Author: "Klenerman, P." / Publisher: elsevier b.v. - Searchworks@Jio Institute Digital Library Search Results

58 results on '"Klenerman, P."'

1. SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination

Author: Baillie, J. Kenneth, Openshaw, Peter J.M., Semple, Malcolm G., Alex, Beatrice, Andrikopoulos, Petros, Bach, Benjamin, Barclay, Wendy S., Bogaert, Debby, Chand, Meera, Chechi, Kanta, Cooke, Graham S., da Silva Filipe, Ana, de Silva, Thushan, Docherty, Annemarie B., dos Santos Correia, Gonçalo, Dumas, Marc-Emmanuel, Dunning, Jake, Fletcher, Tom, Green, Christopher A., Greenhalf, William, Griffin, Julian, Gupta, Rishi K., Harrison, Ewen M., Ho, Antonia Y.W., Holden, Karl, Horby, Peter W., Ijaz, Samreen, Khoo, Say, Klenerman, Paul, Law, Andrew, Lewis, Matthew, Liggi, Sonia, Lim, Wei Shen, Maslen, Lynn, Mentzer, Alexander J., Merson, Laura, Meynert, Alison M, Moore, Shona C., Noursadeghi, Mahdad, Olanipekun, Michael, Osagie, Anthonia, Palmarini, Massimo, Palmieri, Carlo, Paxton, William A., Pollakis, Georgios, Price, Nicholas, Rambaut, Andrew, Robertson, David L, Russell, Clark D., Sancho-Shimizu, Vanessa, Sands, Caroline, Scott, Janet T., Sigfrid, Louise, Solomon, Tom, Sriskandan, Shiranee, Stuart, David, Summers, Charlotte, Swann, Olivia V., Takats, Zoltan, Takis, Panteleimon, Tedder, Richard S., Thompson, A.A. 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Petousi, N., Petrie, J., Pfeffer, P., Phipps, J., Pimm, J., Piper Hanley, K., Pius, R., Plant, H., Plein, S., Plekhanova, T., Plowright, M., Poinasamy, K., Polgar, O., Poll, L., Porter, J.C., Porter, J., Portukhay, S., Powell, N., Prabhu, A., Pratt, J., Price, A., Price, C., Price, D., Price, L., Prickett, A., Propescu, J., Prosper, S., Pugmire, S., Quaid, S., Quigley, J., Quint, J., Qureshi, H., Qureshi, I.N., Radhakrishnan, K., Rahman, N.M., Ralser, M., Raman, B., Ramos, A., Ramos, H., Rangeley, J., Rangelov, B., Ratcliffe, L., Ravencroft, P., Reddington, A., Reddy, R., Redfearn, H., Redwood, D., Reed, A., Rees, M., Rees, T., Regan, K., Reynolds, W., Ribeiro, C., Richards, A., Richardson, E., Richardson, M., Rivera-Ortega, P., Roberts, K., Robertson, E., Robinson, E., Robinson, L., Roche, L., Roddis, C., Rodger, J., Ross, A., Ross, G., Rossdale, J., Rostron, A., Rowe, A., Rowland, A., Rowland, J., Rowland, M.J., Rowland-Jones, S.L., Roy, K., Roy, M., Rudan, I., Russell, R., Russell, 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N., Steiner, M., Stensel, D., Stephens, G., Stephenson, L., Stern, M., Stewart, I., Stimpson, R., Stockdale, S., Stockley, J., Stoker, W., Stone, R., Storrar, W., Storrie, A., Storton, K., Stringer, E., Strong-Sheldrake, S., Stroud, N., Subbe, C., Sudlow, C.L., Suleiman, Z., Summers, C., Summersgill, C., Sutherland, D., Sykes, D.L., Sykes, R., Talbot, N., Tan, A.L., Tarusan, L., Tavoukjian, V., Taylor, A., Taylor, C., Taylor, J., Te, A., Tedd, H., Tee, C.J., Teixeira, J., Tench, H., Terry, S., Thackray-Nocera, S., Thaivalappil, F., Thamu, B., Thickett, D., Thomas, C., Thomas, D.C., Thomas, S., Thomas, A.K., Thomas-Woods, T., Thompson, T., Thompson, A.A.R., Thornton, T., Thorpe, M., Thwaites, R.S., Tilley, J., Tinker, N., Tiongson, G.F., Tobin, M., Tomlinson, J., Tong, C., Toshner, M., Touyz, R., Tripp, K.A., Tunnicliffe, E., Turnbull, A., Turner, E., Turner, S., Turner, V., Turner, K., Turney, S., Turtle, L., Turton, H., Ugoji, J., Ugwuoke, R., Upthegrove, R., Valabhji, J., Ventura, M., Vere, J., Vickers, C., Vinson, B., Wade, E., Wade, P., Wain, L.V., Wainwright, T., Wajero, L.O., Walder, S., Walker, S., Wall, E., Wallis, T., Walmsley, S., Walsh, J.A., Walsh, S., Warburton, L., Ward, T.J.C., Warwick, K., Wassall, H., Waterson, S., Watson, E., Watson, L., Watson, J., Weir McCall, J., Welch, C., Welch, H., Welsh, B., Wessely, S., West, S., Weston, H., Wheeler, H., White, S., Whitehead, V., Whitney, J., Whittaker, S., Whittam, B., Whitworth, V., Wight, A., Wild, J., Wilkins, M., Wilkinson, D., Williams, B., Williams, N., Williams, J., Williams-Howard, S.A., Willicombe, M., Willis, G., Willoughby, J., Wilson, A., Wilson, D., Wilson, I., Window, N., Witham, M., Wolf-Roberts, R., Wood, C., Woodhead, F., Woods, J., Wootton, D.G., Wormleighton, J., Worsley, J., Wraith, D., Wrey Brown, C., Wright, C., Wright, L., Wright, S., Wyles, J., Wynter, I., Xu, M., Yasmin, N., Yasmin, S., Yates, T., Yip, K.P., Young, B., Young, S., Young, A., Yousuf, A.J., Zawia, A., Zeidan, L., Zhao, B., Zheng, B., Zongo, O., Liew, Felicity, Talwar, Shubha, Cross, Andy, Willett, Brian J., Scott, Sam, Logan, Nicola, Siggins, Matthew K., Swieboda, Dawid, Sidhu, Jasmin K., Efstathiou, Claudia, Davis, Chris, Mohamed, Noura, Nunag, Jose, King, Clara, Rowland-Jones, Sarah L., Chalmers, James D., Ho, Ling-Pei, Horsley, Alexander, Raman, Betty, Poinasamy, Krisnah, Marks, Michael, Kon, Onn Min, Howard, Luke, Wootton, Daniel G., Dunachie, Susanna, Quint, Jennifer K., Evans, Rachael A., Wain, Louise V., Fontanella, Sara, de Silva, Thushan I., Ho, Antonia, Harrison, Ewen, Brightling, Christopher, and Turtle, Lance
Published: 2023
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2. Thrombotic and hemorrhagic complications of COVID-19 in adults hospitalized in high-income countries compared with those in adults hospitalized in low- and middle-income countries in an international registry

