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3. Global phylogeny of Treponema pallidum lineages reveals recent expansion and spread of contemporary syphilis

Author

Beale, Mathew A., Marks, Michael, Cole, Michelle J., Lee, Min-Kuang, Pitt, Rachel, Ruis, Christopher, Balla, Eszter, Crucitti, Tania, Ewens, Michael, Fernández-Naval, Candela, Grankvist, Anna, Guiver, Malcolm, Kenyon, Chris R., Khairullin, Rafil, Kularatne, Ranmini, Arando, Maider, Molini, Barbara J., Obukhov, Andrey, Page, Emma E., Petrovay, Fruzsina, Rietmeijer, Cornelis, Rowley, Dominic, Shokoples, Sandy, Smit, Erasmus, Sweeney, Emma L., Taiaroa, George, Vera, Jaime H., Wennerås, Christine, Whiley, David M., Williamson, Deborah A., Hughes, Gwenda, Naidu, Prenilla, Unemo, Magnus, Krajden, Mel, Lukehart, Sheila A., Morshed, Muhammad G., Fifer, Helen, and Thomson, Nicholas R.

Published
2021
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5. Genomic Evidence of In-Flight Transmission of SARS-CoV-2 Despite Predeparture Testing

Author

Swadi, Tara, Geoghegan, Jemma L., Devine, Tom, McElnay, Caroline, Sherwood, Jillian, Shoemack, Phil, Ren, Xiaoyun, Storey, Matt, Jefferies, Sarah, Smit, Erasmus, Hadfield, James, Kenny, Aoife, Jelley, Lauren, Sporle, Andrew, McNeill, Andrea, Reynolds, G. Edwin, Mouldey, Kip, Lowe, Lindsay, Sonder, Gerard, Drummond, Alexei J., Huang, Sue, Welch, David, Holmes, Edward C., French, Nigel, Simpson, Colin R., and de Ligt, Joep

Subjects
Epidemics -- Distribution -- New Zealand, Airline passengers -- Health aspects, Disease transmission -- Demographic aspects -- Causes of, Company distribution practices, Health
Abstract

In response to the growing international risks associated with importation of coronavirus disease (COVID-19), on March 20, 2020, New Zealand closed its borders to all but New Zealand citizens, permanent [...]

Published
2021
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6. Associations between baseline characteristics, CD4 cell count response and virological failure on first-line efavirenz + tenofovir + emtricitabine for HIV

Author

Stirrup, Oliver T., Sabin, Caroline A., Phillips, Andrew N., Williams, Ian, Churchill, Duncan, Tostevin, Anna, Hill, Teresa, Dunn, David T., Asboe, David, Pozniak, Anton, Cane, Patricia, Chadwick, David, Clark, Duncan, Collins, Simon, Delpech, Valerie, Douthwaite, Samuel, Dunn, David, Fearnhill, Esther, Porter, Kholoud, Stirrup, Oliver, Fraser, Christophe, Geretti, Anna Maria, Gunson, Rory, Hale, Antony, Hué, Stéphane, Lazarus, Linda, Leigh-Brown, Andrew, Mbisa, Tamyo, Mackie, Nicola, Orkin, Chloe, Nastouli, Eleni, Pillay, Deenan, Phillips, Andrew, Sabin, Caroline, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Volz, Erik, Zhang, Hongyi, Fairbrother, Keith, Dawkins, Justine, O’Shea, Siobhan, Mullen, Jane, Cox, Alison, Tandy, Richard, Fawcett, Tracy, Hopkins, Mark, Booth, Clare, Renwick, Lynne, Schmid, Matthias L., Payne, Brendan, Hubb, Jonathan, Dustan, Simon, Kirk, Stuart, Bradley-Stewart, Amanda, Jose, Sophie, Thornton, Alicia, Huntington, Susie, Glabay, Adam, Shidfar, Shaadi, Lynch, Janet, Hand, James, de Souza, Carl, Perry, Nicky, Tilbury, Stuart, Youssef, Elaney, Gazzard, Brian, Nelson, Mark, Mabika, Tracey, Mandalia, Sundhiya, Anderson, Jane, Munshi, Sajid, Post, Frank, Adefisan, Ade, Taylor, Chris, Gleisner, Zachary, Ibrahim, Fowzia, Campbell, Lucy, Baillie, Kirsty, Gilson, Richard, Brima, Nataliya, Ainsworth, Jonathan, Schwenk, Achim, Miller, Sheila, Wood, Chris, Johnson, Margaret, Youle, Mike, Lampe, Fiona, Smith, Colette, Tsintas, Rob, Chaloner, Clinton, Hutchinson, Samantha, Walsh, John, Mackie, Nicky, Winston, Alan, Weber, Jonathan, Ramzan, Farhan, Carder, Mark, Leen, Clifford, Wilson, Alan, Morris, Sheila, Gompels, Mark, Allan, Sue, Palfreeman, Adrian, Lewszuk, Adam, Kegg, Stephen, Faleye, Akin, Ogunbiyi, Victoria, Mitchell, Sue, Hay, Phillip, Kemble, Christian, Martin, Fabiola, Russell-Sharpe, Sarah, Gravely, Janet, Allan, Sris, Harte, Andrew, Tariq, Anjum, Spencer, Hazel, Jones, Ron, Pritchard, Jillian, Cumming, Shirley, Atkinson, Claire, Mital, Dushyant, Edgell, Veronica, Allen, Juli, Ustianowski, Andy, Murphy, Cynthia, Gunder, Ilise, Trevelion, Roy, and Babiker, Abdel

Published
2019
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9. Global epidemiology of drug resistance after failure of WHO recommended first-line regimens for adult HIV-1 infection: a multicentre retrospective cohort study

Author

Gregson, John, Tang, Michele, Ndembi, Nicaise, Hamers, Raph L, Rhee, Soo-Yon, Marconi, Vincent C, Diero, Lameck, Brooks, Katherine A, Theys, Kristof, Rinke de Wit, Tobias, Arruda, Monica, Garcia, Frederico, Monge, Susana, Günthard, Huldrych F, Hoffmann, Christopher J, Kanki, Phyllis J, Kumarasamy, Nagalingeshwaran, Kerschberger, Bernard, Mor, Orna, Charpentier, Charlotte, Todesco, Eva, Rokx, Casper, Gras, Luuk, Helvas, Elias K, Sunpath, Henry, Di Carlo, Domenico, Antinori, Antonio, Andreoni, Massimo, Latini, Alessandra, Mussini, Cristina, Aghokeng, Avelin, Sonnerborg, Anders, Neogi, Ujjwal, Fessel, William J, Agolory, Simon, Yang, Chunfu, Blanco, Jose L, Juma, James M, Smit, Erasmus, Schmidt, Daniel, Watera, Christine, Asio, Juliet, Kurungi, Wilford, Tostevin, Anna, El-Hay, Tal, Clumeck, Nathan, Goedhals, Dominique, Van Vuuren, Cloete, Bester, Philip A, Sabin, Caroline, Mukui, Irene, Santoro, MARIA M, Perno, Carlo F, Hunt, Gillian, Morris, Lynn, Camacho, Ricardo, De Oliveira, Tulio, Pillay, Deenan, Schulter, Eugene, Murakami-Ogasawara, Akio, Reyes-Terán, Gustavo, Romero, Karla, Avila-Rios, Santiago, Sirivichayakul, Sunee, Ruxrungtham, Kiat, Mekprasan, Suwanna, Dunn, David, Kaleebu, Pontiano, Raizes, Elliot, Kantor, Rami, Shafer, Robert W, and Gupta, Ravindra K

Published
2016
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11. Using whole-genome sequencing in the rapid response to SARS-CoV-2 in Aotearoa New Zealand

Author

White, Rhys T, Jelley, Lauren, Douglas, Jordan, Xiaoyun Ren, Winter, David, Genomics Team, Covid-19 Wgs, Bunce, Michael, Carr, Sam, Mcneill, Andrea, Q Sue Huang, Swadi, Tara, Devine, Tom, Mcelnay, Caroline, Sherwood, Jillian, Shoemack, Phil, Fox-Lewis, Andrew, Williamson, Felicity, Harrower, Jay, Storey, Matt, Jefferies, Sarah, Smit, Erasmus, Hadfield, James, Kenny, Aoife, Sporle, Andrew, G Edwin Reynolds, Mouldey, Kip, Lowe, Lindsay, Sonder, Gerard, Drummond, Alexei J, Welch, David, Holmes, Edward C, French, Nigel, Simpson, Colin R, De Ligt, Joep, and Geoghegan, Jemma

Published
2023
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15. Real-time, portable genome sequencing for Ebola surveillance

