjusted odds ratio, 1.02; 95% confidence interval, 1.01-1.04; for each 1 h increment]. There were no significant interactions of duration of ruptured membranes with study cohort or with any of the covariates, except maternal AIDS. Among women diagnosed with AIDS, the estimated probability of transmission increased from 8% to 31% with duration of ruptured membranes of 2 h and 24 h respectively (P < 0.01). Conclusions: These results support the importance of duration of ruptured membranes as a risk factor for vertical transmission of HIV and suggest that a diagnosis of AIDS in the mother at the time of delivery may potentiate the effect of duration of ruptured membranes. © 2001 Lippincott Williams & Wilkins.

Published
2001
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22. Human retroviruses and AIDS 1994

Author

Myers, G., primary, Korber, B., additional, Wain-Hobson, S., additional, Jeang, Kuan-Teh, additional, Henderson, L.E., additional, and Pavlakis, G.N., additional

Published
1995
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26. The Mode of Delivery and the Risk of Vertical Transmission of Human Immunodeficiency Virus Type 1 — A Meta-Analysis of 15 Prospective Cohort Studies

Author

Andiman, W., Boucher, M., Burns, D., Bryson, Y., Farley, J., Fowler, H., Gabiano, C., Galli, L., Hutto, C., Kind, C., Korber, B., Kovacs, A., Krogstad, P., Landesman, S., Lapointe, N., Lemay, M., Lew, J., Mandelbrot, L., Mayaux, Mj, Mellins, R., Minkoff, H., Mofenson, L., Nielsen, K., Newell, Ml, Pardi, G., Peavy, H., Peckham, C., Read, J., Rother, C., Rudin, C., Scott, G., Semprini, A., Shearer, W., Simonds, R., Simpson, B., Stek, A., Tovo, Pa, Tuomala, R., Dyke, R., Weedon, J., Martino, M., Lindsay, M., Belair, S., Chan, L., Harris, D., Kalish, L., Muenz, L., Nugent, R., Schluchter, M., Durako, S., Goodwin, S., Mitchell, R., Nourjah, P., Owen, W., Widmayer, S., Bardeguez, A., Hanson, C., Wiznia, A., Luzuriaga, K., Viscarello, R., Ho, D., Koup, R., Chen, I., Mullins, J., Wolinsky, S., Walker, B., Ammann, A., Clapp, S., Mcdonald, D., Fauvel, M., Hankins, C., Samson, J., Bailey, A., Giaquinto, C., Ruga, E., Rossi, A., Truscia, D., Grosch-Worner, I., Schafer, A., Mok, J., Johnstone, F., Jiminez, J., Alba, C., Garcia-Rodriguez, M., Bates, I., Jose, I., Hawkins, F., Zapico, Rm, Asensi-Botet, F., Otero, M., Perez-Tamarit, D., Moya, A., Galbis, M., Scherpbier, H., Boer, K., Bohlin, A., Lindgren, S., Ehrnst, A., Anzen, B., Belfrage, E., Levy, J., Alimenti, A., Barlow, P., Ferrazin, A., Maria, A., Gotta, C., Maritati, V., Mur, A., Rovira, M., Paya, A., Coll, O., Fortuny, C., Boguna, J., Caro, Mc, Canet, Y., Ravizza, M., Castagna, C., Fiore, S., Guerra, B., Lanari, M., Bianchi, S., Bovicelli, L., Prati, E., Duse, M., Soresina, A., Scaravelli, G., Santis, M., Muggiasca, M., Vigano, A., Marchisio, P., Iasci, A., Spinillo, A., Bucceri, A., Grossi, E., Rancilio, L., Della Torre, M., Dallacasa, P., Pachi, A., Principi, N., Zara, C., Vignali, M., Rossi, G., Selvaggi, L., Greco, P., Vimercati, A., Massi, G., Innocenti, T., Fiscella, A., Sansone, M., Benedetto, C., Tibaldi, C., Ziarati, N., Tadrist, B., Thevenicau, D., Gondry, J., Paulard, B., Alisy, C., Brault, D., Tordjeman, P., Mamou, J., Rozan, M., Colombani, D., Pincemaille, O., Salvetti, A., Chabanier, C., Hernandorena, X., Leroy, J., Schaal, J., Balde, P., Faucher, P., Lachassinne, E., Benoit, S., Douard, D., Hocke, C., Barjot, P., Brouard, J., Delattre, P., Stien, L., Audibert, F., Labrune, P., Vial, M., Mazy, F., Sitbon, D., Crenn-Hebert, C., Floch-Tudal, C., Akakpo, R., Daveau, C., Leblanc, A., Cesbron, P., Duval-Arnould, H., Huraux-Rendu, C., Lemerle, S., Touboul, C., Guerin, M., Maingueneau, C., Reynaud, I., Rousseau, T., Ercoil, V., Lanza, M., Denavit, M., Garnier, J., Lahsinat, K., Pia, R., Allouche, C., Nardou, M., Grall, F., May, A., Dallot, M., Lhuillier, P., Cecile, W., Mezin, R., Bech, A., Lobut, J., Algava, G., Dermesay, Ac, Busuttil, R., Jacquemot, M., Bader-Meunier, B., Fridman, S., Codaccioni, X., Maxingue, F., Thomas, D., Alain, J., Lumley, L., Tabaste, J., Salin, Pb, Seaume, H., Guichard, A., Kebaili, K., Roussouly, C., Botto, C., Lanete, A., Wipff, P., Cravello, L., Boisse, P., Leclaire, M., Michel, G., Crumiere, C., Lefevre, V., Le Lorier, B., Pauly, I., Robichez, B., Seguy, D., Dehlinger, M., Rideau, F., Talon, P., Benos, P., Huret, C., Nicolas, J., Heller-Roussin, B., Saint-Leger, S., Delaporte, M., Hubert, C., Sarcus, B., Karoubi, P., Mechinaud, F., Bertcrottiere, D., Bongain, A., Monpoux, F., Gennes, C., Devianne, F., Nisand, I., Rousset, M., Mouchnino, G., Muray, J., Munzer, M., Quereux, C., Brossard, V., Clavier, B., Allemon, M., Rotten, D., Stephan, J., Varlet, M., Guyot, B., Narey, P., Bardinet, F., Caunes, F., Jeny, R., Robin, M., Bouley, Ar, Savey, L., Berrebi, A., Tricoire, J., Borderon, J., Fignon, A., Guillot, F., Maria, B., Broyard, A., Chitrit, Y., Firtion, G., Pillet, Ml, Parat, S., Boissinot, C., Garec, N., Levine, M., Ottenwalter, A., Schaller, F., Vilmer, B., Courpotin, C., Brunner, C., Ciraru-Vigneron, N., Hatem-Gantzer, G., Xavier FRITEL, Wallet, A., Bouille, J., Milliez, J., Mrejen, Db, Dermer, E., Noseda, G., Bardou, D., Cressaty, J., Francoual, C., Moncomble, Cc, Cohen, H., Blanche, S., Bastion, H., Benifla, J., Benkhatar, F., Berkane, N., Herve, F., Ronzier, M., Ferraris, G., Rancillo, L., Tulisso, S., Scolfaro, C., Riva, C., Vierucci, A., Luca, M., Farina, S., Fundaro, C., Genovese, O., Mercu, G., Forni, G., Stegagno, M., Falconieri, P., Zuccotti, G., Riva, E., Cellini, M., Baraldi, C., Consolini, R., Palla, G., Ruggeri, M., Pignata, C., Guarino, A., Osimani, P., Metri, A., Antonellini, A., Benaglia, G., Romano, A., Mattia, D., Caselli, D., Boni, S., Erba, G., Bassanetti, F., Sticca, M., Timpano, C., Magnani, C., Salvatore, C., Gambaretto, G., Lipreri, R., Tornaghi, R., Pinzani, R., Cecchi, M., Bezzi, T., Battisti, L., Bresciani, E., Gattinara, G., Berrino, R., Pellegatta, A., Mazza, A., Baldi, F., Micheletti, E., Altobelli, R., Deiana, M., Colnaghi, C., Tarallo, L., Tondo, U., Anastasio, E., Chiriaco, P., Contardi, I., Ruggeri, C., Ibba, P., O Sullivan, M., Malmsberry, A., Willoughby, A., Goedert, J., Mendez, H., Holman, S., Rubinstein, A., Nesheim, S., Clark, S., Lee, F., Nahmias, A., Sawyer, M., Vink, P., Alger, L., Abrams, E., Bamji, M., Lambert, G., Schoenbaum, E., Thea, D., Thomas, P., Palumbo, P., Denny, T., Oleske, J., Orloff, S., Ethier-Ives, J., Rogers, M., Kutner, M., Kaplan, S., Kattan, M., Lipshultz, S., Sopko, G., Sloand, E., Wu, M., Nadal, D., Siegrist, Ca, Wyler, Ca, Cheseaux, Jj, Aebi, C., Gnehm, H., Schubiger, G., Klingler, J., Hunziker, U., Kuchler, H., Gianinazzi, M., Buhlmann, U., Biedermann, K., Lauper, U., Irion, O., Brunelli, A., Spoletini, G., Schreyer, A., Hosli, I., Saurenmann, E., Drack, G., Isenschmid, M., Poorbeik, M., Schupbach, J., Perrin, L., Erb, P., Joller, H., Dillon, M., Nielsen, R., Boyer, P., Liao, D., Keller, M., Deveikis, A., Khoury, M., Diaz, C., Pacheco-Acosta, E., Cooper, E., Mesthene, D., Pitt, J., Higgins, A., Moroso, G., Rich, K., Turpin, D., Cooper, N., Fowler, M., Smeriglio, V., Mckinlay, S., and Ellis, S.