Author: Griffee, M, Bozza, P, Reyes, L, Eddington, D, Rosenberger, D, Merson, L, Citarella, B, Fanning, J, Alexander, P, Fraser, J, Dalton, H, Cho, S, Abdukahil, S, Abdulkadir, N, Abe, R, Abel, L, Abrous, A, Absil, L, Acker, A, Adam, E, Adriao, D, Al Ageel, S, Ahmed, S, Ainscough, K, Aisa, T, Hssain, A, Tamlihat, Y, Akimoto, T, Akmal, E, Akwani, C, Al Qasim, E, Alalqam, R, Alberti, A, Al-dabbous, T, Alegesan, S, Alessi, M, Alex, B, Alexandre, K, Al-Fares, A, Alfoudri, H, Ali, I, Alidjnou, K, Aliudin, J, Alkhafajee, Q, Allavena, C, Allou, N, Alves, J, Alves, R, Cabrita, J, Amaral, M, Amira, N, Ampaw, P, Andini, R, Andrejak, C, Angheben, A, Angoulvant, F, Ansart, S, Anthonidass, S, Antonelli, M, de Brito, C, Apriyana, A, Arabi, Y, Aragao, I, Arancibia, F, Araujo, C, Arcadipane, A, Archambault, P, Arenz, L, Arlet, J, Arnold-Day, C, Arora, L, Arora, R, Artaud-Macari, E, Aryal, D, Asensio, A, Ashraf, M, Assie, J, Asyraf, A, Atif, M, Atique, A, Auchabie, J, Aumaitre, H, Auvet, A, Azemar, L, Azoulay, C, Bach, B, Bachelet, D, Badr, C, Baig, N, Baillie, J, Bak, E, Bakakos, A, Bakar, N, Bal, A, Balakrishnan, M, Balan, V, Bani-Sadr, F, Barbalho, R, Barbosa, N, Barclay, W, Barnett, S, Barnikel, M, Barrasa, H, Barrelet, A, Barrigoto, C, Bartoli, M, Baruch, J, Basmaci, R, Basri, M, Battaglini, D, Bauer, J, Rincon, D, Beane, A, Bedossa, A, Hong Bee, K, Begum, H, Behilill, S, Beishuizen, A, Beljantsev, A, Bellemare, D, Beltrame, A, Beltrao, B, Beluze, M, Benech, N, Benjiman, L, Benkerrou, D, Bennett, S, Benny, B, Bento, L, Berdal, J, Bergeaud, D, Bergin, H, Sobrino, J, Bertoli, G, Bertolino, L, Bessis, S, Bevilcaqua, S, Bezulier, K, Bhatt, A, Bhavsar, K, Bianco, C, Bidin, F, Singh, M, Humaid, F, Kamarudin, M, Bisoffi, Z, Bissuel, F, Bitker, L, Bitton, J, Blanco-Schweizer, P, Blier, C, Bloos, F, Blot, M, Blumberg, L, Boccia, F, Bodenes, L, Bogaert, D, Boivin, A, Bolanos, I, Bolze, P, Bompart, F, Borges, D, Borie, R, Bosse, H, Botelho-Nevers, E, Bouadma, L, Bouchaud, O, Bouchez, S, 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C., Lima C., Lina B., Lina L., Lind A., Lingas G., Lion-Daolio S., Lissauer S., Liu K., Livrozet M., Lizotte P., Lolong N., Loon L. C., Lopes D., Lopez-Colon D., Loschner A. L., Loubet P., Loufti B., Louis G., Lourenco S., Lee Low L., Lowik M., Loy J. S., Lucet J. -C., Bermejo C. L., Luna C. M., Lungu O., Luong L., Luque N., Luton D., Lwin N., Lyons R., Maasikas O., Mabiala O., Machado M., Machado S., Macheda G., Madiha H., de la Calle G. M., Mahieu R., Mahy S., Maia A. R., Maier L. S., Maillet M., Maitre T., Malfertheiner M., Malik N., Mallon P., Maltez F., Malvy D., Manda V., Mandelbrot L., Manetta F., Mankikian J., Manning E., Manuel A., Sant`Ana Malaque C. M., Marino F., Markowicz S., Marques A., Marquis C., Marsh B., Marsh L., Marshal M., Marshall J., Martelli C. T., Martin E., Martin-Blondel G., Martinez F. E., Martin-Loeches I., Martinot M., Martins J., Martins A., Martins N., Rego C. M., Martucci G., Martynenko O., Marwali E. M., Marzukie M., Maslove D., Mason S., Mat Nor M. B., Matan M., Mathieu D., Mattei M., Maulin L., Maxwell M., Maynar J., Mazzoni T., Sweeney L. M., McArthur C., McCanny P., McCarthy A., McCloskey C., McConnochie R., McDermott S., McDonald S. E., McElroy A., McElwee S., McEneany V., McEvoy N., McGeer A., McKay C., McKeown J., McLean K. A., McNally P., McNicholas B., McPartlan E., Meaney E., Mear-Passard C., Mechlin M., Mehkri O., Mele F., Melo L., Mendes J. J., Menon K., Mentre F., Mentzer A. J., Mercier E., Mercier N., Merckx A., Mergeay-Fabre M., Mergler B., Mesquita A., Metwally O., Meybeck A., Meyer D., Meynert A. M., Meysonnier V., Meziane A., Mezidi M., Michelanglei C., Michelet I., Mihelis E., Mihnovit V., Miller J., Miranda-Maldonado H., Misnan N. A., Mohamed T. J., Eliza Mohamed N. N., Moin A., Molinos E., Molloy B., Monahan S., Mone M., Monteiro A., Montes C., Montrucchio G., Moore S. C., Moore S., Cely L. M., Moro L., Morton B., Motherway C., Motos A., Mouquet H., Perrot C. M., Moyet J., Mudara C., Muh N. Y., Muhamad D., Mullaert J., Muller F., Muller K. E., Murphy A., Murphy L., Murray P., Murris M., Murthy S., Musaab H., Muyandy G., Myrodia D. M., Nagpal D., Nagrebetsky A., Narasimhan M., Narayanan N., Nazerali-Maitland A., Neant N., Neb H., Neto R., Neumann E., Ng P. Y., Ng W. Y., Nghi A., Nguyen D., Choileain O. N., Leathlobhair N. N., Nichol A. D., Nitayavardhana P., Nonas S., Mohd Noordin N. A., Noret M., Izzati Norharizam N. F., Norman L., Noursadeghi M., Nowinski A., Nseir S., Nunez J. I., Nyamankolly E., Brien F. O., Callaghan A. O., O'Callaghan A., Occhipinti G., OConnor D., O'Donnell M., Ogston T., Ogura T., Oh T. -H., O'Halloran S., O'Hearn K., Ohshimo S., Oliveira J., Oliveira L., Olliaro P. L., Ong D. S. Y., Ong J. Y., Oosthuyzen W., Opavsky A., Openshaw P., Orozco-Chamorro C. M., Ortoleva J., Osatnik J., O'Shea L., O'Sullivan M., Othman S. Z., Ouamara N., Ouissa R., Oziol E., Pagadoy M., Pages J., Palacios A., Palmarini M., Panarello G., Panda P. K., Pang L. H., Panigada M., Pansu N., Papadopoulos A., Parke R., Pasquier J., Pastene B., Patauner F., Pathmanathan M. D., Patrao L., Patricio P., Patrier J., Patterson L., Paul C., Paul M., Paulos J., Paxton W. A., Payen J. -F., Peake S. L., Peariasamy K., Jimenez M. P., Peek G. J., Peelman F., Peiffer-Smadja N., Peigne V., Pejkovska M., Pelosi P., Peltan I. D., Pereira R., Perez D., Periel L., Perpoint T., Pesenti A., Pestre V., Petrou L., Petrovic M., Petrov-Sanchez V., Pettersen F. O., Peytavin G., Pharand S., Picard W., Picone O., de Piero M., Pierobon C., Piersma D., Pimentel C., Pinto R., Piquard V., Pires C., Pironneau I., Piroth L., Piubelli C., Pius R., Plantier L., Png H. S., Poissy J., Pokeerbux R., Poli S., Pollakis G., Ponscarme D., Porto D. B., Post A. -M., Postma D. F., Povoa P., Povoas D., Powis J., Prapa S., Preau S., Prebensen C., Preiser J. -C., Prinssen A., Pritchard M. G., Proenca L., Pudota S., Puechal O., Semedi B. P., Purcell G., Quesada L., Gonzalez V. Q., Quist-Paulsen E., Quraishi M., Qutishat F., Rabaud C., Rafael A., Rafiq M., Rahman R. A., Haji Ab Rahman A. K., Rainieri F., Rajahram G. S., Ramakrishnan N., Ramalho J., Ramli A. A., Rammaert B., Ramos G. V., Ranjan R., Rapp C., Rasmin M., Ratsep I., Ravi T., Real A., Rebaudet S., Redl S., Reeve B., Reid L., Reikvam D. H., Reis R., Rello J., Remppis J., Remy M., Ren H., Renk H., Resseguier A. -S., Revest M., Rewa