Author

Quick, Joshua, Loman, Nicholas J., Duraffour, Sophie, Simpson, Jared T., Severi, Ettore, Cowley, Lauren, Bore, Joseph Akoi, Koundouno, Raymond, Dudas, Gytis, Mikhail, Amy, Ouédraogo, Nobila, Afrough, Babak, Bah, Amadou, Baum, Jonathan H. J., Becker-Ziaja, Beate, Boettcher, Jan Peter, Cabeza-Cabrerizo, Mar, Camino-Sánchez, Álvaro, Carter, Lisa L., Doerrbecker, Juliane, Enkirch, Theresa, Dorival, Isabel García-, Hetzelt, Nicole, Hinzmann, Julia, Holm, Tobias, Kafetzopoulou, Liana Eleni, Koropogui, Michel, Kosgey, Abigael, Kuisma, Eeva, Logue, Christopher H., Mazzarelli, Antonio, Meisel, Sarah, Mertens, Marc, Michel, Janine, Ngabo, Didier, Nitzsche, Katja, Pallasch, Elisa, Patrono, Livia Victoria, Portmann, Jasmine, Repits, Johanna Gabriella, Rickett, Natasha Y., Sachse, Andreas, Singethan, Katrin, Vitoriano, Inês, Yemanaberhan, Rahel L., Zekeng, Elsa G., Racine, Trina, Bello, Alexander, Sall, Amadou Alpha, Faye, Ousmane, Faye, Oumar, Magassouba, NʼFaly, Williams, Cecelia V., Amburgey, Victoria, Winona, Linda, Davis, Emily, Gerlach, Jon, Washington, Frank, Monteil, Vanessa, Jourdain, Marine, Bererd, Marion, Camara, Alimou, Somlare, Hermann, Camara, Abdoulaye, Gerard, Marianne, Bado, Guillaume, Baillet, Bernard, Delaune, Déborah, Nebie, Koumpingnin Yacouba, Diarra, Abdoulaye, Savane, Yacouba, Pallawo, Raymond Bernard, Gutierrez, Giovanna Jaramillo, Milhano, Natacha, Roger, Isabelle, Williams, Christopher J., Yattara, Facinet, Lewandowski, Kuiama, Taylor, James, Rachwal, Phillip, Turner, Daniel J., Pollakis, Georgios, Hiscox, Julian A., Matthews, David A., Shea, Matthew K. Oʼ, Johnston, Andrew McD., Wilson, Duncan, Hutley, Emma, Smit, Erasmus, Di Caro, Antonino, Wölfel, Roman, Stoecker, Kilian, Fleischmann, Erna, Gabriel, Martin, Weller, Simon A., Koivogui, Lamine, Diallo, Boubacar, Keïta, Sakoba, Rambaut, Andrew, Formenty, Pierre, Günther, Stephan, and Carroll, Miles W.

Published
2016
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17. Detection of drug resistance mutations at low plasma HIV-1 RNA load in a European multicentre cohort study

Author

Prosperi, Mattia C. F., Mackie, Nicola, Di Giambenedetto, Simona, Zazzi, Maurizio, Camacho, Ricardo, Fanti, Iuri, Torti, Carlo, Sönnerborg, Anders, Kaiser, Rolf, Codoñer, Francisco M., Van Laethem, Kristel, Bansi, Loveleen, van de Vijver, David A. M. C., Geretti, Anna Maria, De Luca, Andrea, Giacometti, Andrea, Butini, Luca, del Gobbo, Romana, Menzo, Stefano, Tacconi, Danilo, Corbelli, Giovanni, Zanussi, Stefania, Monno, Laura, Punzi, Grazia, Maggiolo, Franco, Callegaro, Annapaola, Calza, Leonardo, Carla Re, Maria, Pristerà, Raffaele, Turconi, Paola, Mandas, Antonella, Tini, Sauro, Zoncada, Alessia, Paolini, Elisabetta, Amadio, Giorgio, Sighinolfi, Laura, Zuccati, Giuliano, Morfini, Massimo, Manetti, Roberto, Corsi, Paola, Galli, Luisa, Di Pietro, Massimo, Bartalesi, Filippo, Colao, Grazia, Tosti, Andrea, Di Biagio, Antonio, Setti, Maurizio, Bruzzone, Bianca, Penco, Giovanni, Trezzi, Michele, Orani, Anna, Pardelli, Riccardo, De Gennaro, Michele, Chiodera, Alessandro, Scalzini, Alfredo, Palvarini, Loredana, Almi, Paolo, Todaro, Giovanni, dʼArminio Monforte, Antonella, Cicconi, Paola, Rusconi, Stefano, Gismondo, Maria Rita, Gismondo, Maria Rita, Micheli, Valeria, Biondi, Maria Luisa, Gianotti, Nicola, Capetti, Amedeo, Meraviglia, Paola, Boeri, Enzo, Mussini, Cristina, Pecorari, Monica, Soria, Alessandro, Vecchi, Laura, Santirocchi, Maurizio, Brustia, Diego, Ravanini, Paolo, Bello, Federico Dal, Romano, Nino, Mancuso, Salvatrice, Calzetti, Carlo, Maserati, Renato, Filice, Gaetano, Baldanti, Fausto, Francisci, Daniela, Parruti, Giustino, Polilli, Ennio, Sacchini, Daria, Martinelli, Chiara, Consolini, Rita, Vatteroni, Linda, Vivarelli, Angela, Dionisio, Daniele, Nerli, Alessandro, Lenzi, Lucia, Magnani, Giacomo, Ortolani, Patrizia, Andreoni, Massimo, Palamara, Guido, Fimiani, Caterina, Palmisano, Lucia, De Luca, Andrea, Fadda, Giovanni, Vullo, Vincenzo, Turriziani, Ombretta, Montano, Marco, Cenderello, Giovanni, Gonnelli, Angela, Zazzi, Maurizio, Palumbo, Michele, Ghisetti, Valeria, Bonora, Stefano, Foglie, Palma Delle, Rossi, Cristina, Grossi, Paolo, Seminari, Elena, Poletti, Federica, Mondino, Vincenzo, Malena, Marina, Lattuada, Emanuela, Lengauer, Thomas, Däumer, Martin, Hoffmann, Daniel, Kaiser, Rolf, Schülter, Eugen, Müller, Claudia, Oette, Mark, Reuter, Stefan, Esser, Stefan, Fätkenheuer, Gerd, Rockstroh, Jürgen, van de Vijver, David AMC, Incardona, Francesca, Rosen-Zvi, Michal, Lengauer, Thomas, Camacho, Ricardo, Clotet, Bonaventura, Thalme, Anders, Svedhem, Veronica, Bratt, Göran, Gargiulo, Franco, Lapadula, Giuseppe, Manca, Nino, Paraninfo, Giuseppe, Quiros-Roldan, Eugenia, Carosi, Giampiero, Castelnuovo, Filippo, Vandamme, Anne-Mieke, Van Laethem, Kristel, Van Wijngaerden, Eric, Ainsworth, Jonathan, Anderson, Jane, Babiker, Abdel, Dunn, David, Easterbrook, Philippa, Fisher, Martin, Gazzard, Brian, Garrett, Nigel, Gilson, Richard, Gompels, Mark, Hill, Teresa, Johnson, Margaret, Leen, Clifford, Orkin, Chloe, Phillips, Andrew, Pillay, Deenan, Porter, Kholoud, Post, Frank, Sabin, Caroline, Sadiq, Tariq, Schwenk, Achim, Walsh, John, Delpech, Valerie, Palfreeman, Adrian, Dunn, David, Glabay, Adam, Porter, Kholoud, Bansi, Loveleen, Hill, Teresa, Phillips, Andrew, Sabin, Caroline, Orkin, Chloe, Garrett, Nigel, Lynch, Janet, Hand, James, de Souza, Carl, Fisher, Martin, Perry, Nicky, Tilbury, Stuart, Churchill, Duncan, Gazzard, Brian, Nelson, Mark, Waxman, Matthew, Mandalia, Sundhiya, Delpech, Valerie, Anderson, Jane, Kall, Meaghan, Post, Frank, Korat, Hardik, Taylor, Chris, Ibrahim, Fowzia, Campbell, Lucy, Easterbrook, Philippa, Babiker, Abdel, Dunn, David, Glabay, Adam, Porter, Kholoud, Gilson, Richard, James, Laura, Brima, Nataliya, Williams, Ian, Schwenk, Achim, Johnson, Margaret, Youle, Mike, Lampe, Fiona, Smith, Colette, Grabowska, Helen, Chaloner, Clinton, Puradiredja, Dewi Ismajani, Bansi, Loveleen, Hill, Teresa, Phillips, Andrew, Sabin, Caroline, Walsh, John, Weber, Jonathan, Ramzan, Farhan, Carder, Mark, Leen, Clifford, Wilson, Alan, Gompels, Mark, Dooley, Debbie, Palfreeman, Adrian, Anderson, Jane, Asboe, David, Pozniak, Anton, Cameron, Sheila, Cane, Patricia, Chadwick, David, Churchill, Duncan, Clark, Duncan, Collins, Simon, Delpech, Valerie, Pillay, Deenan, Lazarus, Linda, Dunn, David, Dolling, David, Fearnhill, Esther, Castro, Hannah, Porter, Kholoud, Coughlin, Kate, Dolling, David, Zuckerman, Mark, Anna Maria, Geretti, Booth, Clare, Goldberg, David, Gompels, Mark, Hale, Antony, Kaye, Steve, Kellam, Paul, Leigh-Brown, Andrew, Mackie, Nicola, Orkin, Chloe, Pillay, Deenan, Phillips, Andrew, Sabin, Caroline, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Tong, William, Williams, Ian, Zhang, Hongyi, Zhang, Hongyi, Clark, Duncan, Ushiro-Lumb, Ines, Oliver, Tony, Bibby, David, Mitchell, Suzanne, Smit, Erasmus, Mbisa, Tamyo, Wildfire, Adrian, Tandy, Richard, Shepherd, Jill, Chadwick, David, MacLean, Alasdair, Tong, William, Bennett, Diane, Hopkins, Mark, Tilston, Peter, Booth, Clare, Garcia-Diaz, Ana, Kaye, Steve, and Kirk, Stuart