Subjects
Male, medicine.medical_specialty, Multivariate analysis, Anti-HIV Agents, Birth weight, HIV Infections, Cohort Studies, Pregnancy, Risk Factors, medicine, Birth Weight, Humans, Rupture of membranes, Pregnancy Complications, Infectious, Prospective cohort study, Cesarean Section, Obstetrics, business.industry, Infant, Newborn, General Medicine, Odds ratio, Delivery, Obstetric, medicine.disease, Infectious Disease Transmission, Vertical, Confidence interval, Logistic Models, Multivariate Analysis, Immunology, HIV-1, Female, business, Zidovudine, Cohort study
Abstract

Background To evaluate the relation between elective cesarean section and vertical transmission of human immunodeficiency virus type 1 (HIV-1), we performed a meta-analysis using data on individual patients from 15 prospective cohort studies. Methods North American and European studies of at least 100 mother-child pairs were included in the meta-analysis. Uniform definitions of modes of delivery were used. Elective cesarean sections were defined as those performed before onset of labor and rupture of membranes. Multivariate logistic-regression analysis was used to adjust for other factors known to be associated with vertical transmission. Results The primary analysis included data on 8533 mother-child pairs. After adjustment for receipt of antiretroviral therapy, maternal stage of disease, and infant birth weight, the likelihood of vertical transmission of HIV-1 was decreased by approximately 50 percent with elective cesarean section, as compared with other modes of delivery (adjusted odds ratio, 0.43; 95 percent confidence interval, 0.33 to 0.56). The results were similar when the study population was limited to those with rupture of membranes shortly before delivery. The likelihood of transmission was reduced by approximately 87 percent with both elective cesarean section and receipt of antiretroviral therapy during the prenatal, intrapartum, and neonatal periods, as compared with other modes of delivery and the absence of therapy (adjusted odds ratio, 0.13; 95 percent confidence interval, 0.09 to 0.19). Among mother-child pairs receiving antiretroviral therapy during the prenatal, intrapartum, and neonatal periods, rates of vertical transmission were 2.0 percent among the 196 mothers who underwent elective cesarean section and 7.3 percent among the 1255 mothers with other modes of delivery. Conclusions The results of this meta-analysis suggest that elective cesarean section reduces the risk of transmission of HIV-1 from mother to child independently of the effects of treatment with zidovudine.

Published
1999
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27. Antigenicity and Immunogenicity of Transmitted/Founder, Consensus, and Chronic Envelope Glycoproteins of Human Immunodeficiency Virus Type 1

Author

Chen, H., Montefiori, D. C., Alam, S. M., Scearce, R. M., Haynes, B. F., Swanstrom, R., Foulger, A., Xia, S.-M., Lu, X., Blinn, J. H., Shaw, G. M., Gao, F., Liao, H.-X., Korber, B., Lapedes, A., Sutherland, L. L., Ma, B.-J., Muldoon, M., Bowman, C., Hahn, B. H., Watson, S., Vandergrift, N., Parks, R., and Tsao, C.-Y.

Subjects
viruses, virus diseases
Abstract

Human immunodeficiency virus type 1 (HIV-1) vaccine development requires selection of appropriate envelope (Env) immunogens. Twenty HIV-1 Env glycoproteins were examined for their ability to bind human anti-HIV-1 monoclonal antibodies (MAbs) and then used as immunogens in guinea pigs to identify promising immunogens. These included five Envs derived from chronically infected individuals, each representing one of five common clades and eight consensus Envs based on these five clades, as well as the consensus of the entire HIV-1 M group, and seven transmitted/founder (T/F) Envs from clades B and C. Sera from immunized guinea pigs were tested for neutralizing activity using 36 HIV-1 Env-pseudotyped viruses. All Envs bound to CD4 binding site, membrane-proximal, and V1/V2 MAbs with similar apparent affinities, although the T/F Envs bound with higher affinity to the MAb 17b, a CCR5 coreceptor binding site antibody. However, the various Envs differed in their ability to induce neutralizing antibodies. Consensus Envs elicited the most potent responses, but neutralized only a subset of viruses, including mostly easy-to-neutralize tier 1 and some more-difficult-to-neutralize tier 2 viruses. T/F Envs elicited fewer potent neutralizing antibodies but exhibited greater breadth than chronic or consensus Envs. Finally, chronic Envs elicited the lowest level and most limited breadth of neutralizing antibodies overall. Thus, each group of Env immunogens elicited a different antibody response profile. The complementary benefits of consensus and T/F Env immunogens raise the possibility that vaccines utilizing a combination of consensus and T/F Envs may be able to induce neutralizing responses with greater breadth and potency than single Env immunogens.

Published
2013
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28. The mode of delivery and the risk of vertical transmission of human immunodeficiency virus type 1--a meta-analysis of 15 prospective cohort studies. The International Perinatal HIV Group

