Search

Your search keyword '"Wolinsky S"' showing total 280 results
Start Over Author "Wolinsky S"
280 results on '"Wolinsky S"'

1. LILRB2 Interaction with HLA Class I Correlates with Control of HIV-1 Infection

Author

Deeks, Steven, Bashirova, AA, Martin-Gayo, E, Jones, DC, Qi, Y, Apps, R, Gao, X, Burke, PS, Taylor, CJ, Rogich, J, and Wolinsky, S

Abstract

Natural progression of HIV-1 infection depends on genetic variation in the human major histocompatibility complex (MHC) class I locus, and the CD8+ T cell response is thought to be a primary mechanism of this effect. However, polymorphism within the MHC ma

Published
2014

4. Measuring recent thymic emigrants in blood of normal and HIV-1-infected individuals before and after effective therapy.

Author

Zhang, L, Lewin, SR, Markowitz, M, Lin, HH, Skulsky, E, Karanicolas, R, He, Y, Jin, X, Tuttleton, S, Vesanen, M, Spiegel, H, Kost, R, van Lunzen, J, Stellbrink, HJ, Wolinsky, S, Borkowsky, W, Palumbo, P, Kostrikis, LG, and Ho, DD

Subjects
T-Lymphocytes, Humans, HIV-1, HIV Infections, DNA, Circular, DNA Primers, Anti-HIV Agents, Case-Control Studies, Polymerase Chain Reaction, Cell Movement, Gene Rearrangement, T-Lymphocyte, Base Sequence, Aging, Adolescent, Adult, Child, DNA, Circular, Gene Rearrangement, T-Lymphocyte, Medical and Health Sciences, Immunology
Abstract

The role of the thymus in HIV-1 pathogenesis remains unclear. We developed an assay to quantify the number of recent thymic emigrants in blood based on the detection of a major excisional DNA byproduct (termed alpha1 circle) of T cell receptor rearrangement. By studying 532 normal individuals, we found that alpha1 circle numbers in blood remain high for the first 10-15 yr of life, a sharp drop is seen in the late teen years, and a gradual decline occurs thereafter. Compared with age-matched uninfected control individuals, alpha1 circle numbers in HIV-1-infected adults were significantly reduced; however, there were many individuals with normal alpha1 circle numbers. In 74 individuals receiving highly active antiretroviral therapy, we found no appreciable effect on alpha1 circle numbers in those whose baseline values were already within the normal range, but significant increases were observed in those with a preexisting impairment. The increases in alpha1 circle numbers were, however, numerically insufficient to account for the rise in levels of naive T lymphocytes. Overall, it is difficult to invoke thymic regenerative failure as a generalized mechanism for CD4 lymphocyte depletion in HIV-1 infection, as alpha1 circle numbers are normal in a substantial subset of HIV-1-infected individuals.

Published
1999

5. HIV-1 Nomenclature Proposal

Author

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

Published
2000

10. Search for the Origin of HIV and AIDS

Author

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

Published
2000

11. Sexual Transmission and Propagation of SIV and HIV in Resting and Activated CD4+ T Cells

Author

Zhang, Z.-Q., Schuler, T., Zupancic, M., Wietgrefe, S., Staskus, K. A., Reimann, K. A., Reinhart, T. A., Rogan, M., Cavert, W., Miller, C. J., Veazey, R. S., Notermans, D., Little, S., Danner, S. A., Richman, D. D., Havlir, D., Wong, J., Jordan, H. L., Schacker, T. W., Racz, P., Tenner-Racz, K., Letvin, N. L., Wolinsky, S., and Haase, A. T.

Published
1999

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

Author

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

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

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

Published
2018

13. Protecting HIV databases

Author

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

Published
1995

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

Author

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

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

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

Published
2001

15. P21WAF1/CIP1RNA expression in highly HIV-1 exposed, uninfected individuals

Author

Herbeck, J, Ghorai, S, Chen, L, Rinaldo, CR, Margolick, JB, Detels, R, Jacobson, L, Wolinsky, S, and Mullins, JI

Abstract

© 2015 Herbeck et al. Some individuals remain HIV-1 antibody and PCR negative after repeated exposures to the virus, and are referred to as HIV-exposed seronegatives (HESN). However, the causes of resistance to HIV-1 infection in cases other than those with a homozygous CCR5Δ32 deletion are unclear. We hypothesized that human p21WAF1/CIP1(a cyclin-dependent kinase inhibitor) could play a role in resistance to HIV-1 infection in HESN, as p21 expression has been associated with suppression of HIV-1 in elite controllers and reported to block HIV-1 integration in cell culture. We measured p21 RNA expression in PBMC from 40 HESN and 40 low exposure HIV-1 seroconverters (LESC) prior to their infection using a real-time PCR assay. Comparing the 20 HESN with the highest exposure risk (median = 111 partners/2.5 years prior to the 20 LESC with the lowest exposure risk (median = 1 partner/2.5 years prior), p21 expression trended higher in HESN in only one of two experiments (P = 0.11 vs. P = 0.80). Additionally, comparison of p21 expression in the top 40 HESN (median = 73 partners/year) and lowest 40 LESC (median = 2 partners/year) showed no difference between the groups (P = 0.84). There was a weak linear trend between risk of infection after exposure and increasing p21 gene expression (R2= 0.02, P = 0.12), but again only in one experiment. Hence, if p21 expression contributes to the resistance to viral infection in HESN, it likely plays a minor role evident only in those with extremely high levels of exposure to HIV-1.