O., Reyes T., Ribeiro M. I., Richardson D., Richier L., Atikah Ahmad Ridzuan S. N., Rios A. L., Rishu A., Rispal P., Risso K., Rizer N., Robba C., Roberto A., Roberts S., Robertson D. L., Robineau O., Roche-Campo F., Rodari P., Rodeia S., Roessler B., Roger P. -M., Roger C., Roilides E., Rojek A., Romaru J., Roncon-Albuquerque R., Roriz M., Rosa-Calatrava M., Rose M., Rossanese A., Rossetti M., Rossignol B., Rossignol P., Rousset S., Roy C., Roze B., Russell C. D., Ryan M., Ryckaert S., Holten A. R., Saba I., Sadat M., Sahraei V., Saint-Gilles M., Sakiyalak P., Salazar L., Sales G., Sallaberry S., Gandonniere C. S., Salvator H., Sanchez O., Sanchez E., Sanchez-Miralles A., Sancho-Shimizu V., Sandhu G., Sandhu Z., Sandrine P. -F., Sandulescu O., Santos M., Sarfo-Mensah S., Sarmento Banheiro B., Sarmiento I. C. E., Sarton B., Satyapriya S., Satyawati R., Saviciute E., Savvidou P., Saw Y. T., Schaffer J., Schermer T., Scherpereel A., Schneider M., Schroll S., Schwameis M., Scicluna B., Scott J. T., Scott-Brown J., Sedillot N., Seitz T., Selvarajoo M., Semaille C., Semple M. G., Senian R. B., Senneville E., Sepulveda C., Sequeira F., Sequeira T., Neto A. S., Balazote P. S., Shadowitz E., Shahidan S. A., Shamsah M., Sharjeel S., Sharma P., Shaw C. A., Shaw V., Sheenan J. R., Shi H., Shime N., Shimizu K., Shrapnel S., Shum H. P., Mohammed N. S., Siang N. Y., Sibiude J., Siddiqui A., Sigfrid L., Sillaots P., Silva C., Silva R., Silva M. J., Lim Heng B. S., Sin W. C., Singh P., Singh B. C., Sitompul P. A., Sivam K., Skogen V., Smith S., Smood B., Smyth C., Smyth M., Snacken M., So D., Soh T. V., Solomon J., Solomon T., Somers E., Sommet A., Song R., Song M. J., Song T., Chia J. S., Sonntagbauer M., Soom A. M., Sotto A., Soum E., Sousa M., Sousa A. C., Uva M. S., Souza-Dantas V., Sperry A., Spinuzza E., Sriskandan S., Stabler S., Staudinger T., Stecher S. -S., Steinsvik T., Stienstra Y., Stiksrud B., Stolz E., Stone A., Streinu-Cercel A., Stuart A., Stuart D., Su R., Suen J. Y., Suen G., Sukumar P., Sultana A., Summers C., Supic D., Suppiah D., Surovcova M., Syahrin S., Syrigos K., Sztajnbok J., Szuldrzynski K., Tabrizi S., Taccone F. S., Tagherset L., Taib S. M., Taleb S., Talsma J., Tampubolon M. L., Tan K. K., Tan Y. C., Tanaka H., Tanaka T., Taniguchi H., Tardivon C., Tattevin P., Taufik M. A., Tawfik H., Tedder R. S., Tee T. Y., Teixeira J., Tejada S., Tellier M. -C., Teoh S. K., Teotonio V., Teoule F., Terpstra P., Terrier O., Terzi N., Tessier-Grenier H., Tey A., Mohd Thabit A. A., Tham Z. D., Thangavelu S., Theron E., Thibault V., Thiberville S. -D., Thill B., Thirumanickam J., Thompson S., Thomson D., Thomson E. C., Thorpe M., Thanga Thurai S. R., Thwaites R. S., Tierney P., Tieroshyn V., Timsit J. -F., Tissot N., Toal F., Yang Toh J. Z., Toki M., Tonby K., Tonnii S. L., Torre M., Torres M., Torres A., Torres-Zevallos H., Towers M., Trapani T., Trioux T., Tromeur C., Trontzas I., Trouillon T., Truong J., Tual C., Tubiana S., Tuite H., Turgeon A. F., Turmel J. -M., Turtle L. C. W., Tveita A., Twardowski P., Uchiyama M., Udy A., Ullrich R., Uribe A., Usman A., Uyeki T. M., Vajdovics C., Val-Flores L., Valran A., Van de Velde S., van den Berge M., Van der Feltz M., van der Palen J., van der Valk P., Van Der Vekens N., Van der Voort P., Van Der Werf S., van Gulik L., Van Hattem J., van Netten C., van Someren Greve F., van Veen I., Van Willigen H., Vanel N., Vanoverschelde H., Varghese P., Varrone M., Vasudayan S. R., Vauchy C., Veeran S., Veislinger A., Vencken S., Ventura S., Verbon A., Vidal J. E., Vieira C., Villanueva J. A., Villar J., Villeneuve P. -M., Villoldo A., Visseaux B., Visser H., Vitiello C., Vonkeman H., Vuotto F., Wahab N. H., Wahab S. A., Wahid N. A., Wainstein M., Walsh L., Wang C. -H., Webb S., Wei J., Weil K., Wen T. P., Wesselius S., Wham M., Whelan B., White N., Wicky P. H., Wiedemann A., Wijaya S. O., Wille K., Willems S., Williams B., Williams V., Williams P. J., Wils E. -J., Wittman J., Wong C., Wong X. C., Wong Y. S., Wong T. F., Xian G. E., Xian L. S., Kuan P. X., Xynogalas I., Binti Mohd Yakop S. R., Yamazaki M., Yarad E., Yazdanpanah Y., Liang Hing N. Y., Yelnik C., Yeoh C. H., Yerkovich S., Yokoyama T., Yonis H., Yousif O., Zaaqoq A., Zabbe M., Zacharowski K., Zahid M., Zahran M., Binti Zaidan N. Z., Zambon M., Zambrano M., Zanella A., Zaynah N., Zayyad H., Zoufaly A., and Zucman D.
Abstract: Background: COVID-19 has been associated with a broad range of thromboembolic, ischemic, and hemorrhagic complications (coagulopathy complications). Most studies have focused on patients with severe disease from high-income countries (HICs). Objectives: The main aims were to compare the frequency of coagulopathy complications in developing countries (low- and middle-income countries [LMICs]) with those in HICs, delineate the frequency across a range of treatment levels, and determine associations with in-hospital mortality. Methods: Adult patients enrolled in an observational, multinational registry, the International Severe Acute Respiratory and Emerging Infections COVID-19 study, between January 1, 2020, and September 15, 2021, met inclusion criteria, including admission to a hospital for laboratory-confirmed, acute COVID-19 and data on complications and survival. The advanced-treatment cohort received care, such as admission to the intensive care unit, mechanical ventilation, or inotropes or vasopressors; the basic-treatment cohort did not receive any of these interventions. Results: The study population included 495,682 patients from 52 countries, with 63% from LMICs and 85% in the basic treatment cohort. The frequency of coagulopathy complications was higher in HICs (0.76%-3.4%) than in LMICs (0.09%-1.22%). Complications were more frequent in the advanced-treatment cohort than in the basic-treatment cohort. Coagulopathy complications were associated with increased in-hospital mortality (odds ratio, 1.58; 95% CI, 1.52-1.64). The increased mortality associated with these complications was higher in LMICs (58.5%) than in HICs (35.4%). After controlling for coagulopathy complications, treatment intensity, and multiple other factors, the mortality was higher among patients in LMICs than among patients in HICs (odds ratio, 1.45; 95% CI, 1.39-1.51). Conclusion: In a large, international registry of patients hospitalized for COVID-19, coagulopathy complications were mo
Published: 2023