Published
2011
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19. Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study

Author

Dolling, David I., Dunn, David T., Sutherland, Katherine A., Pillay, Deenan, Mbisa, Jean L., Parry, Chris M., Post, Frank A., Sabin, Caroline A., Cane, Patricia A., Aitken, Celia, Asboe, David, Webster, Daniel, Cane, Patricia, Castro, Hannah, Dunn, David, Dolling, David, Chadwick, David, Churchill, Duncan, Clark, Duncan, Collins, Simon, Delpech, Valerie, Geretti, Anna Maria, Goldberg, David, Hale, Antony, Hué, Stéphane, Kaye, Steve, Kellam, Paul, Lazarus, Linda, Leigh-Brown, Andrew, Mackie, Nicola, Orkin, Chloe, Rice, Philip, Pillay, Deenan, Phillips, Andrew, Sabin, Caroline, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Tong, William, Williams, Ian, Zhang, Hongyi, Zuckerman, Mark, Greatorex, Jane, Wildfire, Adrian, OʼShea, Siobhan, Mullen, Jane, Mbisa, Tamyo, Cox, Alison, Tandy, Richard, Hale, Tony, Fawcett, Tracy, Hopkins, Mark, Ashton, Lynn, Booth, Claire, Garcia-Diaz, Ana, Shepherd, Jill, Schmid, Matthias L., Payne, Brendan, Hay, Phillip, Rice, Phillip, Paynter, Mary, Bibby, David, Kirk, Stuart, MacLean, Alasdair, Gunson, Rory, Coughlin, Kate, Fearnhill, Esther, Fradette, Lorraine, Porter, Kholoud, Ainsworth, Jonathan, Anderson, Jane, Babiker, Abdel, Fisher, Martin, Gazzard, Brian, Gilson, Richard, Gompels, Mark, Hill, Teresa, Johnson, Margaret, Kegg, Stephen, Leen, Clifford, Nelson, Mark, Palfreeman, Adrian, Post, Frank, Sachikonye, Memory, Schwenk, Achim, Walsh, John, Huntington, Susie, Jose, Sophie, Thornton, Alicia, Glabay, Adam, Orkin, C., Garrett, N., Lynch, J., Hand, J., de Souza, C., Fisher, M., Perry, N., Tilbury, S., Gazzard, B., Nelson, M., Waxman, M., Asboe, D., Mandalia, S., Delpech, V., Anderson, J., Munshi, S., Korat, H., Welch, J., Poulton, M., MacDonald, C., Gleisner, Z., Campbell, L., Gilson, R., Brima, N., Williams, I., Schwenk, A., Ainsworth, J., Wood, C., Miller, S., Johnson, M., Youle, M., Lampe, F., Smith, C., Grabowska, H., Chaloner, C., Puradiredja, D., Walsh, J., Weber, J., Ramzan, F., Mackie, N., Winston, A., Leen, C., Wilson, A., Allan, S., Palfreeman, A., Moore, A., and Wakeman, K.

Published
2013
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31. Virological failure and development of new resistance mutations according to CD4 count at combination antiretroviral therapy initiation

Author

Jose, S., Quinn, K., Dunn, D., Cox, A., Sabin, C., Fidler, S., Fisher, Martin, Gazzard, Brian, Gilson, Richard, Gompels, Mark, Hay, Phillip, Johnson, Margaret, Kegg, Stephen, Leen, C., Martin, Fabiola, Nelson, Mark, Palfreeman, Adrian, Post, F., Pritchard, Jillian, Sachikonye, Memory, Schwenk, Achim, Tariq, Anjum, Walsh, John, Hill, Teresa, Jose, Sophie, Phillips, Andrew, Sabin, Caroline, Thornton, Alicia, Dunn, David, Glabay, Adam, Fisher, M., Perry, N., Tilbury, S., Youssef, E., Churchill, D., Gazzard, B., Nelson, M., Everett, R., Asboe, D., Mandalia, S., Korat, H., Taylor, C., Gleisner, Z., Ibrahim, F., Campbell, L., Gilson, R., Brima, N., Williams, I., Johnson, M., Youle, M., Lampe, F., Smith, C., Tsintas, R., Chaloner, C., Hutchinson, S., Phillips, A., Hill, T., Thornton, A., Huntington, S., Walsh, J., Mackie, N., Winston, A., Weber, J., Ramzan, F., Carder, M., Orkin, C., Lynch, J., Hand, J., de Souza, C., Anderson, J., Munshi, S., Ainsworth, J., Schwenk, A., Miller, S., Wood, C., Wilson, A., Morris, S., Gompels, M., Allan, S., Palfreeman, A., Memon, K., Lewszuk, A., Chadwick, D., Cope, E., Gibson, J., Kegg, S., Main, P., Mitchell, Hunter, Hay, P., Dhillon, M., Martin, F., Russell-Sharpe, S., Harte, A., Clay, S., Tariq, A., Spencer, H., Jones, R., Pritchard, J., Cumming, S., Atkinson, C., Delpech, Valerie, Sachikony, M., Aitken, Celia, Asboe, David, Pozniak, Anton, Cane, Patricia, Chadwick, David, Churchill, Duncan, Clark, Duncan, Collins, Simon, Douthwaite, Samuel, Fearnhill, Esther, Porter, Kholoud, Tostevin, Anna, White, Ellen, Fraser, Christophe, Geretti, Anna Maria, Hale, Antony, Hué, Stéphane, Kaye, Steve, Kellam, Paul, Lazarus, Linda, Leigh-Brown, Andrew, Mbisa, Tamyo, Mackie, Nicola, Moses, Samuel, Orkin, Chloe, Nastouli, Eleni, Pillay, Deenan, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Webster, Daniel, Williams, Ian, Zhang, Hongyi, Greatorex, Jane, O'Shea, Siobhan, Mullen, Jane, Cox, Alison, Tandy, Richard, Fawcett, Tracy, Hopkins, Mark, Ashton, Lynn, Booth, Claire, Garcia-Diaz, Ana, Shepherd, Jill, Schmid, Matthias L., Payne, Brendan, Pereira, Spiro, Hubb, Jonathan, Kirk, Stuart, Gunson, Rory, Bradley-Stewart, Amanda, and Medical Research Council (MRC)

Subjects
0301 basic medicine, Male, HAART, HIV Infections, Treatment failure, law.invention, 0302 clinical medicine, Randomized controlled trial, law, Antiretroviral Therapy, Highly Active, Pharmacology (medical), 030212 general & internal medicine, Treatment Failure, virological failure, Health Policy, UK CHIC and UK HDRD Steering Committees, Virological failure, 3. Good health, Antiretroviral therapy, Patient benefit, Infectious Diseases, Female, medicine.symptom, Life Sciences & Biomedicine, Viral load, Cart, medicine.medical_specialty, Anti-HIV Agents, Short Communication, antiretroviral therapy, CD4 count, Asymptomatic, 03 medical and health sciences, HIV-INFECTION, Virology, Internal medicine, Drug Resistance, Viral, medicine, Humans, Science & Technology, business.industry, HIV resistance, 1103 Clinical Sciences, 030112 virology, CD4 Lymphocyte Count, Immunology, Mutation, business
Abstract

Objectives No randomized controlled trials have yet reported an individual patient benefit of initiating combination antiretroviral therapy (cART) at CD4 counts > 350 cells/μL. It is hypothesized that earlier initiation of cART in asymptomatic and otherwise healthy individuals may lead to poorer adherence and subsequently higher rates of resistance development. Methods In a large cohort of HIV-positive individuals, we investigated the emergence of new resistance mutations upon virological treatment failure according to the CD4 count at the initiation of cART. Results Of 7918 included individuals, 6514 (82.3%), 996 (12.6%) and 408 (5.2%) started cART with a CD4 count ≤ 350, 351–499 and ≥ 500 cells/μL, respectively. Virological rebound occurred while on cART in 488 (7.5%), 46 (4.6%) and 30 (7.4%) with a baseline CD4 count ≤ 350, 351–499 and ≥ 500 cells/μL, respectively. Only four (13.0%) individuals with a baseline CD4 count > 350 cells/μL in receipt of a resistance test at viral load rebound were found to have developed new resistance mutations. This compared to 107 (41.2%) of those with virological failure who had initiated cART with a CD4 count

Published
2015
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33. Integrase inhibitor (INI) genotypic resistance in treatment-naive and raltegravir-experienced patients infected with diverse HIV-1 clades

Author

Doyle, Tomas, Dunn, David T., Ceccherini-Silberstein, Francesca, De Mendoza, Carmen, Garcia, Frederico, Smit, Erasmus, Fearnhill, Esther, Marcelin, Anne-Genevieve, Martinez-Picado, Javier, Kaiser, Rolf, Geretti, Anna Maria, CORONET Study Group, [Doyle,T] Department of Infectious Diseases, King's College London, London, UK. [Dunn,DT, Fearnhill,E] MRC Clinical Trial Unit at UCL, London, UK. [Ceccherini-Silberstein,F] Faculty of Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy. [De Mendoza,C] Research Institute and Hospital Puerta de Hierro, Madrid, Spain. [Garcia,F] HU San Cecilio, Granada, Spain. [Smit,E] Heart of England NHS Foundation Trust, Birmingham, UK. [Marcelin,AG] AP-HP, Hôpital Pitié-Salpêtrière, INSERM-Sorbonne Universités, Paris, France. [Martinez-Picado,J] IrsiCaixa, ICREA and UVic-UCC, Barcelona, Spain. [Kaiser,R] Institute of Virology, University of Cologne, Cologne, Germany. [Geretti,AM] Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK., and The study was supported by a research award made by Merck to the Royal Free Charitable Trust.