Author

Andiman W., Boucher M., Burns D., Bryson Y., Farley J., Fowler H., Gabiano C., Galli L., Hutto C., Kind C., Korber B., Kovacs A., Krogstad P., Landesman S., Lapointe N., Lemay M., Lew J., Mandelbrot L., Mayaux M.J., Mellins R., Minkoff H., Mofenson L., Nielsen K., Newell M.L., Pardi G., Peavy H., Peckham C., Read J., Rother C., Rudin C., Scott G., Semprini A., Shearer W., Simonds R., Simpson B., Stek A., Tovo P.A., Tuomala R., Van Dyke R., Weedon J., de Martino M., Lindsay M., Belair S., Chan L., Harris D., Kalish L., Muenz L., Nugent R., Schluchter M., Durako S., Goodwin S., Mitchell R., Nourjah P., Owen W., Widmayer S., Bardeguez A., Hanson C., Wiznia A., Luzuriaga K., Viscarello R., Ho D., Koup R., Chen I., Mullins J., Wolinsky S., Walker B., Ammann A., Clapp S., McDonald D., Fauvel M., Hankins C., Samson J., Bailey A., Giaquinto C., Ruga E., De Rossi A., Truscia D., Grosch Worner I., Schafer A., Mok J., Johnstone F., Jiminez J., de Alba C., Garcia Rodriguez M., Bates I., de Jose I., Hawkins F., Zapico R.M., Asensi Botet F., Otero M., Perez Tamarit D., Moya A., Galbis M., Scherpbier H., Boer K., Bohlin A., Lindgren S., Ehrnst A., Anzen B., Belfrage E., Levy J., Alimenti A., Barlow P., Ferrazin A., De Maria A., Gotta C., Maritati V., Mur A., Rovira M., Paya A., Coll O., Fortuny C., Boguna J., Caro M.C., Canet Y., Ravizza M., Castagna C., Fiore S., Guerra B., Lanari M., Bianchi S., Bovicelli L., Prati E., Duse M., Soresina A., Scaravelli G., De Santis M., Muggiasca M., Vigano A., Marchisio P., Iasci A., Spinillo A., Bucceri A., Grossi E., Rancilio L., Della Torre M., Dallacasa P., Pachi A., Principi N., Zara C., Vignali M., Rossi G., Selvaggi L., Greco P., Vimercati A., Massi G., Innocenti T., Fiscella A., Sansone M., Benedetto C., Tibaldi C., Ziarati N., Tadrist B., Thevenicau D., Gondry J., Paulard B., Alisy C., Brault D., Tordjeman P., Mamou J., Rozan M., Colombani D., Pincemaille O., Salvetti A., Chabanier C., Hernandorena X., Leroy J., Schaal J., Balde P., Faucher P., Lachassinne E., Benoit S., Douard D., Hocke C., Barjot P., Brouard J, Delattre P, Stien L, Audibert F, Labrune P, Vial M, Mazy F, Sitbon D, Crenn Hebert C, Floch Tudal C, Akakpo R, Daveau C, Leblanc A, Cesbron P, Duval Arnould H, Huraux Rendu C, Lemerle S, Touboul C, Guerin M, Maingueneau C, Reynaud I, Rousseau T, Ercoil V, Lanza M, Denavit M, Garnier J, Lahsinat K, Pia R, Allouche C, Nardou M, Grall F, May A, Dallot M, Lhuillier P, Cecile W, Mezin R, Balde P, Bech A, Lobut J, Algava G, Dermesay AC, Busuttil R, Jacquemot M, Bader Meunier B, Fridman S, Codaccioni X, Maxingue F, Thomas D, Alain J, De Lumley L, Tabaste J, Salin PB, Seaume H, Guichard A, Kebaili K, Roussouly C, Botto C, De Lanete A, Wipff P, Cravello L, De Boisse P, Leclaire M, Michel G, Crumiere C, Lefevre V, Le Lorier B, Pauly I, Robichez B, Seguy D, Dehlinger M, Rideau F, Talon P, Benos P, Huret C, Nicolas J, Heller Roussin B, Saint Leger S, Delaporte M, Hubert C, De Sarcus B, Karoubi P, Mechinaud F, Bertcrottiere D, Bongain A, Monpoux F, De Gennes C, Devianne F, Nisand I, Rousset M, Mouchnino G, Muray J, Munzer M, Quereux C, Brossard V, Clavier B, Allemon M, Rotten D, Stephan J, Varlet M, Guyot B, Narey P, Bardinet F, De Caunes F, Jeny R, Robin M, Bouley AR, Savey L, Berrebi A, Tricoire J, Borderon J, Fignon A, Guillot F, Maria B, Broyard A, Chitrit Y, Firtion G, Mandelbrot L, Pillet ML, Parat S, Boissinot C, Garec N, Levine M, Ottenwalter A, Schaller F, Vilmer B, Courpotin C, Brunner C, Ciraru Vigneron N, Hatem Gantzer G, Fritel X, Wallet A, Bouille J, Milliez J, Mrejen DB, Dermer E, Noseda G, Bardou D, Cressaty J, Francoual C, Moncomble CC, Cohen H, Blanche S, Bastion H, Benifla J, Benkhatar F, Berkane N, Herve F, Ronzier M, Mayaux MJ, de Martino M, Tovo PA, Galli L, Gabiano C, Ferraris G, Rancillo L, Bucceri A, Tulisso S, Scolfaro C, Riva C, Vierucci A, de Luca M, Farina S, Fundaro C, Genovese O, Mercu G, Forni G, Stegagno M, Falconieri P, Zuccotti G, Riva E, Cellini M, Baraldi C, Consolini R, Palla G, Ruggeri M, Osimani P, Metri A, Antonellini A, Benaglia G, Romano A, Dallacasa P, De Mattia D, Caselli D, Boni S, Dell'Erba G, Bassanetti F, Sticca M, Timpano C, Magnani C, Salvatore C, Gambaretto G, Lipreri R, Tornaghi R, Pinzani R, Cecchi M, Bezzi T, Battisti L, Bresciani E, Gattinara G, Berrino R, Pellegatta A, Mazza A, Baldi F, Micheletti E, Ruga E, Altobelli R, Deiana M, Colnaghi C, Tarallo L, Tondo U, Anastasio E, Duse M, Chiriaco P, Contardi I, Ruggeri C, Ibba P, Scott G, Hutto C, O'Sullivan M, Malmsberry A, Willoughby A, Burns D, Goedert J, Landesman S, Minkoff H, Mendez H, Holman S, Rubinstein A, Durako S, Muenz L, Goodwin S, Nesheim S, Lindsay M, Clark S, Lee F, Nahmias A, Sawyer M, Vink P, Farley J, Alger L, Abrams E, Bamji M, Lambert G, Schoenbaum E, Thea D, Thomas P, Weedon J, Palumbo P, Bardeguez A, Denny T, Oleske J, Simonds R, Orloff S, Ethier Ives J, Rogers M, Schluchter M, Kutner M, Kaplan S, Kattan M, Lipshultz S, Mellins R, Shearer W, Peavy H, Sopko G, Sloand E, Wu M, Kind C, Nadal D, Rudin C, Siegrist CA, Wyler CA, Cheseaux JJ, Aebi C, Gnehm H, Schubiger G, Klingler J, Hunziker U, Kuchler H, Gianinazzi M, Buhlmann U, Biedermann K, Lauper U, Irion O, Brunelli A, Spoletini G, Schreyer A, Hosli I, Saurenmann E, Drack G, Isenschmid M, Poorbeik M, Schupbach J, Perrin L, Erb P, Joller H, Bryson Y, Dillon M, Nielsen R, Boyer P, Liao D, Keller M, Deveikis A, Kovacs A, Stek A, Chan L, Rother C, Khoury M, Diaz C, Pacheco Acosta E, Tuomala R, Cooper E, Mesthene D, Pitt J, Higgins A, Moroso G, Rich K, Turpin D, Cooper N, Fowler M, Nugent R, Smeriglio V, McKinlay S, Kalish L, Ellis S, Andiman W, PIGNATA, CLAUDIO, GUARINO, ALFREDO, Andiman, W., Boucher, M., Burns, D., Bryson, Y., Farley, J., Fowler, H., Gabiano, C., Galli, L., Hutto, C., Kind, C., Korber, B., Kovacs, A., Krogstad, P., Landesman, S., Lapointe, N., Lemay, M., Lew, J., Mandelbrot, L., Mayaux, M. J., Mellins, R., Minkoff, H., Mofenson, L., Nielsen, K., Newell, M. L., Pardi, G., Peavy, H., Peckham, C., Read, J., Rother, C., Rudin, C., Scott, G., Semprini, A., Shearer, W., Simonds, R., Simpson, B., Stek, A., Tovo, P. A., Tuomala, R., Van