3. Role of mucosal-associated invariant T cells in coronavirus disease 2019 vaccine immunogenicity.

Author: Amini, Ali, Klenerman, Paul, and Provine, Nicholas M
Abstract: Mucosal-associated invariant T (MAIT) cells are an unconventional T cell population that are highly abundant in humans. They possess a semi-invariant T cell receptor (TCR) that recognises microbial metabolites formed during riboflavin biosynthesis, presented on a nonpolymorphic MHC-like molecule MR1. MAIT cells possess an array of effector functions, including type 1, type 17, and tissue repair activity. Deployment of these functions depends on the stimuli they receive through their TCR and/or cytokine receptors. Strong cytokine signalling, such as in response to vaccination, can bypass TCR triggering and provokes a strong proinflammatory response. Although data are still emerging, multiple aspects of MAIT cell biology are associated with modulation of immunity induced by the coronavirus disease 2019 mRNA and adenovirus vector vaccines. In this review, we will address how MAIT cells may play a role in immunogenicity of vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and how these cells can be harnessed as cellular adjuvants. [ABSTRACT FROM AUTHOR]
Published: 2024
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4. Novel genetically-modified chimpanzee adenovirus and MVA-vectored respiratory syncytial virus vaccine safely boosts humoral and cellular immunity in healthy older adults.

Author: Green, Christopher A., Sande, Charles J., Scarselli, Elisa, Capone, Stefania, Vitelli, Alessandra, Nicosia, Alfredo, Silva-Reyes, Laura, Thompson, Amber J., de Lara, Catherine M., Taylor, Kathryn S., Haworth, Kathryn, Hutchings, Claire L., Cargill, Tamsin, Angus, Brian, Klenerman, Paul, and Pollard, Andrew J.
Abstract: Objectives: Respiratory syncytial virus (RSV) causes respiratory infection across the world, with infants and the elderly at particular risk of developing severe disease and death. The replication-defective chimpanzee adenovirus (PanAd3-RSV) and modified vaccinia virus Ankara (MVA-RSV) vaccines were shown to be safe and immunogenic in young healthy adults. Here we report an extension to this first-in-man vaccine trial to include healthy older adults aged 60-75 years.Methods: We evaluated the safety and immunogenicity of a single dose of MVA-RSV given by intra-muscular (IM) injection (n = 6), two doses of IM PanAd3-RSV given 4-weeks apart (n = 6), IM PanAd3-RSV prime and IM MVA-RSV boost 8-weeks later (n = 6), intra-nasal (IN) spray of PanAd3-RSV prime and IM MVA-RSV boost 8-weeks later (n = 6), or no vaccine (n = 6). Safety measures included all adverse events within one week of vaccination and blood monitoring. Immunogenicity measures included serum antibody responses (RSV- and PanAd3-neutralising antibody titres measured by plaque-reduction neutralisation and SEAP assays, respectively), peripheral B-cell immune responses (frequencies of F-specific IgG and IgA antibody secreting cells and memory B-cells by ex vivo and cultured dual-colour ELISpot assays respectively), and peripheral RSV-specific T-cell immune responses (frequencies of IFNγ-producing T-cells by ex vivo ELISpot and CD4+/CD8+/Tfh-like cell frequencies by ICS/FACS assay).Results: The vaccines were safe and well tolerated. Compared with each individual baseline immunity the mean fold-changes in serum RSV-neutralising antibody, appearance and magnitude of F-specific IgG and IgA ASCs and expansion of CD4+/CD8+ IFNγ-producing T-cells in peripheral circulation were comparable to the results seen from younger healthy adults who received the same vaccine combination and dose. There were little/no IgA memory B-cell responses in younger and older adults. Expansion of IFNγ-producing T-cells was most marked in older adults following IM prime, with balanced CD4+ and CD8+ T cell responses. The RSV-specific immune responses to vaccination did not appear to be attenuated in the presence of PanAd3 (vector) neutralising antibody.Conclusions: PanAd3-RSV and MVA-RSV was safe and immunogenic in older adults and the parallel induction of RSV-specific humoral and cellular immunity merits further assessment in providing protection from severe disease. [ABSTRACT FROM AUTHOR]
Published: 2019
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5. SAT-431 - A pan-genotype HCV T cell vaccine, in a simian adenovirus vector, to target T cell epitopes conserved across multiple HCV genotypes

Author: Donnison, T., von Delft, A., Chinnakannan, S.K., Lourenco, J., Hutchings, C., Brown, A., Klenerman, P., and Barnes, E.
Published: 2018
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6. SAT-409 - Highly immunogenic virally vectored T cell vaccine against HCV are able to induce specific CD4+ T cell helper responses

Author: Esposito, I., Hartnell, F., Swadling, L., Phetsouphanh, C., Brown, A., Lara, C.D., Folgori, A., Capone, S., Barnes, E., and Klenerman, P.
Published: 2018
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7. Consequences of Identifying XIAP Deficiency in an Adult Patient With Inflammatory Bowel Disease.

Author: Quaranta, Maria, Wilson, Rachel, Gonçalves Serra, Eva, Pandey, Sumeet, Schwerd, Tobias, Gilmour, Kimberly, Klenerman, Paul, Powrie, Fiona, Keshav, Satish, Travis, Simon P.L., Anderson, Carl A., and Uhlig, Holm H.
Published: 2018
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8. SAT-391 - IGG4-Related Disease is Associatied with CD4+ T Cell Activation and Regulation

Author: Cargill, T., Culver, E., Makuch, M., Manganis, C., Willberg, C., Sadler, R., Vermeulen, E., Lighaam, L., Llibre, A., Swadling, L., Evans, C., Green, C., Kurioka, A., Brown, A., de Lara, C., van Ham, M., Klenerman, P., Rispens, T., and Barnes, E.
Published: 2016
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9. SAT-376 - Helicobacter Pylori as a Microbial Antigen in IGG4-Related Disease

Author: Culver, E.L., Smit, W., Evans, C., Sadler, R., Cargill, T., Wang, L.-M., Klenerman, P., Ferry, B., and Barnes, E.
Published: 2016
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10. FRI-235 - Vaccine-Induced HCV-Specific CD8+ T Cell Response Restricted by the Protective HLA Allele B*27: Broad Cross-Recognition of Evolving Viral Variants

Author: Frohnmüller, K., Swadling, L., Nitschke, K., Klenerman, P., Thimme, R., Barnes, E., and Neumann-Haefelin, C.
Published: 2016
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11. FRI-209 - The Generation of an Immunogenic Second-Generation Conserved Segment HCV T Cell Vaccine to Target Multiple HCV Genotypes