Subjects
Genotype, Anti-HIV Agents, Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Enzyme Inhibitors::Integrase Inhibitors [Medical Subject Headings], Estudios de cohortes, Mutation, Missense, HIV Infections, Integrase Inhibitors, Diseases::Virus Diseases::RNA Virus Infections::Retroviridae Infections::Lentivirus Infections::HIV Infections [Medical Subject Headings], Organisms::Viruses::RNA Viruses::Retroviridae::Lentivirus::Lentiviruses, Primate::HIV [Medical Subject Headings], Europa (continente), Cohort Studies, Mutación Missense, Raltegravir Potassium, Inhibidores de integrasa, Drug Resistance, Viral, Humans, Original Research, Farmacorresistencia viral, Geographicals::Geographic Locations::Europe [Medical Subject Headings], Infecciones por VIH, Europe, Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation::Mutation, Missense [Medical Subject Headings], Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Anti-Infective Agents::Antiviral Agents::Anti-Retroviral Agents::Anti-HIV Agents [Medical Subject Headings], Fármacos anti-VIH, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Cohort Studies [Medical Subject Headings], HIV-1, VIH-1, Phenomena and Processes::Microbiological Phenomena::Drug Resistance, Microbial::Drug Resistance, Viral [Medical Subject Headings]
Abstract

Journal Article; Research Support, Non-U.S. Gov't; OBJECTIVES The aim of this study was to characterize the prevalence and patterns of genotypic integrase inhibitor (INI) resistance in relation to HIV-1 clade. METHODS The cohort comprised 533 INI-naive subjects and 255 raltegravir recipients with viraemia who underwent integrase sequencing in routine care across Europe, including 134/533 (25.1%) and 46/255 (18.0%), respectively, with non-B clades (A, C, D, F, G, CRF01, CRF02, other CRFs, complex). RESULTS No major INI resistance-associated mutations (RAMs) occurred in INI-naive subjects. Among raltegravir recipients with viraemia (median 3523 HIV-1 RNA copies/mL), 113/255 (44.3%) had one or more major INI RAMs, most commonly N155H (45/255, 17.6%), Q148H/R/K + G140S/A (35/255, 13.7%) and Y143R/C/H (12/255, 4.7%). In addition, four (1.6%) raltegravir recipients showed novel mutations at recognized resistance sites (E92A, S147I, N155D, N155Q) and novel mutations at other integrase positions that were statistically associated with raltegravir exposure (K159Q/R, I161L/M/T/V, E170A/G). Comparing subtype B with non-B clades, Q148H/R/K occurred in 42/209 (20.1%) versus 2/46 (4.3%) subjects (P = 0.009) and G140S/A occurred in 36/209 (17.2%) versus 1/46 (2.2%) subjects (P = 0.005). Intermediate- to high-level cross-resistance to twice-daily dolutegravir was predicted in 40/255 (15.7%) subjects, more commonly in subtype B versus non-B clades (39/209, 18.7% versus 1/46, 2.2%; P = 0.003). A glycine (G) to serine (S) substitution at integrase position 140 required one nucleotide change in subtype B and two nucleotide changes in all non-B clades. CONCLUSIONS No major INI resistance mutations occurred in INI-naive subjects. Reduced occurrence of Q148H/R/K + G140S/A was seen in non-B clades versus subtype B, and was explained by the higher genetic barrier to the G140S mutation observed in all non-B clades analysed. Yes

Published
2015

34. An association between K65R and HIV-1 subtype C viruses in patients treated with multiple NRTIs.

Author

Smit, Erasmus, White, Ellen, Clark, Duncan, Churchill, Duncan, Hongyi Zhang, Collins, Simon, Pillay, Deenan, Sabin, Caroline, Nelson, Mark, Winston, Alan, Jose, Sophie, Tostevin, Anna, Dunn, David T., Zhang, Hongyi, and UK HIV Drug Resistance Database and the UK Collaborative HIV Cohort

Subjects
*HIV-positive persons, *HIV, *TENOFOVIR, *MEDICAL care, *HIV infections, *THERAPEUTICS, *ANTI-HIV agents, *REVERSE transcriptase inhibitors, *DRUG resistance in microorganisms, *GENETIC techniques, *MULTIVARIATE analysis, *GENETIC mutation, *RESEARCH funding, *HIGHLY active antiretroviral therapy, *DIDANOSINE (Drug), *STAVUDINE, *DEOXYRIBONUCLEOSIDES, *SEQUENCE analysis, *GENOTYPES
Abstract

Objectives: HIV-1 subtype C might have a greater propensity to develop K65R mutations in patients with virological failure compared with other subtypes. However, the strong association between viral subtype and confounding factors such as exposure groups and ethnicity affects the calculation of this propensity. We exploited the diversity of viral subtypes within the UK to undertake a direct comparative analysis.Patients and methods: We analysed only sequences with major IAS-defined mutations from patients with virological failure. Prevalence of K65R was related to subtype and exposure to the NRTIs that primarily select for this mutation (tenofovir, abacavir, didanosine and stavudine). A multivariate logistic regression model quantified the effect of subtype on the prevalence of K65R, adjusting for previous and current exposure to all four specified drugs.Results: Subtype B patients ( n  =   3410) were mostly MSM (78%) and those with subtype C ( n  =   810) were mostly heterosexual (82%). K65R was detected in 7.8% of subtype B patients compared with 14.2% of subtype C patients. The subtype difference in K65R prevalence was observed irrespective of NRTI exposure and K65R was frequently selected by abacavir, didanosine and stavudine in patients with no previous exposure to tenofovir. Multivariate logistic regression confirmed that K65R was significantly more common in subtype C viruses (adjusted OR = 2.02, 95% CI = 1.55-2.62, P  <   0.001).Conclusions: Patients with subtype C HIV-1 have approximately double the frequency of K65R in our database compared with other subtypes. The exact clinical implications of this finding need to be further elucidated. [ABSTRACT FROM AUTHOR]

Published
2017
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35. Dried blood spot and mini-tube blood sample collection kits for postal HIV testing services: a comparative review of successes in a real-world setting.

Author

Page, Matthew, Atabani, Sowsan F., Wood, Martyn, Smit, Erasmus, Wilson, Steven, Atherton, Carol, Davenport, Clare F., Hartland, Daniel, Simpson, Mark, and Taylor, Stephen

Subjects
DIAGNOSIS of HIV infections, BLOOD testing, BLOOD collection, COMPARATIVE studies, DIAGNOSTIC errors, HETEROSEXUALITY, HIV infections, RESEARCH methodology, MEDICAL cooperation, MEDICAL screening, POSTAL service, RESEARCH, SERODIAGNOSIS, TELEMEDICINE, VIRAL antibodies, VIRAL antigens, EVALUATION research
Abstract

Objectives: This is a comparative review between using dried blood spot (DBS) and mini-tube (MT) HIV sampling kits as part of an online sexually transmitted infection (STI) postal testing service. England has recently seen increases in internet-based and postal (eHealth) STI services. Expanding accessibility and testing for patients, cost implications and narrowing the HIV undiagnosed margin are drivers for this.Methods: In 2017, data were reviewed from an online postal STI kit requesting service at a time of transitioning from MT to DBS. We compared the STI postal kit and HIV blood sample return rates, and the successful processing/analysis rates of the DBS and MT kits. Descriptive statistics were applied to participant characteristics, with Pearson's χ2 or Fisher exact test used to demonstrate statistical differences. We also describe and calculate a 'request-to-result ratio' (RRR) for both kit types. The RRR is defined as the number of online kit requests required to produce one successfully analysed result.Results: 550 STI postal kit requests from a North-West of England region were reviewed from 13 June 2017 to 22 September 2017 (275 MT, 275 DBS). Baseline characteristics between the two groups were comparable (63% woman, 90% white British and 86% heterosexual with a median age of 26 years). The successful processing rate for the DBS was 98.8% c.f. 55.7% for the MT (p<0.001). The RRR for MT was 2.96, c.f. 1.70 for DBS. There was a 5.4% false positive HIV rate in the MT c.f. none in the DBS.Conclusions: This comparative analysis suggests that in this community setting, the use of postal HIV DBS kits resulted in a significantly improved RRR compared with MT. The biggest factor was the large number of MT samples not analysed due to inadequate blood volumes. The unexpected level of false positive results in the MT samples needs confirming in larger studies. [ABSTRACT FROM AUTHOR]

Published
2019
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37. Whole genome sequencing and de novo assembly identifies Sydney-like variant noroviruses and recombinants during the winter 2012/2013 outbreak in England.