Dyke, R., Weedon, J., de Martino, M., Lindsay, M., Belair, S., Chan, L., Harris, D., Kalish, L., Muenz, L., Nugent, R., Schluchter, M., Durako, S., Goodwin, S., Mitchell, R., Nourjah, P., Owen, W., Widmayer, S., Bardeguez, A., Hanson, C., Wiznia, A., Luzuriaga, K., Viscarello, R., Ho, D., Koup, R., Chen, I., Mullins, J., Wolinsky, S., Walker, B., Ammann, A., Clapp, S., Mcdonald, D., Fauvel, M., Hankins, C., Samson, J., Bailey, A., Giaquinto, C., Ruga, E., De Rossi, A., Truscia, D., Grosch Worner, I., Schafer, A., Mok, J., Johnstone, F., Jiminez, J., de Alba, C., Garcia Rodriguez, M., Bates, I., de Jose, I., Hawkins, F., Zapico, R. M., Asensi Botet, F., Otero, M., Perez Tamarit, D., Moya, A., Galbis, M., Scherpbier, H., Boer, K., Bohlin, A., Lindgren, S., Ehrnst, A., Anzen, B., Belfrage, E., Levy, J., Alimenti, A., Barlow, P., Ferrazin, A., De Maria, A., Gotta, C., Maritati, V., Mur, A., Rovira, M., Paya, A., Coll, O., Fortuny, C., Boguna, J., Caro, M. C., Canet, Y., Ravizza, M., Castagna, C., Fiore, S., Guerra, B., Lanari, M., Bianchi, S., Bovicelli, L., Prati, E., Duse, M., Soresina, A., Scaravelli, G., De Santis, M., Muggiasca, M., Vigano, A., Marchisio, P., Iasci, A., Spinillo, A., Bucceri, A., Grossi, E., Rancilio, L., Della Torre, M., Dallacasa, P., Pachi, A., Principi, N., Zara, C., Vignali, M., Rossi, G., Selvaggi, L., Greco, P., Vimercati, A., Massi, G., Innocenti, T., Fiscella, A., Sansone, M., Benedetto, C., Tibaldi, C., Ziarati, N., Tadrist, B., Thevenicau, D., Gondry, J., Paulard, B., Alisy, C., Brault, D., Tordjeman, P., Mamou, J., Rozan, M., Colombani, D., Pincemaille, O., Salvetti, A., Chabanier, C., Hernandorena, X., Leroy, J., Schaal, J., Balde, P., Faucher, P., Lachassinne, E., Benoit, S., Douard, D., Hocke, C., Barjot, P., Brouard, J, Delattre, P, Stien, L, Audibert, F, Labrune, P, Vial, M, Mazy, F, Sitbon, D, Crenn Hebert, C, Floch Tudal, C, Akakpo, R, Daveau, C, Leblanc, A, Cesbron, P, Duval Arnould, H, Huraux Rendu, C, Lemerle, S, Touboul, C, Guerin, M, Maingueneau, C, Reynaud, I, Rousseau, T, Ercoil, V, Lanza, M, Denavit, M, Garnier, J, Lahsinat, K, Pia, R, Allouche, C, Nardou, M, Grall, F, May, A, Dallot, M, Lhuillier, P, Cecile, W, Mezin, R, Balde, P, Bech, A, Lobut, J, Algava, G, Dermesay, Ac, Busuttil, R, Jacquemot, M, Bader Meunier, B, Fridman, S, Codaccioni, X, Maxingue, F, Thomas, D, Alain, J, De Lumley, L, Tabaste, J, Salin, Pb, Seaume, H, Guichard, A, Kebaili, K, Roussouly, C, Botto, C, De Lanete, A, Wipff, P, Cravello, L, De Boisse, P, Leclaire, M, Michel, G, Crumiere, C, Lefevre, V, Le Lorier, B, Pauly, I, Robichez, B, Seguy, D, Dehlinger, M, Rideau, F, Talon, P, Benos, P, Huret, C, Nicolas, J, Heller Roussin, B, Saint Leger, S, Delaporte, M, Hubert, C, De Sarcus, B, Karoubi, P, Mechinaud, F, Bertcrottiere, D, Bongain, A, Monpoux, F, De Gennes, C, Devianne, F, Nisand, I, Rousset, M, Mouchnino, G, Muray, J, Munzer, M, Quereux, C, Brossard, V, Clavier, B, Allemon, M, Rotten, D, Stephan, J, Varlet, M, Guyot, B, Narey, P, Bardinet, F, De Caunes, F, Jeny, R, Robin, M, Bouley, Ar, Savey, L, Berrebi, A, Tricoire, J, Borderon, J, Fignon, A, Guillot, F, Maria, B, Broyard, A, Chitrit, Y, Firtion, G, Mandelbrot, L, Pillet, Ml, Parat, S, Boissinot, C, Garec, N, Levine, M, Ottenwalter, A, Schaller, F, Vilmer, B, Courpotin, C, Brunner, C, Ciraru Vigneron, N, Hatem Gantzer, G, Fritel, X, Wallet, A, Bouille, J, Milliez, J, Mrejen, Db, Dermer, E, Noseda, G, Bardou, D, Cressaty, J, Francoual, C, Moncomble, Cc, Cohen, H, Blanche, S, Bastion, H, Benifla, J, Benkhatar, F, Berkane, N, Herve, F, Ronzier, M, Mayaux, Mj, de Martino, M, Tovo, Pa, Galli, L, Gabiano, C, Ferraris, G, Rancillo, L, Bucceri, A, Tulisso, S, Scolfaro, C, Riva, C, Vierucci, A, de Luca, M, Farina, S, Fundaro, C, Genovese, O, Mercu, G, Forni, G, Stegagno, M, Falconieri, P, Zuccotti, G, Riva, E, Cellini, M, Baraldi, C, Consolini, R, Palla, G, Ruggeri, M, Pignata, Claudio, Guarino, Alfredo, Osimani, P, Metri, A, Antonellini, A, Benaglia, G, Romano, A, Dallacasa, P, De Mattia, D, Caselli, D, Boni, S, Dell'Erba, G, Bassanetti, F, Sticca, M, Timpano, C, Magnani, C, Salvatore, C, Gambaretto, G, Lipreri, R, Tornaghi, R, Pinzani, R, Cecchi, M, Bezzi, T, Battisti, L, Bresciani, E, Gattinara, G, Berrino, R, Pellegatta, A, Mazza, A, Baldi, F, Micheletti, E, Ruga, E, Altobelli, R, Deiana, M, Colnaghi, C, Tarallo, L, Tondo, U, Anastasio, E, Duse, M, Chiriaco, P, Contardi, I, Ruggeri, C, Ibba, P, Scott, G, Hutto, C, O'Sullivan, M, Malmsberry, A, Willoughby, A, Burns, D, Goedert, J, Landesman, S, Minkoff, H, Mendez, H, Holman, S, Rubinstein, A, Durako, S, Muenz, L, Goodwin, S, Nesheim, S, Lindsay, M, Clark, S, Lee, F, Nahmias, A, Sawyer, M, Vink, P, Farley, J, Alger, L, Abrams, E, Bamji, M, Lambert, G, Schoenbaum, E, Thea, D, Thomas, P, Weedon, J, Palumbo, P, Bardeguez, A, Denny, T, Oleske, J, Simonds, R, Orloff, S, Ethier Ives, J, Rogers, M, Schluchter, M, Kutner, M, Kaplan, S, Kattan, M, Lipshultz, S, Mellins, R, Shearer, W, Peavy, H, Sopko, G, Sloand, E, Wu, M, Kind, C, Nadal, D, Rudin, C, Siegrist, Ca, Wyler, Ca, Cheseaux, Jj, Aebi, C, Gnehm, H, Schubiger, G, Klingler, J, Hunziker, U, Kuchler, H, Gianinazzi, M, Buhlmann, U, Biedermann, K, Lauper, U, Irion, O, Brunelli, A, Spoletini, G, Schreyer, A, Hosli, I, Saurenmann, E, Drack, G, Isenschmid, M, Poorbeik, M, Schupbach, J, Perrin, L, Erb, P, Joller, H, Bryson, Y, Dillon, M, Nielsen, R, Boyer, P, Liao, D, Keller, M, Deveikis, A, Kovacs, A, Stek, A, Chan, L, Rother, C, Khoury, M, Diaz, C, Pacheco Acosta, E, Tuomala, R, Cooper, E, Mesthene, D, Pitt, J, Higgins, A, Moroso, G, Rich, K, Turpin, D, Cooper, N, Fowler, M, Nugent, R, Smeriglio, V, Mckinlay, S, Kalish, L, Ellis, S, and Andiman, W