Author: Von Delft, A., Donnison, T., Chinnakannan, S., Lourenco, J., Hutchings, C., Brown, A., Klenerman, P., and Barnes, E.
Published: 2016
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12. THU-262 - Genome-To-Genome Virus-Host Analysis Reveals HCV Genotype 3 Viral Polymorphisms Linked Viral Load and to Host HLA Class-I/II and IL28B Alleles

Author: Azim Ansari, M., Pedergnana, V., Bonsall, D., Chaturvedi, N., Bartha, I., Fellay, J., Smith, D., Bowden, R., Ip, C., Trebes, A., Piazza, P., Foster, G., Cooke, G., Klenerman, P., Barnes, E., and Spencer, C.
Published: 2016
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13. THU-253 - Comparison of next Generation Sequencing Technologies for the Comprehensive Assessment of Full-Length Hepatitis C Viral Genomes

Author: Thomson, E., Ip, C., Badhan, A., Christiansen, M., Adamson, W., Ansari, A., Bibby, D., Bonsall, D., Bowden, R., Breuer, J., Brown, A., Bryant, J., Da Silva Filipe, A., Hinds, C., Hudson, E., Klenerman, P., Lythgow, K., Mbisa, J., McLauchlan, J., Myers, R., Piazza, P., Roy, S., Trebes, A., Vattipally, S., Witteveldt, J., Simmonds, P., and Barnes, E.
Published: 2016
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14. THU-252 - Sequencing Methods Developed for Hepatitis C Identifies a New Virus, Human Hepegivirus 1, in Patients with Advanced Cirrhosis

Author: Bonsall, D.G., Gregory, W.F., Ip, C.L., Donfield, S., Iles, J., Ansari, M.A., Piazza, P., Trebes, A., Frater, J., Pybus, O., Goulder, P., Klenerman, P., Brown, A., Bowden, R., Gomperts, E.G., Barnes, E., Kapoor, A., Sharp, C., and Simmonds, P.
Published: 2016
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15. PS031 - Characterisation of the Specificity, Functionality and Durability of Host T-Cell Responses against the Full HEV Genome

Author: Halliday, J., Brown, A., Swadling, L., Madden, R., Bendall, R., Jubb, S., Hunter, J., Maggs, J., Simmonds, P., Smith, D., Vine, L., McLaughlin, C., Collier, J., Jeffery, K., Klenerman, P., Izopet, J., Kamar, N., Dalton, H., and Barnes, E.
Published: 2016
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16. CD161intCD8+ T cells: a novel population of highly functional, memory CD8+ T cells enriched within the gut.

Author: Fergusson, J R, Hühn, M H, Swadling, L, Walker, L J, Kurioka, A, Llibre, A, Bertoletti, A, Holländer, G, Newell, E W, Davis, M M, Sverremark-Ekström, E, Powrie, F, Capone, S, Folgori, A, Barnes, E, Willberg, C B, Ussher, J E, and Klenerman, P
Published: 2016
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17. P1191 : Increased IgG4 responses to multiple environmental antigens indicate a polyclonal expansion and differentiation of pre-existing B cells in autoimmune pancreatitis and IgG4 -related cholangitis

Author: Culver, E.L., Makuch, M., Vermeulen, E., van Leeuwen, A., Sadler, R., Cargill, T., Klenerman, P., Aalberse, R.C., Van Ham, S.M., Barnes, E., and Rispens, T.
Published: 2015
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18. P1173 : Mait cells are enriched in portal tracts and respond to biliary epithelial cells presenting bacterial ligands during liver inflammation

Author: Jeffery, H., van Wilgenburg, B., Hunter, S., Kurioka, A., Parekh, K., Stirling, K., Roberts, S., Adams, D., Klenerman, P., and Oo, Y.H.
Published: 2015
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19. MAIT cells are licensed through granzyme exchange to kill bacterially sensitized targets.

Author: Kurioka, A, Ussher, J E, Cosgrove, C, Clough, C, Fergusson, J R, Smith, K, Kang, Y-H, Walker, L J, Hansen, T H, Willberg, C B, and Klenerman, P
Published: 2015
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20. Liver Sinusoidal Endothelial Cells: An Antiviral “Defendothelium”.

Author: Klenerman, Paul and Ramamurthy, Narayan
Published: 2015
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21. 1163: BOTH VEDOLIZUMAB AND ANTI-TNF THERAPY ARE ASSOCIATED WITH ATTENUATION OF SEROLOGICAL AND NEUTRALIZING RESPONSES TO SARS-COV-2 INFECTION IN INFLAMMATORY BOWEL DISEASE.

Author: Wellens, Judith, Edmans, Matthew, Obolski, Uri, Marlow, Luke, Brann, Stephanie, Dunachie, Susanna, Eyre, David W., Helmus, Drew, Barnes, Eleanor, Colombel, Jean Frederic, Wong, Serre-Yu, Klenerman, Paul, Lindsay, James O., Thompson, Craig, and Satsangi, Jack J.
Published: 2022
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22. P.1.e.012 Effect of interferon-alfa on cortical glutamate in patients with hepatitis C: a proton magnetic resonance spectroscopy study

Author: Godlewska, B.R., Taylor, M.J., Near, J., Christmas, D., Potokar, J., Collier, J., Klenerman, P., Barnes, E., and Cowen, P.J.
Published: 2012
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23. Temporal Analysis of Early Immune Responses in Patients With Acute Hepatitis B Virus Infection.

Author: Dunn, Claire, Peppa, Dimitra, Khanna, Pooja, Nebbia, Gaia, Jones, Meleri, Brendish, Nathan, Lascar, R. Monica, Brown, David, Gilson, Richard J., Tedder, Richard J., Dusheiko, Geoffrey M., Jacobs, Michael, Klenerman, Paul, and Maini, Mala K.
Subjects: IMMUNE response, HEPATITIS B, DENDRITIC cells, ENZYME-linked immunosorbent assay, HIV, TUMOR necrosis factors, INTERFERONS, VIREMIA, NATURAL immunity, PATIENTS
Abstract: Background & Aims: Hepatitis B virus (HBV) causes more than 1 million deaths annually from immune-mediated liver damage. The long incubation period has been difficult to study; by the time most patients present, massive viremia and the majority of viral clearance have already occurred. The aim of this study was to investigate the contribution of innate and adaptive immune mechanisms in early acute HBV through access to an unusual cohort of patients sampled in the preclinical phase and followed up to resolution of their infection. Methods: Twenty-one patients with acute HBV were studied, 8 of them from before the peak of viremia. Circulating innate cytokines were quantitated by enzyme-linked immunosorbent assay and natural killer (NK) and T-cell effector function by flow cytometry. Results were correlated with temporal changes in viral load, serology, and liver inflammation and compared with healthy controls. Results: Type I interferon (IFN) remained barely detectable throughout, with concentrations no higher than those found in healthy controls. Similarly, interleukin-15 and IFN-λ1 were not induced during peak viremia. NK cell activation and capacity for IFN-γ production were reduced at peak viremia. Early functional HBV-specific CD4 and CD8 T-cell responses were attenuated as viral load increased and recovered again as infection resolved. The transient inhibition of NK and T-cell responses coincided with a surge in the immunosuppressive cytokine interleukin-10 accompanying HBV viremia. Conclusions: The early stages of acute HBV are characterized by induction of interleukin-10 rather than type I IFN, accompanied by a temporary attenuation of NK and T-cell responses. [Copyright &y& Elsevier]
Published: 2009
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24. Resistance to apoptosis underpins the corticosteroid insensitivity of group 2 innate lymphoid cells.