Author

Wong, T. H. Nicholas, Dearlove, Bethany L., Hedge, Jessica, Giess, Adam P., Piazza, Paolo, Trebes, Amy, Paul, John, Smit, Erasmus, Smith, E. Grace, Sutton, Julian K., Wilcox, Mark H., Dingle, Kate E., Peto, Tim E. A., Crook, Derrick W., Wilson, Daniel J., and Wyllie, David H.

Subjects
NOROVIRUSES, GASTROENTERITIS, GENOMES, NUCLEOTIDE sequence, PHYLOGENY
Abstract

Background Norovirus is the commonest cause of epidemic gastroenteritis among people of all ages. Outbreaks frequently occur in hospitals and the community, costing the UK an estimated £110 m per annum. An evolutionary explanation for periodic increases in norovirus cases, despite some host-specific post immunity is currently limited to the identification of obvious recombinants. Our understanding could be significantly enhanced by full length genome sequences for large numbers of intensively sampled viruses, which would also assist control and vaccine design. Our objective is to develop rapid, high-throughput, end-to-end methods yielding complete norovirus genome sequences. We apply these methods to recent English outbreaks, placing them in the wider context of the international norovirus epidemic of winter 2012. Method Norovirus sequences were generated from 28 unique clinical samples by Illumina RNA sequencing (RNA-Seq) of total faecal RNA. A range of de novo sequence assemblers were attempted. The best assembler was identified by validation against three replicate samples and two norovirus qPCR negative samples, together with an additional 20 sequences determined by PCR and fractional capillary sequencing. Phylogenetic methods were used to reconstruct evolutionary relationships from the whole genome sequences. Results Full length norovirus genomes were generated from 23/28 samples. 5/28 partial norovirus genomes were associated with low viral copy numbers. The de novo assembled sequences differed from sequences determined by capillary sequencing by <0.003%. Intra-host nucleotide sequence diversity was rare, but detectable by mapping short sequence reads onto its de novo assembled consensus. Genomes similar to the Sydney 2012 strain caused 78% (18/23) of cases, consistent with its previously documented association with the winter 2012 global outbreak. Interestingly, phylogenetic analysis and recombination detection analysis of the consensus sequences identified two related viruses as recombinants, containing sequences in prior circulation to Sydney 2012 in open reading frame (ORF) 2. Conclusion Our approach facilitates the rapid determination of complete norovirus genomes. This method provides high resolution of full norovirus genomes which, when coupled with detailed epidemiology, may improve the understanding of evolution and control of this important healthcare-associated pathogen. [ABSTRACT FROM AUTHOR]

Published
2013
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38. HIV-Positive-to-HIV-Positive Liver Transplantation.

Author

Hathorn, Emma, Smit, Erasmus, Mutimer, David, Elsharkawy, Ahmed M, Bramhall, Simon R, Bufton, Sally A, and Allan, Sris

Subjects
*LIVER transplantation, *HIV, *HEPATITIS C, *ANTIRETROVIRAL agents, *HEPATOCELLULAR carcinoma, *HIV infections, *LIVER tumors, *RNA, *VIRAL load, *HIV seroconversion, *SUPERINFECTION
Abstract

A letter to the editor is presented concerning the case of liver transplantation from a donor positive for human immunodeficiency virus type 1 (HIV-1) to a recipient co-infected with hepatitis C virus and HIV-1 who required transplantation for primary liver cancer complicating cirrhosis.

Published
2016
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39. The management of isolated positive syphilis enzyme immunoassay results in HIV-negative patients attending a sexual health clinic.

Author

Thorley, Nicola, Adebayo, Michael, Smit, Erasmus, and Radcliffe, Keith

Subjects
DIAGNOSIS of syphilis, ENZYME-linked immunosorbent assay, SEXUAL health, SEROLOGY, TREPONEMA pallidum, RETROSPECTIVE studies
Abstract

An unconfirmed positive treponemal enzyme immunoassay (enzyme immunoassay positive, Treponema pallidum particle agglutination negative and rapid plasma reagin negative) presents a clinical challenge to distinguish early syphilis infection from false-positive results. These cases are referred for syphilis line assay (INNO-LIA) and recalled for repeat syphilis serology. We performed a retrospective audit to establish the proportion of HIV-negative cases with unconfirmed positive enzyme immunoassay results, the proportion of these cases that received an INNO-LIA test and repeat syphilis serology testing and reviewed the clinical outcomes; 0.35% (80/22687) cases had an unconfirmed positive treponemal enzyme immunoassay result. Repeat syphilis serology was performed in 80% (64/80) cases, but no additional cases of syphilis were identified. Eighty-eight per cent (70/80) received an INNO-LIA test; 14% (5/37) unconfirmed enzyme immunoassay-positive cases with no prior history of syphilis were confirmed on INNO-LIA assay, supporting a diagnosis of latent syphilis. As a confirmatory treponemal test, the INNO-LIA assay may be more useful than repeat syphilis serological testing. [ABSTRACT FROM AUTHOR]

Published
2016
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41. Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study

Author

Dolling, David I., Dunn, David T., Sutherland, Katherine A., Pillay, Deenan, Mbisa, Jean L., Parry, Chris M., Post, Frank A., Sabin, Caroline A., Cane, Patricia A., Aitken, Celia, Asboe, David, Webster, Daniel, Cane, Patricia, Castro, Hannah, Dunn, David, Dolling, David, Chadwick, David, Churchill, Duncan, Clark, Duncan, Collins, Simon, Delpech, Valerie, Geretti, Anna Maria, Goldberg, David, Hale, Antony, Hué, Stéphane, Kaye, Steve, Kellam, Paul, Lazarus, Linda, Leigh-Brown, Andrew, Mackie, Nicola, Orkin, Chloe, Rice, Philip, Phillips, Andrew, Sabin, Caroline, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Tong, William, Williams, Ian, Zhang, Hongyi, Zuckerman, Mark, Greatorex, Jane, Wildfire, Adrian, O'Shea, Siobhan, Mullen, Jane, Mbisa, Tamyo, Cox, Alison, Tandy, Richard, Hale, Tony, Fawcett, Tracy, Hopkins, Mark, Ashton, Lynn, Booth, Claire, Garcia-Diaz, Ana, Shepherd, Jill, Schmid, Matthias L., Payne, Brendan, Hay, Phillip, Rice, Phillip, Paynter, Mary, Bibby, David, Kirk, Stuart, MacLean, Alasdair, Gunson, Rory, Coughlin, Kate, Fearnhill, Esther, Fradette, Lorraine, Porter, Kholoud, Ainsworth, Jonathan, Anderson, Jane, Babiker, Abdel, Fisher, Martin, Gazzard, Brian, Gilson, Richard, Gompels, Mark, Hill, Teresa, Johnson, Margaret, Kegg, Stephen, Leen, Clifford, Nelson, Mark, Palfreeman, Adrian, Post, Frank, Sachikonye, Memory, Schwenk, Achim, Walsh, John, Huntington, Susie, Jose, Sophie, Thornton, Alicia, Glabay, Adam, Orkin, C., Garrett, N., Lynch, J., Hand, J., de Souza, C., Fisher, M., Perry, N., Tilbury, S., Gazzard, B., Nelson, M., Waxman, M., Asboe, D., Mandalia, S., Delpech, V., Anderson, J., Munshi, S., Korat, H., Welch, J., Poulton, M., MacDonald, C., Gleisner, Z., Campbell, L., Gilson, R., Brima, N., Williams, I., Schwenk, A., Ainsworth, J., Wood, C., Miller, S., Johnson, M., Youle, M., Lampe, F., Smith, C., Grabowska, H., Chaloner, C., Puradiredja, D., Walsh, J., Weber, J., Ramzan, F., Mackie, N., Winston, A., Leen, C., Wilson, A., Allan, S., Palfreeman, A., Moore, A., and Wakeman, K.