Published
2015

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

Author

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

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

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

Published
1999

17. P21WAF1/CIP1 RNA expression in highly HIV-1 exposed, uninfected individuals

Author

Herbeck, J, Ghorai, S, Chen, L, Rinaldo, CR, Margolick, JB, Detels, R, Jacobson, L, Wolinsky, S, Mullins, JI, Herbeck, J, Ghorai, S, Chen, L, Rinaldo, CR, Margolick, JB, Detels, R, Jacobson, L, Wolinsky, S, and Mullins, JI

Abstract

Some individuals remain HIV-1 antibody and PCR negative after repeated exposures to the virus, and are referred to as HIV-exposed seronegatives (HESN). However, the causes of resistance to HIV-1 infection in cases other than those with a homozygous CCR5Δ32 deletion are unclear. We hypothesized that human p21WAF1/CIP1 (a cyclin-dependent kinase inhibitor) could play a role in resistance to HIV-1 infection in HESN, as p21 expression has been associated with suppression of HIV-1 in elite controllers and reported to block HIV-1 integration in cell culture. We measured p21 RNA expression in PBMC from 40 HESN and 40 low exposure HIV-1 seroconverters (LESC) prior to their infection using a real-time PCR assay. Comparing the 20 HESN with the highest exposure risk (median = 111 partners/2.5 years prior to the 20 LESC with the lowest exposure risk (median = 1 partner/2.5 years prior), p21 expression trended higher in HESN in only one of two experiments (P = 0.11 vs. P = 0.80). Additionally, comparison of p21 expression in the top 40 HESN (median = 73 partners/year) and lowest 40 LESC (median = 2 partners/year) showed no difference between the groups (P = 0.84). There was a weak linear trend between risk of infection after exposure and increasing p21 gene expression (R2 = 0.02, P = 0.12), but again only in one experiment. Hence, if p21 expression contributes to the resistance to viral infection in HESN, it likely plays a minor role evident only in those with extremely high levels of exposure to HIV-1.

Published
2015

18. A chemokine receptor CCR2 allele delays HIV-1 disease progression and is associated with a CCR5 promoter mutation

Author

Deutsch, L., Kostrikis, Leontios G., Huang, Y., Moore, J. P., Wolinsky, S. M., Zhang, L., Guo, Y., Phair, J., Neumann, A. U., Ho, David D., and Kostrikis, Leontios G. [0000-0002-5340-7109]

Subjects
Male, Heterozygote, CCR2, Genotype, Receptors, CCR5, Molecular Sequence Data, HIV Infections, t lymphocyte, human immunodeficiency virus infection, Biology, General Biochemistry, Genetics and Molecular Biology, Virus, Cohort Studies, Loss of heterozygosity, Chemokine receptor, promoter region, HIV Seroprevalence, HIV Seropositivity, Humans, Coding region, controlled study, human, gene mutation, Allele, Alleles, Genetics, Human immunodeficiency virus, disease course, human cell, Point mutation, Homozygote, article, allele, immunopathogenesis, chemokine receptor, General Medicine, Prognosis, major clinical study, CD4 Lymphocyte Count, cd4 antigen, priority journal, Mutation, Disease Progression, HIV-1, Receptors, Chemokine, Promoter Regions (Genetics), virus cell interaction, human immunodeficiency virus 1
Abstract

Viral and host factors influence the rate of HIV-1 disease progression. For HIV-1 to fuse, a CD4+ cell must express a co-receptor that the virus can use. The chemokine receptors CCR5 and CXCR4 are used by R5 and X4 viruses, respectively. Most new infections involve transmission of R5 viruses, but variants can arise later that also use CXCR4 (R5-X4 or X4 viruses). This is associated with an increased rate of CD4+ T-cell loss and poor prognosis. The ability of host cells to support HIV-1 entry also influences progression. The absence of CCR5 in approximately 1% of the Caucasian population, due to homozygosity for a 32-nucleotide deletion in the coding region (Δ32-CCR5 allele), very strongly protects against HIV-1 transmission. Heterozygosity for the Δ32-CCR5 allele delays progression typically by 2 years. A recent study showed that a conservative substitution (V641) in the coding region of CCR2 also has a significant impact on disease progression, but not on HIV-1 transmission. This was unexpected, since CCR2 is rarely used as a co-receptor in vitro and the V641 change is in a transmembrane region. Because a subsequent study did not confirm this effect on progression to disease, we analyzed CCR2-V641 using subjects in the Chicago MACS. We show that CCR2- V641 is indeed protective against disease progression and go on to show that the CCR2-V641 allele is in complete linkage disequilibrium with a point mutation in the CCR5 regulatory region. 4 350 353 Cited By :335

Published
1998

19. A genome-wide association study of resistance to HIV infection in highly exposed uninfected individuals with hemophilia A