Author: Luo, Jian, Wu, Yanqiu, Shrimanker, Rahul, Go, Simei, Ye, Yuan, Hardman, Clare, Nahler, Janina, Chen, Yi-Ling, Stöger, Linda, Zeng, Ni, Liu, Wei, Reed, Lara, Tolkovsky, Aviva M., Klenerman, Paul, Ogg, Graham, Pavord, Ian D., and Xue, Luzheng
Published: 2019
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25. HLA contributes to immune control of hepatitis B in HIV-positive African adults.

Author: Matthews, Philippa, Beloukas, Apostolos, Malik, Amna, Carlson, Jonathan, Jooste, Pieter, Ogwu, Anthony, Shapiro, Roger, Riddell, Lynn, Chen, Fabian, Luzzi, Graz, Jaggernath, Manjeetha, Jesuthasan, Gerald, Jeffery, Katie, Ndung'u, Thumbi, Goulder, Philip, Geretti, Anna Maria, and Klenerman, Paul
Published: 2015
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26. Cysteinyl leukotriene E4 activates human group 2 innate lymphoid cells and enhances the effect of prostaglandin D2 and epithelial cytokines.

Author: Salimi, Maryam, Stöger, Linda, Liu, Wei, Go, Simei, Pavord, Ian, Klenerman, Paul, Ogg, Graham, and Xue, Luzheng
Abstract: Background Group 2 innate lymphoid cells (ILC2s) are a potential innate source of type 2 cytokines in the pathogenesis of allergic conditions. Epithelial cytokines (IL-33, IL-25, and thymic stromal lymphopoietin [TSLP]) and mast cell mediators (prostaglandin D 2 [PGD 2 ]) are critical activators of ILC2s. Cysteinyl leukotrienes (cysLTs), including leukotriene (LT) C 4 , LTD 4 , and LTE 4 , are metabolites of arachidonic acid and mediate inflammatory responses. Their role in human ILC2s is still poorly understood. Objectives We sought to determine the role of cysLTs and their relationship with other ILC2 stimulators in the activation of human ILC2s. Methods For ex vivo studies, fresh blood from patients with atopic dermatitis and healthy control subjects was analyzed with flow cytometry. For in vitro studies, ILC2s were isolated and cultured. The effects of cysLTs, PGD 2 , IL-33, IL-25, TSLP, and IL-2 alone or in combination on ILC2s were defined by using chemotaxis, apoptosis, ELISA, Luminex, quantitative RT-PCR, and flow cytometric assays. The effect of endogenous cysLTs was assessed by using human mast cell supernatants. Results Human ILC2s expressed the LT receptor CysLT 1 , levels of which were increased in atopic subjects. CysLTs, particularly LTE 4 , induced migration, reduced apoptosis, and promoted cytokine production in human ILC2s in vitro . LTE 4 enhanced the effect of PGD 2 , IL-25, IL-33, and TSLP, resulting in increased production of type 2 and other proinflammatory cytokines. The effect of LTE 4 was inhibited by montelukast, a CysLT 1 antagonist. Interestingly, addition of IL-2 to LTE 4 and epithelial cytokines significantly amplified ILC2 activation and upregulated expression of the receptors for IL-33 and IL-25. Conclusion CysLTs, particularly LTE 4 , are important contributors to the triggering of human ILC2s in inflammatory responses, particularly when combined with other ILC2 activators. [ABSTRACT FROM AUTHOR]
Published: 2017
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27. Mo1447 - Clinical and Translational Outcomes in Patients with Primary Sclerosing Cholangitis and Inflammatory Bowel Disease Receiving Vedolizumab.

Author: Williamson, Kate D., Slevin, Stephanie, Willberg, Christian, Chapman, Roger W., Klenerman, Paul, and Keshav, Satish
Published: 2017
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28. Prostaglandin D2 and leukotriene E4 synergize to stimulate diverse TH2 functions and TH2 cell/neutrophil crosstalk.

Author: Xue, Luzheng, Fergusson, Joannah, Salimi, Maryam, Panse, Isabel, Ussher, James E., Hegazy, Ahmed N., Vinall, Shân L., Jackson, David G., Hunter, Michael G., Pettipher, Roy, Ogg, Graham, and Klenerman, Paul
Abstract: Background Prostaglandin D 2 (PGD 2 ) and cysteinyl leukotrienes (cysLTs) are lipid mediators derived from mast cells, which activate T H 2 cells. The combination of PGD 2 and cysLTs (notably cysteinyl leukotriene E 4 [LTE 4 ]) enhances T H 2 cytokine production. However, the synergistic interaction of cysLTs with PGD 2 in promoting T H 2 cell activation is still poorly understood. The receptors for these mediators are drug targets in the treatment of allergic diseases, and hence understanding their interaction is likely to have clinical implications. Objective We aimed to comprehensively define the roles of PGD 2 , LTE 4 , and their combination in activating human T H 2 cells and how such activation might allow the T H 2 cells to engage downstream effectors, such as neutrophils, which contribute to the pathology of allergic responses. Methods The effects of PGD 2 , LTE 4 , and their combination on human T H 2 cell gene expression were defined by using a microarray, and changes in specific inflammatory pathways were confirmed by means of PCR array, quantitative RT-PCR, ELISA, Luminex, flow cytometry, and functional assays, including analysis of downstream neutrophil activation. Blockade of PGD 2 and LTE 4 was tested by using TM30089, an antagonist of chemoattractant receptor-homologous molecule expressed on T H 2 cells, and montelukast, an antagonist of cysteinyl leukotriene receptor 1. Results PGD 2 and LTE 4 altered the transcription of a wide range of genes and induced diverse functional responses in T H 2 cells, including cell adhesion, migration, and survival and cytokine production. The combination of these lipids synergistically or additively enhanced T H 2 responses and, strikingly, induced marked production of diverse nonclassical T H 2 inflammatory mediators, including IL-22, IL-8, and GM-CSF, at concentrations sufficient to affect neutrophil activation. Conclusions PGD 2 and LTE 4 activate T H 2 cells through different pathways but act synergistically to promote multiple downstream effector functions, including neutrophil migration and survival. Combined inhibition of both PGD 2 and LTE 4 pathways might provide an effective therapeutic strategy for allergic responses, particularly those involving interaction between T H 2 cells and neutrophils, such as in patients with severe asthma. [ABSTRACT FROM AUTHOR]
Published: 2015
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29. Prostaglandin D2 activates group 2 innate lymphoid cells through chemoattractant receptor-homologous molecule expressed on TH2 cells.

Author: Xue, Luzheng, Salimi, Maryam, Panse, Isabel, Mjösberg, Jenny M., McKenzie, Andrew N.J., Spits, Hergen, Klenerman, Paul, and Ogg, Graham
Abstract: Background: Activation of the group 2 innate lymphoid cell (ILC2) population leads to production of the classical type 2 cytokines, thus promoting type 2 immunity. Chemoattractant receptor-homologous molecule expressed on TH2 cells (CRTH2), a receptor for prostaglandin D2 (PGD2), is expressed by human ILC2s. However, the function of CRTH2 in these cells is unclear. Objectives: We sought to determine the role of PGD2 and CRTH2 in human ILC2s and compare it with that of the established ILC2 activators IL-25 and IL-33. Methods: The effects of PGD2, IL-25, and IL-33 on the cell migration, cytokine production, gene regulation, and receptor expression of ILC2s were measured with chemotaxis, ELISA, Luminex, flow cytometry, quantitative RT-PCR, and QuantiGene assays. The effects of PGD2 under physiologic conditions were evaluated by using the supernatant from activated mast cells. Results: PGD2 binding to CRTH2 induced ILC2 migration and production of type 2 cytokines and many other cytokines. ILC2 activation through CRTH2 also upregulated the expression of IL-33 and IL-25 receptor subunits (ST2 and IL-17RA). The effects of PGD2 on ILC2s could be mimicked by the supernatant from activated human mast cells and inhibited by a CRTH2 antagonist. Conclusions: PGD2 is an important and potent activator of ILC2s through CRTH2 mediating strong proallergic inflammatory responses. Through IgE-mediated mast cell degranulation, these innate cells can also contribute to adaptive type 2 immunity; thus CRTH2 bridges the innate and adaptive pathways in human ILC2s. [Copyright &y& Elsevier]
Published: 2014
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30. An adenoviral model to unlock the secrets of memory inflation?