Subjects
Male, Mutation rate, Pyridines, Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, THERAPY, Cohort Studies, 0302 clinical medicine, HIV Protease, Mutation Rate, 1108 Medical Microbiology, Genotype, Pharmacology (medical), 030212 general & internal medicine, Pharmacology & Pharmacy, Treatment Failure, drug resistance mutations, Original Research, 0303 health sciences, virological failure, UK Collaborative HIV Cohort Study (UK CHIC), Proteolytic enzymes, virus diseases, Middle Aged, 3. Good health, Infectious Diseases, Female, 1115 Pharmacology and Pharmaceutical Sciences, Life Sciences & Biomedicine, Oligopeptides, medicine.drug, Cohort study, 0605 Microbiology, Microbiology (medical), Adult, medicine.medical_specialty, Anti-HIV Agents, Atazanavir Sulfate, protease inhibitors, Mutation, Missense, RITONAVIR, Biology, Microbiology, Medication Adherence, 03 medical and health sciences, Internal medicine, SCORE, Drug Resistance, Viral, medicine, Humans, 030304 developmental biology, Pharmacology, Science & Technology, HIV, Virology, naive patients, United States, Atazanavir, Regimen, HIV-1, Ritonavir, UK HIV Drug Resistance Database (UKHDRD)
Abstract

Author(s): Dolling, David I; Dunn, David T; Sutherland, Katherine A; Pillay, Deenan; Mbisa, Jean L; Parry, Chris M; Post, Frank A; Sabin, Caroline A; Cane, Patricia A; UK HIV Drug Resistance Database (UKHDRD); UK Collaborative HIV Cohort Study (UK CHIC) | Abstract: ObjectivesTo determine protease mutations that develop at viral failure for protease inhibitor (PI)-naive patients on a regimen containing the PI atazanavir.MethodsResistance tests on patients failing atazanavir, conducted as part of routine clinical care in a multicentre observational study, were randomly matched by subtype to resistance tests from PI-naive controls to account for natural polymorphisms. Mutations from the consensus B sequence across the protease region were analysed for association and defined using the IAS-USA 2011 classification list.ResultsFour hundred and five of 2528 (16%) patients failed therapy containing atazanavir as a first PI over a median (IQR) follow-up of 1.76 (0.84-3.15) years and 322 resistance tests were available for analysis. Recognized major atazanavir mutations were found in six atazanavir-experienced patients (P l 0.001), including I50L and N88S. The minor mutations most strongly associated with atazanavir experience were M36I, M46I, F53L, A71V, V82T and I85V (P l 0.05). Multiple novel mutations, I15S, L19T, K43T, L63P/V, K70Q, V77I and L89I/T/V, were also associated with atazanavir experience.ConclusionsViral failure on atazanavir-containing regimens was not common and major resistance mutations were rare, suggesting that adherence may be a major contributor to viral failure. Novel mutations were described that have not been previously documented.

43. Global epidemiology of drug resistance after failure of WHO recommended first-line regimens for adult HIV-1 infection: a multicentre retrospective cohort study

Author

Gregson, J, Tang, M, Ndembi, N, Hamers, Rl, Marconi, Vc, Brooks, K, Theys, K, Arruda, M, Garcia, F, Monge, S, Kanki, Pj, Kumarasamy, N, Kerschberger, B, Mor, O, Charpentier, C, Todesco, E, Rokx, C, Gras, L, Halvas, Ek, Sunpath, H, Carlo, Dd, Antinori, A, Andreoni, M, Latini, A, Mussini, C, Aghokeng, A, Sonnerborg, A, Neogi, U, Fessel, Wj, Agolory, S, Yang, C, Blanco, Jl, Juma, Jm, Smit, E, Schmidt, D, Watera, C, Asio, J, Kirungi, W, Tostevin, A, Clumeck, N, Goedhals, D, Bester, Pa, Sabin, C, Mukui, I, Santoro, M, Perno, Cf, Hunt, G, Morris, L, Pillay, D, Schulter, E, Reyes-Teran, G, Romero, K, Avila-Rios, S, Sirivichayakul, S, Ruxrungtham, K, Mekprasan, S, Dunn, D, Kaleebu, P, Raizes, E, Kantor, R, Gupta, Rk, Rhee, S, Shafer, Rw, de Wit, Tfr, Diero, L, Camacho, R, Gunthard, Hf, Hoffmann, Cj, Di Carlo, D, El-Hay, T, van Vuuren, C, de Oliveira, T, Murakami-Ogasawara, A, [Pillay, Deenan] UCL, Dept Infect, London WC1E 6BT, England, [Gupta, Ravindra K.] UCL, Dept Infect, London WC1E 6BT, England, [Tang, Michele] Stanford Univ, Dept Med, Stanford, CA 94305 USA, [Rhee, Soo-Yon] Stanford Univ, Dept Med, Stanford, CA 94305 USA, [Shafer, Robert W.] Stanford Univ, Dept Med, Stanford, CA 94305 USA, [Gregson, John] London Sch Hyg & Trop Med, Dept Stat, London, England, [Ndembi, Nicaise] Inst Human Virol Nigeria, Abuja, Federal Capital, Nigeria, [Hamers, Raph L.] Univ Amsterdam, Acad Med Ctr, Amsterdam Inst Global Hlth & Dev, Dept Global Hlth, NL-1012 WX Amsterdam, Netherlands, [de Wit, Tobias F. Rinke] Univ Amsterdam, Acad Med Ctr, Amsterdam Inst Global Hlth & Dev, Dept Global Hlth, NL-1012 WX Amsterdam, Netherlands, [Hamers, Raph L.] Univ Amsterdam, Acad Med Ctr, Dept Internal Med, NL-1012 WX Amsterdam, Netherlands, [de Wit, Tobias F. Rinke] Univ Amsterdam, Acad Med Ctr, Dept Internal Med, NL-1012 WX Amsterdam, Netherlands, [Marconi, Vincent C.] Emory Univ, Rollins Sch Publ Hlth, Dept Global Hlth, Atlanta, GA 30322 USA, [Marconi, Vincent C.] Emory Univ, Sch Med, Div Infect Dis, Atlanta, GA USA, [Diero, Lameck] Moi Univ, Eldoret, Kenya, [Diero, Lameck] Acad Model Providing Access Healthcare, Eldoret, Kenya, [Brooks, Katherine] Brown Univ, Alpert Med Sch, Div Infect Dis, Providence, RI 02912 USA, [Theys, Kristof] KU Leuven Univ Leuven, Rega Inst Med Res, Dept Microbiol & Immunol, B-3000 Leuven, Belgium, [Camacho, Ricardo] KU Leuven Univ Leuven, Rega Inst Med Res, Dept Microbiol & Immunol, B-3000 Leuven, Belgium, [Kantor, Rami] KU Leuven Univ Leuven, Rega Inst Med Res, Dept Microbiol & Immunol, B-3000 Leuven, Belgium, [Arruda, Monica] Univ Fed Rio de Janeiro, Inst Biol, LVM, BR-21941 Rio De Janeiro, Brazil, [Garcia, Frederico] Complejo Hosp Univ Granada, Granada, Spain, Univ Alcala de Henares, E-28871 Alcala De Henares, Spain, [Monge, Susana] CIBERESP, Madrid, Spain, [Gunthard, Huldrych F.] Univ Zurich, Div Infect Dis & Hosp Epidemiol, Zurich, Switzerland, [Gunthard, Huldrych F.] Univ Zurich, Inst Med Virol, Zurich, Switzerland, [Hoffmann, Christopher J.] Johns Hopkins Univ, Baltimore, MD USA, [Hoffmann, Christopher J.] Aurum Inst, Johannesburg, South Africa, [Kanki, Phyllis J.] Harvard Univ, TH Chan Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA, [Kumarasamy, Nagalingeshwaran] VHS, YRGCARE Med Ctr, Chennai, Tamil Nadu, India, [Kerschberger, Bernard] Med Sans Frontieres Operat Ctr Geneva, Mbabane, Eswatini, [Mor, Orna] Israel Minist Hlth, Publ Hlth Serv, Cent Virol Lab, Jerusalem, Israel, [Charpentier, Charlotte] Univ Paris Diderot, Sorbonne Paris Cite, IAME, UMR 1137, Paris, France, [Charpentier, Charlotte] INSERM, IAME, UMR 1137, Paris, France, [Charpentier, Charlotte] Hop Bichat Claude Bernard, AP HP, Virol Lab, F-75018 Paris, France, [Todesco, Eva] Hop La Pitie Salpetriere, Lab Virol, Paris, France, [Rokx, Casper] Erasmus Univ, Med Ctr, Dept Internal Med Infect Dis, Rotterdam, Netherlands, [Gras, Luuk] Stichting HIV Monitoring, Amsterdam, Netherlands, [Halvas, Elias K.] Univ Pittsburgh, Pittsburgh, PA USA, [Sunpath, Henry] Ethekwini Dist Hlth Off, Kwa Zulu, South Africa, [Di Carlo, Domenico] Univ Roma Tor Vergata, Dept Expt Med & Surg, Rome, Italy, [Santoro, Maria M.] Univ Roma Tor Vergata, Dept Expt Med & Surg, Rome, Italy, [Antinori, Antonio] INMI L Spallanzani, Infect Dis Unit, Rome, Italy, [Andreoni, Massimo] Univ Hosp Tor Vergata, Clin Infect Dis, Rome, Italy, [Latini, Alessandra] San Gallicano Dermatol Inst, HIV AIDS Unit, Rome, Italy, [Mussini, Cristina] Azienda Osped Univ Policlin, Clin Infect Dis, Modena, Italy, [Aghokeng, Avelin] Virol Lab CREMER IMPM, Yaounde, Cameroon, [Sonnerborg, Anders] Karolinska Inst, Div Clin Microbiol, Stockholm, Sweden, [Neogi, Ujjwal] Karolinska Inst, Div Clin Microbiol, Stockholm, Sweden, [Sonnerborg, Anders] Karolinska Inst, Infect Dis Unit, Stockholm, Sweden, [Neogi, Ujjwal] Karolinska Inst, Infect Dis Unit, Stockholm, Sweden, [Sonnerborg, Anders] Karolinska Univ Hosp, Stockholm, Sweden, [Neogi, Ujjwal] Karolinska Univ Hosp, Stockholm, Sweden, [Fessel, William J.] Kaiser Permanente Med Care Program Northern Calif, San Francisco, CA USA, [Agolory, Simon] Ctr Dis Control & Prevent, Div Global HIV AIDS, Ctr Global Hlth, Atlanta, GA USA, [Raizes, Elliot] Ctr Dis Control & Prevent, Div Global HIV AIDS, Ctr Global Hlth, Atlanta, GA USA, [Yang, Chunfu] Ctr Dis Control & Prevent, Int Lab Branch, Div Global HIV AIDS, Ctr Global Hlth, Atlanta, GA USA, [Blanco, Jose L.] Univ Barcelona, Inst Invest Biomed August Pi i Sunyer, Clin Univ, Barcelona, Spain, [Juma, James M.] Minist Hlth & Social Welf, Dar Es Salaam, Tanzania, [Smit, Erasmus] Publ Hlth England, Publ Hlth Lab, Birmingham, W Midlands, England, [Schmidt, Daniel] Robert Koch Inst, Dept Infect Dis Epidemiol HIV AIDS STI & Blood Bo, Berlin, Germany, [Watera, Christine] Uganda Res Unit AIDS, Entebbe, Uganda, [Asio, Juliet] Uganda Res Unit AIDS, Entebbe, Uganda, [Kaleebu, Pontiano] Uganda Res Unit AIDS, Entebbe, Uganda, [Tostevin, Anna] Minist Hlth, Kampala, Uganda, [Tostevin, Anna] UCL, MRC Clin Trials Unit, London, England, [Dunn, David] UCL, MRC Clin Trials Unit, London, England, [El-Hay, Tal] IBM Haifa Res Lab, Haifa, Israel, [Clumeck, Nathan] Univ Libre Bruxelles, St Pierre Univ Hosp, Brussels, Belgium, [Goedhals, Dominique] Univ Orange Free State, Dept Med Microbiol & Virol, Natl Hlth Lab Serv, Bloemfontein, South Africa, [van Vuuren, Cloete] Univ Orange Free State, Dept Med Microbiol & Virol, Natl Hlth Lab Serv, Bloemfontein, South Africa, [Sabin, Caroline] UCL, Infect & Populat Hlth, London, England, [Mukui, Irene] Minist Hlth, Natl AIDS & STI Control Programme, Nairobi, Kenya, [Perno, Carlo F.] INMI L Spallanzani, Antiretroviral Drugs Monitoring Unit, Rome, Italy, [Hunt, Gillian] Natl Inst Communicable Dis, Johannesburg, South Africa, [Morris, Lynn] Natl Inst Communicable Dis, Johannesburg, South Africa, [de Oliveira, Tulio] Wellcome Trust Africa Ctr Hlth & Populat Studies, Durban, South Africa, [Pillay, Deenan] Wellcome Trust Africa Ctr Hlth & Populat Studies, Durban, South Africa, [de Oliveira, Tulio] Univ KwaZulu Natal, Coll Hlth Sci, Durban, South Africa, [Schulter, Eugene] Univ Cologne, Inst Virol, D-50931 Cologne, Germany, [Murakami-Ogasawara, Akio] Natl Inst Resp Dis, Ctr Res Infect Dis, Mexico City, DF, Mexico, [Sirivichayakul, Sunee] Chulalongkorn Univ, Dept Med, Bangkok, Thailand, [Ruxrungtham, Kiat] Chulalongkorn Univ, Dept Med, Bangkok, Thailand, [Mekprasan, Suwanna] Chulalongkorn Univ, Dept Med, Bangkok, Thailand, [Kaleebu, Pontiano] MRC UVRI Uganda Res Unit AIDS, Entebbe, Uganda, Wellcome Trust, MRC, NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES, and Medical Research Council