Abstract

To evaluate the relation between elective cesarean section and vertical transmission of human immunodeficiency virus type 1 (HIV-1), we performed a meta-analysis using data on individual patients from 15 prospective cohort studies. North American and European studies of at least 100 mother-child pairs were included in the meta-analysis. Uniform definitions of modes of delivery were used. Elective cesarean sections were defined as those performed before onset of labor and rupture of membranes. Multivariate logistic-regression analysis was used to adjust for other factors known to be associated with vertical transmission. The primary analysis included data on 8533 mother-child pairs. After adjustment for receipt of antiretroviral therapy, maternal stage of disease, and infant birth weight, the likelihood of vertical transmission of HIV-1 was decreased by approximately 50 percent with elective cesarean section, as compared with other modes of delivery (adjusted odds ratio, 0.43; 95 percent confidence interval, 0.33 to 0.56). The results were similar when the study population was limited to those with rupture of membranes shortly before delivery. The likelihood of transmission was reduced by approximately 87 percent with both elective cesarean section and receipt of antiretroviral therapy during the prenatal, intrapartum, and neonatal periods, as compared with other modes of delivery and the absence of therapy (adjusted odds ratio, 0.13; 95 percent confidence interval, 0.09 to 0.19). Among mother-child pairs receiving antiretroviral therapy during the prenatal, intrapartum, and neonatal periods, rates of vertical transmission were 2.0 percent among the 196 mothers who underwent elective cesarean section and 7.3 percent among the 1255 mothers with other modes of delivery. The results of this meta-analysis suggest that elective cesarean section reduces the risk of transmission of HIV-1 from mother to child independently of the effects of treatment with zidovudine.

Published
1999

30. Deciphering Human Immunodeficiency Virus Type 1 Transmission and Early Envelope Diversification by Single-Genome Amplification and Sequencing

Author

Guffey, M. B., Anderson, J. A., Korber, B. T. M., Pham, K. T., Keele, B. F., Haynes, B. F., Salazar-Gonzalez, J. F., Manigart, O., Salazar, M. G., Allen, S., Mulenga, J., Swanstrom, R., Sharp, P. M., Athreya, G. S., Derdeyn, C. A., Hunter, E., Shaw, G. M., Bailes, E., Hahn, B. H., and Farmer, P.

Subjects
viruses
Abstract

Accurate identification of the transmitted virus and sequences evolving from it could be instrumental in elucidating the transmission of human immunodeficiency virus type 1 (HIV-1) and in developing vaccines, drugs, or microbicides to prevent infection. Here we describe an experimental approach to analyze HIV-1 env genes as intact genetic units amplified from plasma virion RNA by single-genome amplification (SGA), followed by direct sequencing of uncloned DNA amplicons. We show that this strategy precludes in vitro artifacts caused by Taq-induced nucleotide substitutions and template switching, provides an accurate representation of the env quasispecies in vivo, and has an overall error rate (including nucleotide misincorporation, insertion, and deletion) of less than 8 × 10−5. Applying this method to the analysis of virus in plasma from 12 Zambian subjects from whom samples were obtained within 3 months of seroconversion, we show that transmitted or early founder viruses can be identified and that molecular pathways and rates of early env diversification can be defined. Specifically, we show that 8 of the 12 subjects were each infected by a single virus, while 4 others acquired more than one virus; that the rate of virus evolution in one subject during an 80-day period spanning seroconversion was 1.7 × 10−5 substitutions per site per day; and that evidence of strong immunologic selection can be seen in Env and overlapping Rev sequences based on nonrandom accumulation of nonsynonymous mutations. We also compared the results of the SGA approach with those of more-conventional bulk PCR amplification methods performed on the same patient samples and found that the latter is associated with excessive rates of Taq-induced recombination, nucleotide misincorporation, template resampling, and cloning bias. These findings indicate that HIV-1 env genes, other viral genes, and even full-length viral genomes responsible for productive clinical infection can be identified by SGA analysis of plasma virus sampled at intervals typical in large-scale vaccine trials and that pathways of viral diversification and immune escape can be determined accurately.

Published
2008
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31. Maternal viral load and rate of disease progression among vertically HIV-1-infected children: an international meta-analysis

Author

Ioannidis, J. P., Tatsioni, A., Abrams, E. J., Bulterys, M., Coombs, R. W., Goedert, J. J., Korber, B. T., Mayaux, M. J., Mofenson, L. M., Moye, J., Jr., Newell, M. L., Shapiro, D. E., Teglas, J. P., Thompson, B., and Wiener, J.

Subjects
Infectious Disease Transmission, Vertical, Infant, Newborn, Infant, Mothers, HIV Infections/blood/transmission/*virology, Prognosis, Anti-Retroviral Agents/therapeutic use, CD4 Lymphocyte Count, Hiv-1, Viral Load/*methods, Disease Progression, Odds Ratio, Humans, Female, Prospective Studies, RNA, Viral/blood
Abstract

OBJECTIVE: To evaluate whether maternal human immunodeficiency virus type 1 (HIV-1) RNA levels in the serum/plasma of mothers at or close to the time of delivery affects the rate of disease progression among vertically HIV-1-infected children and whether it correlates with other parameters affecting infant disease progression. METHODS: International meta-analysis of eight studies with 574 HIV-1 infected infants with available maternal HIV-1 RNA measurements at or close to delivery and clinical follow-up. The primary outcome was disease progression (stage C disease or death, n = 178). Cohort-stratified Cox models were used. RESULTS: Higher maternal HIV-1 RNA level at or close to delivery significantly increased disease progression risk [hazard ratio (HR), 1.25; 95% confidence interval (CI), 1.04-1.52 per 1 log10 increase; P = 0.02) with a borderline effect on mortality (HR, 1.26; 95% CI, 0.96-1.65; P = 0.10]. The association with disease progression risk was strong in the first 6 months of life (HR, 1.77; 95% CI, 1.28-2.45; P = 0.001), but not subsequently (HR, 1.03; 95% CI, 0.81-1.30). Maternal HIV-1 RNA, early infant HIV-1 RNA (at 30-200 days after birth) and infant CD4 were independent predictors of disease progression in the first 6 months. Maternal HIV-1 RNA at or close to delivery correlated with early infant HIV-1 RNA (r = 0.26, P < 0.001). Effects were independent of maternal and infant treatment. CONCLUSIONS: Higher maternal HIV-1 RNA at or close to delivery strongly predicts disease progression for HIV-1-infected infants, especially in their first 6 months of life and correlates with the early peak of viremia in the infected child. AIDS

Published
2004

32. Perinatal transmission of human immunodeficiency virus type 1 by pregnant women with RNA virus loads <1000 copies/ml

Author

Ioannidis, J. P., Abrams, E. J., Ammann, A., Bulterys, M., Goedert, J. J., Gray, L., Korber, B. T., Mayaux, M. J., Mofenson, L. M., Newell, M. L., Shapiro, D. E., Teglas, J. P., and Wilfert, C. M.

Subjects
Clinical Trials as Topic, Infectious Disease Transmission, Vertical, HIV-1/*physiology, International Cooperation, Pregnancy Complications, Infectious/drug therapy/*virology, RNA, Viral/*blood, Infant, Newborn, Gestational Age, United States, Europe, HIV Infections/drug therapy/*transmission/virology, Viral Load, Pregnancy, Risk Factors, Anti-HIV Agents/therapeutic use, Humans, Female, Prospective Studies, Registries, Viremia
Abstract

In a collaboration of 7 European and United States prospective studies, 44 cases of vertical human immunodeficiency virus type 1 (HIV-1) transmission were identified among 1202 women with RNA virus loads 500 copies/mL. Perinatal HIV-1 transmission occurs in only 1% of treated women with RNA virus loads

Published
2001

33. Timing the ancestor of the HIV-1 pandemic strains

Author

Muldoon, M., Theiler, J., Lapedes, A., Wolinsky, S., Gao, F., Gupta, R., Korber, B., Hahn, Bh H., and Bhattacharya, T.