Author: Colston, Julia, Bolinger, Beatrice, Turner, Alison, Gilbert, Sarah, and Klenerman, Paul
Published: 2013
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31. HLA alleles in combination with innate immune genes are key determinants of viral outcome in Hepatitis C virus infection.

Author: Fitzmaurice, Karen, Hurst, Jacob, Dring, Megan, Gardiner, Clair, and Klenerman, Paul
Published: 2013
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32. Inflammation in common variable immunodeficiency is associated with a distinct CD8+ response to cytomegalovirus.

Author: Marashi, Sayed Mahdi, Raeiszadeh, Mohammad, Workman, Sarita, Rahbar, Afsar, Soderberg-Naucler, Cecilia, Klenerman, Paul, Chee, Ronnie, Webster, A. David, Milne, Richard S.B., and Emery, Vincent C.
Subjects: INFLAMMATION, IMMUNODEFICIENCY, CYTOMEGALOVIRUSES, PHENOTYPES, IMMUNOHISTOCHEMISTRY, BIOLOGICAL assay, T cell receptors, BIOMARKERS, EPSTEIN-Barr virus
Abstract: Background: Common variable immunodeficiency is the most common primary immunodeficiency. A subset of patients has debilitating inflammatory complications. Objectives: We investigated the role of cytomegalovirus (CMV), and the T-cell response targeted at this virus, in this inflammatory disease. Methods: Phenotypic and functional assays were used to profile CMV-specific T cells in patients with common variable immunodeficiency with and without inflammatory complications. Highly sensitive immunohistochemistry was used to detect CMV antigens at sites of inflammation. Results: Cytomegalovirus was significantly associated with inflammatory disease, which occurred in 31 of 43 (72%) virus-exposed patients and 8 of 31 (26%) naive patients (P = .0001). CMV pp65-NLVPMVATV epitope–specific CD8+ T-cell frequencies were significantly elevated in inflammatory patients, but these cells did not show evidence of exhaustion, with low levels of programmed death-1 and high T-cell receptor avidity. Rather, they showed features consistent with high in vivo functionality and proliferative activity including reduced levels of the anti-inflammatory marker CD73 (1.67% of NLV+ cells were CD73+ vs 42.01% in noninflammatory patients; P = .004) and increased Ki-67 expression (37% vs 2% in noninflammatory patients; P < .0001). In vitro, the CMV-specific T cells showed high antigen-specific proliferative potential compared with cells from noninflammatory patients. By using sensitive immunohistochemistry, we detected for the first time viral antigen at the sites of inflammation, indicative of active viral replication. Conclusion: Our data strongly support a direct role for CMV and a hyperreactive CMV-specific immune response in the debilitating chronic inflammatory complications of common variable immunodeficiency. [ABSTRACT FROM AUTHOR]
Published: 2011
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33. HLA footprinting reveals a novel protective CD8 + T cell response in Hepatitis C virus infection.

Author: Fitzmaurice, Karen, Petrovic, Danijela, Gaudieri, Silvana, Freitas, Elizabeth, Sims, Stuart, Long, Aideen, Kelleher, Dermot, and Klenerman, Paul
Published: 2009
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34. It's not what you've got it's what you do with it: Identifying the components of a Better Immune Response to HIV.

Author: Northfield, J.W., Loo, C., Michaelsson, J., Nixon, D., and Klenerman, P.
Published: 2007
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35. Humoral and cellular immunity to RSV in infants, children and adults.

Author: Green, C.A., Sande, C.J., de Lara, C., Thompson, A.J., Silva-Reyes, L., Napolitano, F., Pierantoni, A., Capone, S., Vitelli, A., Klenerman, P., and Pollard, A.J.
Subjects: *RESPIRATORY syncytial virus, *CELLULAR immunity, *HUMORAL immunity, *IMMUNOGLOBULIN A, *IMMUNE response
Abstract: Abstract Background Respiratory syncytial virus (RSV) causes respiratory disease throughout life. Here we report differences in naturally acquired immunity with age and presumed exposure. Methods A longitudinal, non-interventional, observational study was performed in healthy adults (20 paediatric healthcare workers and 10 non-healthcare workers), children (10 aged 3–6 years) and infants (5 aged 2–4 months and 20 aged 6–12 months). Blood samples were analysed for RSV-neutralising antibody titre, F/Ga/Gb-specific antibody titres, F-specific IgG/IgA memory B-cell frequencies and T-cell production of IFNγ, IL-4, IL-13 and IL-17. Results Serum G-specific antibody titres were significantly lower in infants and children than adults. However, serum titres of F-specific and RSV-neutralising antibody and IFNγ-producing T-cell frequencies were low or absent in the infants, but comparable between children and adults. Interestingly, F-specific memory IgA B-cells could not be detected in paediatric samples and in samples from non-healthcare workers, but recordable IgA memory B-cells were found in 9/18 paediatric healthcare workers and 2/8 non-healthcare workers at the end of the RSV season. These responses waned 4–6 months later. By contrast, F-specific IgG memory B-cells were detectable in samples from all adults without significant variation across time points. T-cells producing IL-4, IL-13 and IL-17 responses were not detectable in peripheral blood from a subset of volunteers. Conclusions Repeated RSV exposure in early life generates immune responses that are inversely related to frequency of severe disease. Induction of F-specific antibody and cellular immune responses through infant vaccination might help to accelerate the development of protective immune responses at an early age. Clinicaltrials.gov reference NCT01563692 and NCT01640652. [ABSTRACT FROM AUTHOR]
Published: 2018
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36. Occult cytomegalovirus in vivarium-housed mice may influence transplant allograft acceptance.

Author: Thomas, A. C., Forster, M. R., Bickerstaff, A. A., Zimmerman, P. D., Wing, B. A., Trgovcich, J., Bergdall, V. K., Klenerman, P., and Cook, C. H.
Subjects: *CYTOMEGALOVIRUSES, *TRANSPLANTATION immunology, *T cells, *LABORATORY rats, *HEART transplantation, *HOMOGRAFTS
Abstract: We have recently shown that latent murine cytomegalovirus (MCMV) can influence murine transplant allograft acceptance. During these studies we became aware that vivarium-housed control mice can acquire occult MCMV infection. The purpose of this investigation was to confirm occult MCMV transmission and determine the timing, vehicle, and possible consequences of transmission. Mice arriving from a commercial vendor were negative for MCMV both by commercial serologic testing and by our nested PCR. Mice housed in our vivarium became positive for MCMV DNA 30-60 days after arrival, but remained negative for MCMV by commercial serologic testing. To confirm MCMV we sequenced PCR products for several genes and showed >99% homology to MCMV. Further sequence analyses show that the occult MCMV is similar to a laboratory strain of MCMV, but the vehicle of transmission remains unclear. Control tissues from historical experiments with unexplained graft losses were evaluated for occult MCMV, and mice with unexplained allograft losses showed significantly higher incidence of occult MCMV than did allograft acceptors. Deliberate infection with very low titer MCMV confirmed that viral transmission can occur without measurable virus specific antibody or T-cell responses. These data suggest that vivarium-housed mice can develop occult MCMV that is missed by currently available commercial serologic testing, and that these infections may influence transplant allograft acceptance. Copyright (c) 2010 Elsevier B.V. All rights reserved. [ABSTRACT FROM AUTHOR]
Published: 2010
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37. Tracking epitope-specific antiviral CD4+ T cell responses to a live attenuated vaccine reveals ongoing functional responses