Subjects
Cyclopropanes, Anti-HIV Agents, K65r, Drug Resistance, Antiretroviral Therapy, HIV Infections, Global Health, Settore MED/07, Virological failure, Tenofovir disoproxil fumarate, Antiretroviral Therapy, Highly Active, Drug Resistance, Viral, Humans, Emtricitabine, Transmission, Highly Active, Viral, Tenofovir, Africa South of the Sahara, Benzoxazines, HIV-1, Lamivudine, Pre-Exposure Prophylaxis, Retrospective Studies, Reverse Transcriptase Inhibitors, Viral Load, Hiv-1-infected patients, virus diseases, Articles, Antiretroviral therapy, Naive patients, Alkynes, Efavirenz
Abstract

Summary Background Antiretroviral therapy (ART) is crucial for controlling HIV-1 infection through wide-scale treatment as prevention and pre-exposure prophylaxis (PrEP). Potent tenofovir disoproxil fumarate-containing regimens are increasingly used to treat and prevent HIV, although few data exist for frequency and risk factors of acquired drug resistance in regions hardest hit by the HIV pandemic. We aimed to do a global assessment of drug resistance after virological failure with first-line tenofovir-containing ART. Methods The TenoRes collaboration comprises adult HIV treatment cohorts and clinical trials of HIV drug resistance testing in Europe, Latin and North America, sub-Saharan Africa, and Asia. We extracted and harmonised data for patients undergoing genotypic resistance testing after virological failure with a first-line regimen containing tenofovir plus a cytosine analogue (lamivudine or emtricitabine) plus a non-nucleotide reverse-transcriptase inhibitor (NNRTI; efavirenz or nevirapine). We used an individual participant-level meta-analysis and multiple logistic regression to identify covariates associated with drug resistance. Our primary outcome was tenofovir resistance, defined as presence of K65R/N or K70E/G/Q mutations in the reverse transcriptase (RT) gene. Findings We included 1926 patients from 36 countries with treatment failure between 1998 and 2015. Prevalence of tenofovir resistance was highest in sub-Saharan Africa (370/654 [57%]). Pre-ART CD4 cell count was the covariate most strongly associated with the development of tenofovir resistance (odds ratio [OR] 1·50, 95% CI 1·27–1·77 for CD4 cell count

Published
2016

44. Integrase inhibitor (INI) genotypic resistance in treatment-naive and raltegravir-experienced patients infected with diverse HIV-1 clades.

Author

Doyle T, Dunn DT, Ceccherini-Silberstein F, De Mendoza C, Garcia F, Smit E, Fearnhill E, Marcelin AG, Martinez-Picado J, Kaiser R, and Geretti AM

Subjects
Anti-HIV Agents therapeutic use, Cohort Studies, Europe, Genotype, HIV-1 classification, HIV-1 isolation & purification, Humans, Integrase Inhibitors therapeutic use, Mutation, Missense, Raltegravir Potassium therapeutic use, Anti-HIV Agents pharmacology, Drug Resistance, Viral, HIV Infections drug therapy, HIV Infections virology, HIV-1 genetics, Integrase Inhibitors pharmacology, Raltegravir Potassium pharmacology
Abstract

Objectives: The aim of this study was to characterize the prevalence and patterns of genotypic integrase inhibitor (INI) resistance in relation to HIV-1 clade., Methods: The cohort comprised 533 INI-naive subjects and 255 raltegravir recipients with viraemia who underwent integrase sequencing in routine care across Europe, including 134/533 (25.1%) and 46/255 (18.0%), respectively, with non-B clades (A, C, D, F, G, CRF01, CRF02, other CRFs, complex)., Results: No major INI resistance-associated mutations (RAMs) occurred in INI-naive subjects. Among raltegravir recipients with viraemia (median 3523 HIV-1 RNA copies/mL), 113/255 (44.3%) had one or more major INI RAMs, most commonly N155H (45/255, 17.6%), Q148H/R/K + G140S/A (35/255, 13.7%) and Y143R/C/H (12/255, 4.7%). In addition, four (1.6%) raltegravir recipients showed novel mutations at recognized resistance sites (E92A, S147I, N155D, N155Q) and novel mutations at other integrase positions that were statistically associated with raltegravir exposure (K159Q/R, I161L/M/T/V, E170A/G). Comparing subtype B with non-B clades, Q148H/R/K occurred in 42/209 (20.1%) versus 2/46 (4.3%) subjects (P = 0.009) and G140S/A occurred in 36/209 (17.2%) versus 1/46 (2.2%) subjects (P = 0.005). Intermediate- to high-level cross-resistance to twice-daily dolutegravir was predicted in 40/255 (15.7%) subjects, more commonly in subtype B versus non-B clades (39/209, 18.7% versus 1/46, 2.2%; P = 0.003). A glycine (G) to serine (S) substitution at integrase position 140 required one nucleotide change in subtype B and two nucleotide changes in all non-B clades., Conclusions: No major INI resistance mutations occurred in INI-naive subjects. Reduced occurrence of Q148H/R/K + G140S/A was seen in non-B clades versus subtype B, and was explained by the higher genetic barrier to the G140S mutation observed in all non-B clades analysed., (© The Author 2015. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy.)

Published
2015
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45. Second-line protease inhibitor-based antiretroviral therapy after non-nucleoside reverse transcriptase inhibitor failure: the effect of a nucleoside backbone.