Abstract

HIV-1 sequences were analyzed to estimate the timing of the ancestral sequence of the main group of HIV-1, the strains responsible for the AIDS pandemic. Using parallel supercomputers and assuming a constant rate of evolution, we applied maximum-likelihood phylogenetic methods to unprecedented amounts of data for this calculation. We validated our approach by correctly estimating the timing of two historically documented points. Using a comprehensive full-length envelope sequence alignment, we estimated the date of the last common ancestor of the main group of HIV-1 to be 1931 (1915-41). Analysis of a gag gene alignment, subregions of envelope including additional sequences, and a method that relaxed the assumption of a strict molecular clock also supported these results.

Published
2000

34. The mode of delivery and the risk of vertical transmission of human immunodeficiency virus type 1--a meta-analysis of 15 prospective cohort studies. The International Perinatal HIV Group

Author

Andiman, W., Boucher, M., Burns, D., Bryson, Y., Farley, J., Fowler, H, Gabiano, C., Gall, L., Hutto, C., Kind, C, Korber, B., Kovacs, A., Krogstad, P., Landesman, S., Lapointe, N., Lemay, M, Lew, J, Mandelbrot, L., Mayaux, Mj, Mellins, R., Minkoff, H., Mofenson, L., Nielsen, K, Newell, Ml, Pardi, G., Peavy, H., Peckham, C., Read, J., Rother, C, Rudin, C., Scott, G., Semprini, A., Shearer, W., Simonds, R., Simpson, A, Stek, A., Tovo, Pa, Tuomala, R., Van Dyke, R., Weedon, J., de Martino, M., Lindsay, M., Belair, S., Chan, L., Harris, D, Kalish, L., Muenz, L., Nugent, R., Schluchter, M., Durako, S., Goodwin, S., Mitchell, R., Nourjah, P., Owen, W., Widmayer, S., Ardeguez, A., Hanson, C., Wiznia, A., Luzuriaga, K., Viscarello, R, Ho, D., Koup, R., Chen, I., Mullins, J., Wolinsky, S., Walker, B, Ammann, A., Clapp, S., Mcdonald, D, Fauvel, M., Hankins, C, Samson, J., Bailey, A., Giaquinto, Carlo, Ruga, E., DE ROSSI, Anita, and Truscia, D.

Subjects
ZIDOVUDINE PROPHYLAXIS, INFANT HIV TRANSMISSION, MOTHER-TO-CHILD, MOTHER-TO-CHILD, INFANT HIV TRANSMISSION, CESAREAN-SECTION, ZIDOVUDINE PROPHYLAXIS, CESAREAN-SECTION
Published
1999

35. A polymorphism in the regulatory region of the CC-chemokine receptor 5 gene influences perinatal transmission of human immunodeficiency virus type 1 to African-American infants

Author

Deutsch, L., Kostrikis, Leontios G., Neumann, A. U., Thomson, B., Korber, B. T., McHardy, P., Karanicolas, R., Huang, Y., Lew, J. F., McIntosh, K., Pollack, H., Borkowsky, W., Spiegel, H. M. L., Palumbo, P., Oleske, J., Bardeguez, A., Luzuriaga, K., Sullivan, J., Wolinsky, S. M., Koup, R. A., Ho, David D., Moore, J. P., and Kostrikis, Leontios G. [0000-0002-5340-7109]

Subjects
Adult, Genotype, Receptors, CCR5, Anti-HIV Agents, regulatory mechanism, European Continental Ancestry Group, HIV Infections, Regulatory Sequences, Nucleic Acid, Linkage Disequilibrium, Cohort Studies, ethnic group, Gene Frequency, chemokine receptor ccr5, newborn, Humans, genetic polymorphism, controlled study, human, gene mutation, Receptors, Cytokine, Alleles, disease transmission, African Americans, Polymorphism, Genetic, Disease Transmission, Vertical, disease course, article, virus diseases, chemokine receptor, major clinical study, infant, Perinatal Care, priority journal, HIV-1, Female, vertical transmission, Receptors, Chemokine, homozygosity, Hispanic Americans, 5' Untranslated Regions, human immunodeficiency virus 1, caucasian, Zidovudine
Abstract

There are natural mutations in the coding and noncoding regions of the human immunodeficiency virus type (HIV-1) CC-chemokine coreceptor 5 (CCR5) and in the related CCR2 protein (the CCR2-64I mutation). Individuals homozygous for the CCRS-Δ32 allele, which prevents CCR5 expression, strongly resist HIV-1 infection. Several genetic polymorphisms have been identified within the CCR5 5' regulatory region, some of which influence the rate of disease progression in adult AIDS study cohorts. We genotyped 1,442 infants (1,235 uninfected and 207 HIV-1 infected) for five CCR5 and CCR2 polymorphisms- CCR5-59353-T/C, CCR5-59356C/T CCR5-59402-A/G, CCRS-Δ32, and CCR2-64I. The clinical significance of each genotype was assessed by measuring whether it influenced the rate of perinatal HIV-1 transmission among 667 AZT-untreated motherinfant pairs (554 uninfected and 113 HIV-1 infected). We found that the mutant CCR5-59356-T allele is relatively common in African-Americans (20.6% allele frequency among 552 infants) and rare in Caucasians and Hispanics (3.4 and 5.6% of 174 and 458 infants, respectively P < 0.001). There were 38 infants homozygous for CCR5-59356-T, of whom 35 were African-Americans. Among the African-American infants in the AZT- untreated group, there was a highly significant increase in HIV-1 transmission to infants with two mutant CCR5-59356-T alleles (47.6% of 21), compared to those with no or one mutant allele (13.4 to 14.1% of 187 and 71, respectively P < 0.001). The increased relative risk was 5.9 (95% confidence interval, 2.3 to 15.3 P < 0.001). The frequency of the CCR5-59356-T mutation varies between population groups in the United States, a low frequency occurring in Caucasians and a higher frequency occurring in African- Americans. Homozygosity for CCR5-59356-T is strongly associated with an increased rate of perinatal HIV-1 transmission. 73 10264 10271 Cited By :109

Published
1999

36. Evaluation of different V3 peptides in an enzyme immunoassay for specific HIV type 1 group 0 antibody detection

Author

Ondoa, P., Willems, B., Fransen, K., Nkengasong, J., Janssens, W., Heyndrickx, L., Zekeng, L., Ndumbe, P., Simon, F., Saragosti, S., Gürtler, L., Peeters, Martine, Korber, B., Goudsmit, J., and Van der Groen, G.