Author: Jones, L., Malavige, G., Jeffery, K., Kemp, E., Breuer, J., Klenerman, P., and Ogg, G.S.
Subjects: *EPITOPES, *ANTIVIRAL agents, *T cells, *IMMUNIZATION, *ANTIGENS, *VARICELLA-zoster virus, *VIRAL vaccines, *PHENOTYPES
Abstract: Abstract: There are few studies that have examined the frequencies of epitope-specific CD4+ T cells following the use of a highly effective vaccine, yet such data would potentially be of value for the development of novel vaccination strategies. In this study we tracked human epitope-specific CD4+ T cell responses over time after immunisation with a live attenuated varicella zoster virus vaccine by MHC Class II tetrameric complexes and functional assays. We show that the peptide-specific responses reflect those against whole virus antigens, and are similar in both frequency and phenotype to those found in healthy volunteers, despite a highly attenuated and clinically inapparent infection. [Copyright &y& Elsevier]
Published: 2009
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38. Positive selection mediated by cytotoxic T lymphocytes influences HIV-1 evolution during primary infection

Author: Price, D.A., Goulder, P.J.R., Klenerman, P., Sewell, A.K., Easterbrook, P.J., Troop, M., Bangham, C.R.M., and Phillips, R.E.
Published: 1997
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39. P1241 A FULLY-AUTOMATED PIPELINE FOR SEQUENCING WHOLE VIRAL GENOMES WITHOUT VIRUS-SPECIFIC PCR AMPLIFICATION TO DETERMINE HCV RESISTANCE TO ANTIVIRAL THERAPY.

Author: Bonsall, D.G., Piazza, P., Trebes, A., Brown, A., Iles, J., Halliday, J., Hurst, J., Batty, E., Ansari, A., Ip, C., Bowden, R., Crook, D., Klenerman, P., and Barnes, E.
Subjects: *POLYMERASE chain reaction, *ANTIVIRAL agents, *HEPATITIS C virus, *DRUG resistance, *VIRAL genomes
Published: 2014
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40. P231 HEPATITIS C VIRUS POTENTLY ACTIVATES HUMAN CD161/MAIT (MUCOSAL ASSOCIATED INVARIANT T) CELLS.

Author: Thompson, F.M., van Wilgenburg, B., Ramamurthy, N., Willberg, C., Oo, Y.H., Fabris, P., and Klenerman, P.
Subjects: *HEPATITIS C treatment, *LIVER diseases, *OXIDATIVE stress, *NADPH oxidase, *VIRAL proteins, *OXYGEN in the body
Published: 2014
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41. P355 GENE EXPRESSION ANALYSIS IDENTIFIES IMMUNE SIGNALING AND COMPLEMENT PATHWAYS IN IgG4-RELATED DISEASE.

Author: Culver, E.L., Marchi, E., Manganis, C., Smit, W., Makuch, M., Ramamurthy, N., Rispens, T., Klenerman, P., and Barnes, E.
Subjects: *GENE expression, *IMMUNOGLOBULIN G, *CELL proliferation, *CELL differentiation, *SMALL interfering RNA
Published: 2014
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42. O161 CROSS-REACTIVITY OF HCV SPECIFIC, VACCINE INDUCED T CELLS, USING AN IN VITRO PRIMING MODEL.

Author: Kelly, C., Capone, S., Folgori, A., Brown, A., Salio, M., Klenerman, P., and Barnes, E.
Subjects: *HEPATITIS C vaccines, *LIVER cells, *T cells, *RAPAMYCIN, *EVEROLIMUS, *VIRAL replication
Published: 2014
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43. P1191 HETEROGENEOUS EVOLUTIONARY DYNAMICS OF CHRONIC HEPATITIS-C INFECTION PREDICT LONG-TERM PERSISTENCE OF VIRUS THROUGH TREATMENT.

Author: Rose, R., Sheridan, I., Suchard, M.A., Lemey, P., Farci, P., Klenerman, P., and Pybus, O.G.
Subjects: *CHRONIC hepatitis C, *BIOLOGICAL evolution, *VIRAL genes, *TREATMENT effectiveness, *CLINICAL trials, *THERAPEUTICS
Published: 2014
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44. 974 SEROPREVALENCE OF HEPATITIS E IN THE SOUTH PACIFIC ISLANDS.

Author: Halliday, J.S., Brown, A., Harrison, G.L., Hunter, J.G., Bendall, R., Penny, D., Klenerman, P., Barnes, E., and Dalton, H.R.
Published: 2013
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45. 1383 IGG4-PLASMA CELL INFILTRATE IN THE LIVER AND COLON OF CHILDREN WITH PRIMARY SCLEROSING CHOLANGITIS

Author: Culver, E.L., Rodriguez, A., Delaney, D., Collier, J., Klenerman, P., Chapman, R.W., and Barnes, E.
Published: 2012
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46. 1183 IN VIVO ANTIGENIC TARGETS OF T CELLS INDUCED BY ADENOVIRAL VECTORED VACCINES IN PATIENTS WITH CHRONIC HCV INFECTION

Author: Kelly, C., Folgori, A., Capone, S., Brown, A.C., Swadling, L., Townsend, R., Halliday, J., Stafford, E., O'Donnell, D., Naddeo, M., Collier, J., Adams, D., Colloca, S., Traboni, C., Cortese, R., Nicosia, A., Klenerman, P., and Barnes, E.
Published: 2012
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47. 45 RAPID AND EFFICIENT ANTIGEN PROCESSING AND PRESENTATION OF A PROTECTIVE AND IMMUNODOMINANT HLA-B*27-RESTRICTED HEPATITIS C VIRUS-SPECIFIC CD8+ T CELL EPITOPE

Author: Schmidt, J., Iversen, A.K.N., Tenzer, S., Gostick, E., Price, D.A., Lohmann, V., Bowness, P., Schild, H., Blum, H.E., Klenerman, P., Neumann-Haefelin, C., and Thimme, R.
Published: 2012
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48. 276 MULTIPLE NOVEL PEPTIDE EPITOPES IN HCV GENOTYPE-3A IDENTIFIED USING TWO PARALLEL APPROACHES

Author: Boehmer, A., Pfafferott, K., Humphreys, I.S., Lucas, M., Swadling, L., Lauer, G.M., Gaudieri, S., Klenerman, P., and Barnes, E.
Published: 2011
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49. 85 IL28B GENETIC STATUS IN ASSOCIATION WITH HCV SPECIFIC T-CELL IMMUNITY

Author: Bucci, C., Rahman, M., Humphreys, I., Brown, A.C., Lucas, M., Pfafferott, K., Collier, J., O'Donnell, D., Stafford, E., Klenerman, P., Gaudieri, S., and Barnes, E.
Published: 2011
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50. 707 CD8AA T CELLS: A NOVEL LINEAGE ENRICHED IN THE LIVER IN CHRONIC HCV

Author: Walker, L.J., Smith, M., Khan, Y., Oo, Y., Barnes, E., Lauer, G., Adams, D., and Klenerman, P.
Published: 2010
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