Author

Waters L, Bansi L, Asboe D, Pozniak A, Smit E, Orkin C, Fearnhill E, Dunn D, and Phillips A

Subjects
Antiretroviral Therapy, Highly Active, CD4 Lymphocyte Count, Drug Resistance, Viral, Female, HIV Infections drug therapy, HIV Infections virology, Humans, Longitudinal Studies, Male, Risk Factors, Treatment Failure, Treatment Outcome, Viral Load, Anti-HIV Agents therapeutic use, HIV Protease Inhibitors therapeutic use, Reverse Transcriptase Inhibitors therapeutic use
Abstract

Background: Virological failures on combined antiretroviral therapy still occur. Boosted protease inhibitor ( Pl/r)- based therapy is a commonly used option after non-nucleoside reverse transcriptase inhibitor ( NNRTI) failure, but whether two fully active nucleoside reverse transciptase inhibitors (NRTIs) are required is unknown. We investigated the effect of an NRTI backbone in individuals receiving Pl/r after failing NNRTI-based combined antiretroviral therapy., Methods: A longitudinal analysis of the UK Collaborative HIV Cohort (CHIC) and the UK HIV Drug Resistance Database to identify individuals who failed first-line NNRTI and two NRTIs, and switched to Pl/r-based therapy between January 1999 and December 2008 was conducted. We investigated the effect of NRTI on suppression., Results: In total, 470 individuals met study criteria: 19.6%, 34.5% and 46.0% started 0, 1 or ≥ 2 NRTIs, respectively. Median CD4+ T-cell count was 223 cells/mm3 and HIV-RNA was 4.3 log10 copies/ml; 246 (52.3%) underwent genotyping before switch. virological failure occurred in 10.9% and 13% after 48 and 96 weeks, respectively. In multivariable analysis, heterosexual risk group and HIV RNA were independently associated with virological failure; higher CD4+ T-cell count was protective (HR= 0.92). Number of new NRTIs or genotypic sensitivity score of backbone had no effect on treatment success rates when modelled as categorical or continuous variables., Conclusions: Successful treatment with a second-line Pl/r may not require two active NRTIs. If replicated in clinincal trials, these findings could guide future recommendations.

Published
2013
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46. Time trends in drug resistant HIV-1 infections in the United Kingdom up to 2009: multicentre observational study.

Author

Dolling D, Sabin C, Delpech V, Smit E, Pozniak A, Asboe D, Brown AL, Churchill D, Williams I, Geretti AM, Phillips A, Mackie N, Murphy G, Castro H, Pillay D, Cane P, Dunn D, and Dolling D

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Cohort Studies, Female, HIV Infections drug therapy, HIV Infections epidemiology, HIV-1 drug effects, Humans, Linear Models, Logistic Models, Male, Microbial Sensitivity Tests, Middle Aged, Mutation Rate, Prevalence, United Kingdom epidemiology, Young Adult, Anti-Retroviral Agents pharmacology, Anti-Retroviral Agents therapeutic use, Drug Resistance, Viral genetics, HIV Infections virology, HIV-1 genetics
Abstract

Objective: To evaluate whether the prevalence of HIV-1 transmitted drug resistance has continued to decline in infections probably acquired within the United Kingdom., Design: Multicentre observational study., Setting: All UK public laboratories conducting tests for genotypic HIV resistance as a part of routine care., Participants: 14,584 patients infected with HIV-1 subtype B virus, who were first tested for resistance before receiving antiretroviral therapy between January 2002 and December 2009., Main Outcome Measure: Prevalence of transmitted drug resistance, defined as one or more resistance mutations from the surveillance list recommended by the World Health Organization., Results: 1654 (11.3%, 95% confidence interval 10.8% to 11.9%) patients had one or more mutations associated with transmitted HIV-1 drug resistance; prevalence was found to decline from 15.5% in 2002 to 9.6% in 2007, followed by a slight increase to 10.9% in 2009 (P=0.21). This later rise was mainly a result of increases in resistance to nucleos(t)ide reverse transcriptase inhibitors (from 5.4% in 2007 to 6.6% in 2009, P=0.24) and protease inhibitors (1.5% to 2.1%, P=0.12). Thymidine analogue mutations, including T215 revertants, remained the most frequent mutations associated with nucleos(t)ide reverse transcriptase inhibitors, despite a considerable fall in stavudine and zidovudine use between 2002 and 2009 (from 29.4% of drug regimens in 2002 to 0.8% in 2009, from 47.9% to 8.8%, respectively)., Conclusions: The previously observed decline in the prevalence of transmitted drug resistance in HIV-1 infections probably acquired in the UK seems to have stabilised. The continued high prevalence of thymidine analogue mutations suggests that the source of this resistance may be increasingly from patients who have not undergone antiretroviral therapy and who harbour resistant viruses. Testing of all newly diagnosed HIV-1 positive people should be continued.

Published
2012
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47. HIV-1 superinfection.

Author

Waters L and Smit E

Subjects
Counseling methods, HIV Infections complications, HIV Infections virology, Humans, Incidence, Practice Guidelines as Topic, Species Specificity, Superinfection complications, Superinfection virology, HIV Infections epidemiology, HIV-1 classification, Superinfection epidemiology
Abstract

Purpose of Review: This review describes the nature and frequency of HIV-1 superinfection and provides advice regarding counselling of patients in accordance with national guidelines., Recent Findings: Recent studies have demonstrated conflicting results, from no superinfection to an incidence of over 18%. We discuss the difficulties comparing studies due to population and methodological differences., Summary: HIV-infected individuals should be counselled that there is risk of superinfection at all stages of HIV, but this is unlikely to be clinically significant unless transmission of resistance occurs. The risk may be as high as the risk of new incident infection in the presence of on-going exposure.

Published
2012
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48. Dynamics of raltegravir resistance profile in an HIV type 2-infected patient.

Author

Xu L, Anderson J, Garrett N, Ferns B, Wildfire A, Cook P, Workman J, Graham S, and Smit E

Subjects
Amino Acid Substitution, Evolution, Molecular, HIV Infections drug therapy, HIV Integrase analysis, HIV Integrase genetics, RNA, Viral analysis, RNA, Viral genetics, Raltegravir Potassium, Sequence Analysis, RNA, Treatment Failure, Drug Resistance, Viral genetics, HIV Infections virology, HIV Integrase Inhibitors therapeutic use, HIV-2 drug effects, HIV-2 genetics, Pyrrolidinones therapeutic use
Abstract

The evolutionary dynamics of RAL resistance in the HIV-2 virus were examined through population and clonal sequence analysis of the IN from baseline, during treatment, and after stopping RAL therapy. The treatment failure of an RAL regimen in the HIV-2 patient studied was associated with the emergence of mutations via the N155H resistance pathway and subsequent switching to the Y143C mutational route. This study has also identified four novel secondary mutations, Q91R, S147G, A153G, and M183I, not previously reported in HIV-1 patients failing RAL therapy. Resistant variants involving the Y143C pathway were noted to have persisted beyond 4 weeks following the cessation of RAL therapy. All resistance-associated mutations were lost at 20 weeks after stopping RAL therapy. Our findings provide evidence supporting the supposition that substantial cross-resistance between strand transfer IN-Is is likely in HIV-2 as shown in HIV-1.

Published
2009
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50. Time trends in primary resistance to HIV drugs in the United Kingdom: multicentre observational study.

Author

Cane P, Chrystie I, Dunn D, Evans B, Geretti AM, Green H, Phillips A, Pillay D, Porter K, Pozniak A, Sabin C, Smit E, Weber J, and Zuckerman M

Subjects
Adolescent, Adult, Aged, HIV Infections epidemiology, HIV Infections genetics, Humans, Middle Aged, Prevalence, Regression Analysis, Reverse Transcriptase Inhibitors therapeutic use, Risk Factors, United Kingdom epidemiology, Anti-HIV Agents therapeutic use, Drug Resistance, Viral genetics, HIV Infections drug therapy, Mutation genetics
Abstract

Objective: To examine whether the level of primary resistance to HIV drugs is increasing in the United Kingdom., Design: Multicentre observational study., Setting: All virology laboratories in the United Kingdom carrying out tests for HIV resistance as part of routine clinical care., Participants: 2357 people infected with HIV who were tested for resistance before receiving antiretroviral therapy., Main Outcome Measure: Prevalence of drug resistance on basis of the Stanford genotypic interpretation system., Results: Over the study period (February 1996 to May 2003), 335 (14.2%, 95% confidence interval 12.8% to 15.7%) samples had mutations that conferred resistance to one or more antiretroviral drugs (9.3% high level resistance, 5.9% medium level resistance). The prevalence of primary resistance has increased markedly over time, although patterns are specific to drug class; the largest increase was for non-nucleoside reverse transcriptase inhibitors. In 2002-3, the prevalence of resistance to any antiretroviral drug to nucleoside or nucleotide reverse transcriptase inhibitors, to non-nucleoside reverse transcriptase inhibitors, or to protease inhibitors was 19.2% (15.7% to 23.2%), 12.4% (9.5% to 15.9%), 8.1% (5.8% to 11.1%), and 6.6% (4.4% to 9.3%), respectively. The risk of primary resistance was only weakly related to most demographic and clinical factors, including ethnicity and viral subtype., Conclusions: The United Kingdom has one of the highest reported rates of primary resistance to HIV drugs worldwide. Prevalence seems still to be increasing and is high in all demographic subgroups.

Published
2005
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