Subjects
EPIDEMIOLOGIE, DIAGNOSTIC, TEST, SIDA, VIRUS, IMMUNOLOGIE, VIH-1 GROUPE O, ANTICORPS
Abstract

Strategies to discriminate group O from group M infections need to be improved. We have developed and evaluated an HIV-1 group O V3 peptide-based enzyme immunoassay (PEIA) for specific HIV-1 group O antibody detection among HIV-1-infected patients. Synthetic peptides, derived from the amino acid sequences of the V3 loop of 15 different group O strains and 7 group O consensus sequences, were evaluated in a PEIA against a panel of genetically confirmed group O (n=33), group M (n=90), and HIV-1 antibody-negative sera (n=17). The best-performing PEIA(s) were then used to screen 134 sera of European and 336 sera of Cameroonian origin for the presence of anti-HIV-1 group O antibodies. The reactivity of reference ("gold standard") sera to individual peptides in the PEIA resulted in the selection of five different peptides with sensitivities (sens), specificities (spec), and test efficiencies (TEs) in the range of 90 to 100%. Improvement of the PEIA was obtained with simultaneous reactivity of at least two different peptides in separate wells of an ELISA plate, together with stringent criteria for positivity. We were able to select seven peptide combinations each with a sens, spec, and TE of 96.9, 100, and 99.2%, respectively. None of the 134 European and 4 (1.2%) of the 336 Cameroonian samples sera were group O positive in the optimized HIV-1 group O PEIA ; this was confirmed by the repeated presence of reactives, in agreement with the present knowledge of group O infection distribution. Finally, we were able to develop a strategy with a higher TE (99.2%) than the previously used ANT-70 (98.5%) and ANT-70/MVP5180 (95.7%). Our results show that optimal specificity rather than optimal sensitivity makes the V3 PEIA a sufficiently accurate epidemiological tool to be useful in estimating specifically group O infection among HIV-1-infected patients. (Résumé d'auteur)

Published
1998

37. Extensive HLA class I allele promiscuity among viral CTL epitopes

Author

Frahm, N., Yusim, K., Suscovich, T., Adams, S., Sidney, J., Hraber, P., Hewitt, H., Linde, C., Kavanagh, D., Woodberry, Tonia, Henry, L., Faircloth, K., Listgarten, J., Kadie, C., Jojic, N., Sango, K., Brown, N., Pae, E., Zaman, M., Bihl, F., Khatri, A., John, M., Mallal, S., Marincola, F., Walker, B., Sette, A., Heckerman, D., Korber, B., Brander, C., Frahm, N., Yusim, K., Suscovich, T., Adams, S., Sidney, J., Hraber, P., Hewitt, H., Linde, C., Kavanagh, D., Woodberry, Tonia, Henry, L., Faircloth, K., Listgarten, J., Kadie, C., Jojic, N., Sango, K., Brown, N., Pae, E., Zaman, M., Bihl, F., Khatri, A., John, M., Mallal, S., Marincola, F., Walker, B., Sette, A., Heckerman, D., Korber, B., and Brander, C.

Abstract

Promiscuous binding of T helper epitopes to MHC class II molecules has been well established, but few examples of promiscuous class I-restricted epitopes exist. To address the extent of promiscuity of HLA class I peptides, responses to 242 well-defined viral epitopes were tested in 100 subjects regardless of the individuals HLA type. Surprisingly, half of all detected responses were seen in the absence of the originally reported restricting HLA class I allele, and only 3% of epitopes were recognized exclusively in the presence of their original allele. Functional assays confirmed the frequent recognition of HLA class I-restricted T cell epitopes on several alternative alleles across HLA class I supertypes and encoded on different class I loci. These data have significant implications for the understanding of MHC class I-restricted antigen presentation and vaccine development.

Published
2007

38. Founder effects in the assessment of HIV polymorphisms and HLA allele associations

Author

Bhattacharya, T., Daniels, M., Heckerman, D., Foley, B., Frahm, N., Kadie, C., Carlson, J., Yusim, K., McMahon, B., Gaschen, B., Mallal, S., Mullins, J.I., Nickle, D.C., Herbeck, J., Rousseau, C, Learn, G.H., Miura, T., Brander, C., Walker, B., Korber, B., Bhattacharya, T., Daniels, M., Heckerman, D., Foley, B., Frahm, N., Kadie, C., Carlson, J., Yusim, K., McMahon, B., Gaschen, B., Mallal, S., Mullins, J.I., Nickle, D.C., Herbeck, J., Rousseau, C, Learn, G.H., Miura, T., Brander, C., Walker, B., and Korber, B.

Abstract

Escape from T cell–mediated immune responses affects the ongoing evolution of rapidly evolving viruses such as HIV. By applying statistical approaches that account for phylogenetic relationships among viral sequences, we show that viral lineage effects rather than immune escape often explain apparent human leukocyte antigen (HLA)–mediated immune-escape mutations defined by older analysis methods. Phylogenetically informed methods identified immune-susceptible locations with greatly improved accuracy, and the associations we identified with these methods were experimentally validated. This approach has practical implications for understanding the impact of host immunity on pathogen evolution and for defining relevant variants for inclusion in vaccine antigens.

Published
2007

39. Transmission and accumulation of CTL escape variants drive negative associations between HIV polymorphisms and HLA

Author

Leslie, A., Kavanagh, D., Honeyborne, I., Pfafferott, K., Edwards, C., Pillay, T., Hilton, L., Thobakgale, C., Ramduth, D., Draenert, R., Le Gall, S., Luzzi, G., Edwards, A., Brander, C., Sewell, A.K., Moore, S., Mullins, J., Moore, C., Mallal, S., Bhardwaj, N., Yusim, K., Phillips, R., Klenerman, P., Korber, B., Kiepiela, P., Walker, B., Goulder, P., Leslie, A., Kavanagh, D., Honeyborne, I., Pfafferott, K., Edwards, C., Pillay, T., Hilton, L., Thobakgale, C., Ramduth, D., Draenert, R., Le Gall, S., Luzzi, G., Edwards, A., Brander, C., Sewell, A.K., Moore, S., Mullins, J., Moore, C., Mallal, S., Bhardwaj, N., Yusim, K., Phillips, R., Klenerman, P., Korber, B., Kiepiela, P., Walker, B., and Goulder, P.

Abstract

Human immunodeficiency virus (HIV)-1 amino acid sequence polymorphisms associated with expression of specific human histocompatibility leukocyte antigen (HLA) class I alleles suggest sites of cytotoxic T lymphocyte (CTL)-mediated selection pressure and immune escape. The associations most frequently observed are between expression of an HLA class I molecule and variation from the consensus sequence. However, a substantial number of sites have been identified in which particular HLA class I allele expression is associated with preservation of the consensus sequence. The mechanism behind this is so far unexplained. The current studies, focusing on two examples of “negatively associated” or apparently preserved epitopes, suggest an explanation for this phenomenon: negative associations can arise as a result of positive selection of an escape mutation, which is stable on transmission and therefore accumulates in the population to the point at which it defines the consensus sequence. Such negative associations may only be in evidence transiently, because the statistical power to detect them diminishes as the mutations accumulate. If an escape variant reaches fixation in the population, the epitope will be lost as a potential target to the immune system. These data help to explain how HIV is evolving at a population level. Understanding the direction of HIV evolution has important implications for vaccine development.

Published
2005

40. HLA-restricted immune responses have driven the evolution of HIV-1 clades

Author

Park, L., Goulder, P., Kiepiela, P., Brander, C., Walker, B., Korber, B., Szinger, J., Keller, J., John, M., Nolan, D., Mallal, S., Park, L., Goulder, P., Kiepiela, P., Brander, C., Walker, B., Korber, B., Szinger, J., Keller, J., John, M., Nolan, D., and Mallal, S.

Abstract

Background. HIV mutates to escape selective pressure from antiretroviral medications and HLA-mediated immune responses. Escape mutations can, but do not necessarily, revert to “wild type” (WT) when the selective pressure is withdrawn. Worldwide, HIV has diversified into numerous clades and recombinant forms, and these variations generally follow geopolitical boundaries. Genetically similar human populations also follow these boundaries, so we hypothesized that population HLA has driven HIV evolution and its diversification into the clades. Methods. HIV isolates from 2 HLA-typed cohorts of antiretroviral-naïve patients were analyzed; these isolates included 107 sequences from Caucasian patients in Australia infected with clade B, and 96 from patients in Durban, Africa, infected with clade C. Polymorphism rates were calculated for each amino acid residue in p24 and p17. Associations between HLA and each amino acid residue (comparing consensus vs all nonconsensus) were quantified using multiple logistic regression models with stepwise selection of HLA class I genotype as covariates. Consensus protein sequences for clades A, B, C, D, F, and G obtained from the Los Alamos HIV database were aligned and compared with the locations of polymorphism and HLA association. Results. In p24 and p17, amino acid polymorphism (> 10% of the isolates differed from consensus) occurred at 50 and 56 residues in the Australian and African sequences, respectively. Of these, 33 were in common. Most of the alternative residues found in the Australian and African cohorts were the consensus amino acids for clades other than B and C, respectively. In each cohort, we found 38 residues with significant (p < 0.05) positive and/or negative associations between HLA and sequence polymorphism. The consensus protein sequences for clades A, B, C, D, F, and G differed at 79 residues. In both cohorts almost all of the polymorphic residues—42 (84%) for Australia and 46 (82%) for Africa—and HLA associations—

Published
2005

41. Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA

Author

Kiepiela, P., Leslie, A.J., Honeyborne, I., Ramduth, D., Thobakgale, C., Chetty, S., Rathnavalu, P., Moore, C.B., Pfafferott, K.J., Hilton, L., Zimbwa, P., Moore, S., Allen, T., Brander, C., Addo, M.M., Altfeld, M., James, I., Mallal, S., Bunce, M., Barber, L.D., Szinger, J., Day, C., Klenerman, P., Mullins, J., Korber, B., Coovadia, H.M., Walker, B.D., Goulder, P.J.R., Kiepiela, P., Leslie, A.J., Honeyborne, I., Ramduth, D., Thobakgale, C., Chetty, S., Rathnavalu, P., Moore, C.B., Pfafferott, K.J., Hilton, L., Zimbwa, P., Moore, S., Allen, T., Brander, C., Addo, M.M., Altfeld, M., James, I., Mallal, S., Bunce, M., Barber, L.D., Szinger, J., Day, C., Klenerman, P., Mullins, J., Korber, B., Coovadia, H.M., Walker, B.D., and Goulder, P.J.R.

Abstract

The extreme polymorphism in the human leukocyte antigen (HLA) class I region of the human genome is suggested to provide an advantage in pathogen defence mediated by CD8+ T cells. HLA class I molecules present pathogen-derived peptides on the surface of infected cells for recognition by CD8+ T cells. However, the relative contributions of HLA-A and -B alleles have not been evaluated. We performed a comprehensive analysis of the class I restricted CD8+ T-cell responses against human immunodeficiency virus (HIV-1), immune control of which is dependent upon virus-specific CD8+ T-cell activity. In 375 HIV-1-infected study subjects from southern Africa, a significantly greater number of CD8+ T-cell responses are HLA-B-restricted, compared to HLA-A (2.5-fold; P = 0.0033). Here we show that variation in viral set-point, in absolute CD4 count and, by inference, in rate of disease progression in the cohort, is strongly associated with particular HLA-B but not HLA-A allele expression (P < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design

Published
2004

43. P16-42. Characterisation of HIV-1 specific T-cell responses in exposed uninfected individuals from a London cohort

Author

Ritchie, AJ, primary, Kopycinski, J, additional, Campion, S, additional, Moore, S, additional, Liu, M, additional, Tanner, R, additional, Kuldanek, K, additional, Legg, K, additional, Wang, M, additional, Moodie, Z, additional, Korber, B, additional, Fidler, S, additional, McMichael, A, additional, and Goonetilleke, N, additional

Published
2009
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47. Quantitating the Multiplicity of Infection with Human Immunodeficiency Virus Type 1 Subtype C Reveals a Non-Poisson Distribution of Transmitted Variants

Author

Abrahams, M.-R., primary, Anderson, J. A., additional, Giorgi, E. E., additional, Seoighe, C., additional, Mlisana, K., additional, Ping, L.-H., additional, Athreya, G. S., additional, Treurnicht, F. K., additional, Keele, B. F., additional, Wood, N., additional, Salazar-Gonzalez, J. F., additional, Bhattacharya, T., additional, Chu, H., additional, Hoffman, I., additional, Galvin, S., additional, Mapanje, C., additional, Kazembe, P., additional, Thebus, R., additional, Fiscus, S., additional, Hide, W., additional, Cohen, M. S., additional, Karim, S. Abdool, additional, Haynes, B. F., additional, Shaw, G. M., additional, Hahn, B. H., additional, Korber, B. T., additional, Swanstrom, R., additional, and Williamson, C., additional

Published
2009
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49. Approaches to the development of broadly protective HIV vaccines: Challenges posed by the genetic, biological and antigenic variability of HIV-1

Author

Barre-Sinoussi, F, Berkley, S, Bhamarapravati, N, Birx, D, Bloom, B, Carvalheiro, J, Ganguly, N, Johnston, M, Kazatchkine, M, Makgoba, WM, Monico, SM, Nathanson, N, Schild, G, Wigzell, H, Yamasaki, S, Aubertin, AM, Bartos, M, Bermann, P, Bradac, J, Burke, D, Cao, H, Desrosiers, R, Ensoli, B, Fenyö, EM, Ferrari, G, Galvao-Castro, B, Godal, T, Goudsmit, J, Frachette, MJ, Ginsberg, R, Heeney, J, Holmes, H, Jin, X, Kalish, M, Klein, M, Korber, B, Liu, M, McMichael, A, McCutchan, F, Mhalu, F, Moscola, J, Moss, R, Mathieson, B, Mbidde, E, M'Boup, S, Mullins, J, Musonda, R, Numberg, J, Owili, M, Peeters, M, Pletschette, M, Redfield, R, Roudil, MP, Salk, P, Scarlatti, G, Schultz, A, Sheppard, H, Stamatos, L, Sutthent, R, Takebe, Y, Tramont, E, Van der Groen, G, Virelizier, JL, Voss, G, Walker, B, Weber, J, Wyatt, R, Young, P, Zolla-Pazner, S, Seck, AC, Dias-Ferrao, V, Esparza, J, Melgaard, B, Osmanov, S, Pattou, C, Piot, P, Ntounga, RS, Toure, C, Barre-Sinoussi, F, Berkley, S, Bhamarapravati, N, Birx, D, Bloom, B, Carvalheiro, J, Ganguly, N, Johnston, M, Kazatchkine, M, Makgoba, WM, Monico, SM, Nathanson, N, Schild, G, Wigzell, H, Yamasaki, S, Aubertin, AM, Bartos, M, Bermann, P, Bradac, J, Burke, D, Cao, H, Desrosiers, R, Ensoli, B, Fenyö, EM, Ferrari, G, Galvao-Castro, B, Godal, T, Goudsmit, J, Frachette, MJ, Ginsberg, R, Heeney, J, Holmes, H, Jin, X, Kalish, M, Klein, M, Korber, B, Liu, M, McMichael, A, McCutchan, F, Mhalu, F, Moscola, J, Moss, R, Mathieson, B, Mbidde, E, M'Boup, S, Mullins, J, Musonda, R, Numberg, J, Owili, M, Peeters, M, Pletschette, M, Redfield, R, Roudil, MP, Salk, P, Scarlatti, G, Schultz, A, Sheppard, H, Stamatos, L, Sutthent, R, Takebe, Y, Tramont, E, Van der Groen, G, Virelizier, JL, Voss, G, Walker, B, Weber, J, Wyatt, R, Young, P, Zolla-Pazner, S, Seck, AC, Dias-Ferrao, V, Esparza, J, Melgaard, B, Osmanov, S, Pattou, C, Piot, P, Ntounga, RS, and Toure, C

Published
2001

50. Targeting of a CD8 T Cell Env Epitope Presented by HLA-B*5802 Is Associated with Markers of HIV Disease Progression and Lack of Selection Pressure

Author

Ngumbela, K.C., primary, Day, C.L., additional, Mncube, Z., additional, Nair, K., additional, Ramduth, D., additional, Thobakgale, C., additional, Moodley, E., additional, Reddy, S., additional, de Pierres, C., additional, Mkhwanazi, N., additional, Bishop, K., additional, van der Stok, M., additional, Ismail, N., additional, Honeyborne, I., additional, Crawford, H., additional, Kavanagh, D.G., additional, Rousseau, C., additional, Nickle, D., additional, Mullins, J., additional, Heckerman, D., additional, Korber, B., additional, Coovadia, H., additional, Kiepiela, P., additional, Goulder, P.J.R., additional, and Walker, B.D., additional

Published
2008
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