Author

Lane, J., Mclaren, P. J., Dorrell, L., Shianna, K. V., Stemke, A., Pelak, K., Moore, S., Oldenburg, J., Alvarez-Roman, M. T., Angelillo-Scherrer, A., Boehlen, F., Bolton-Maggs, P. H. B., Brand, B., Brown, D., Chiang, E., Cid-Haro, A. R., Clotet, B., Collins, P., Colombo, S., Dalmau, J., Fogarty, P., Giangrande, P., Gringeri, A., Iyer, R., Katsarou, O., Kempton, C., Kuriakose, P., Lin, J., Makris, M., Manco-Johnson, M., Tsakiris, D. A., Martinez-Picado, J., Mauser-Bunschoten, E., Neff, A., Oka, S., Oyesiku, L., Parra, R., Peter-Salonen, K., Powell, J., Recht, M., Shapiro, A., Stine, K., Talks, K., Telenti, A., Wilde, J., Yee, T. T., Wolinsky, S. M., Martinson, J., Hussain, S. K., Bream, J. H., Jacobson, L. P., Carrington, M., Goedert, J. J., Haynes, B. F., Mcmichael, A. J., Goldstein, D. B., Fellay, J., and NIAID Ctr HIV AIDS Vaccine

Abstract

Human genetic variation contributes to differences in susceptibility to HIV-1 infection. To search for novel host resistance factors, we performed a genome-wide association study (GWAS) in hemophilia patients highly exposed to potentially contaminated factor VIII infusions. Individuals with hemophilia A and a documented history of factor VIII infusions before the introduction of viral inactivation procedures (1979-1984) were recruited from 36 hemophilia treatment centers (HTCs), and their genome-wide genetic variants were compared with those from matched HIV-infected individuals. Homozygous carriers of known CCR5 resistance mutations were excluded. Single nucleotide polymorphisms (SNPs) and inferred copy number variants (CNVs) were tested using logistic regression. In addition, we performed a pathway enrichment analysis, a heritability analysis, and a search for epistatic interactions with CCR5 32 heterozygosity. A total of 560 HIV-uninfected cases were recruited: 36 (6.4%) were homozygous for CCR5 32 or m303. After quality control and SNP imputation, we tested 1 081 435 SNPs and 3686 CNVs for association with HIV-1 serostatus in 431 cases and 765 HIV-infected controls. No SNP or CNV reached genome-wide significance. The additional analyses did not reveal any strong genetic effect. Highly exposed, yet uninfected hemophiliacs form an ideal study group to investigate host resistance factors. Using a genome-wide approach, we did not detect any significant associations between SNPs and HIV-1 susceptibility, indicating that common genetic variants of major effect are unlikely to explain the observed resistance phenotype in this population.

Published
2013

20. Correction: Copy Number Variation of KIR Genes Influences HIV-1 Control

Author

Pelak, K, Need, A, Fellay, J, Shianna, K, Feng, S, Urban, T, Ge, D, De Luca, A, Martinez-Picado, J, Wolinsky, S, Martinson, J, Jamieson, B, Bream, J, Martin, M, Borrow, P, Letvin, N, McMichael, A, Haynes, B, Telenti, A, Carrington, M, Goldstein, D, Alter, G, and (CHAVI), on behalf of NIAID Center for HIV/AIDS Vaccine Immunology

Subjects
Genetics, General Immunology and Microbiology, QH301-705.5, General Neuroscience, Human immunodeficiency virus (HIV), Cancer, Correction, Biology, medicine.disease_cause, medicine.disease, General Biochemistry, Genetics and Molecular Biology, medicine, Copy-number variation, Biology (General), General Agricultural and Biological Sciences, Gene
Abstract

The affiliation for the twentieth author was incorrect. Mary Carrington is not affiliated with #10 but with #12 Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland, United States of America. The author’s affiliation to #18 is unaffected.

Published
2011

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

Author

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

Abstract

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

Published
1999

22. LILRB2 Interaction with HLA Class I Correlates with Control of HIV-1 Infection

Author

Bashirova, AA, Martin-Gayo, E, Jones, DC, Qi, Y, Apps, R, Gao, X, Burke, PS, Taylor, CJ, Rogich, J, Wolinsky, S, Bream, JH, Duggal, P, Hussain, S, Martinson, J, Weintrob, A, Kirk, GD, Fellay, J, Buchbinder, SP, Goedert, JJ, Deeks, SG, Pereyra, F, Trowsdale, J, Lichterfeld, M, Telenti, A, Walker, BD, Allen, RL, Carrington, M, Yu, XG, Bashirova, AA, Martin-Gayo, E, Jones, DC, Qi, Y, Apps, R, Gao, X, Burke, PS, Taylor, CJ, Rogich, J, Wolinsky, S, Bream, JH, Duggal, P, Hussain, S, Martinson, J, Weintrob, A, Kirk, GD, Fellay, J, Buchbinder, SP, Goedert, JJ, Deeks, SG, Pereyra, F, Trowsdale, J, Lichterfeld, M, Telenti, A, Walker, BD, Allen, RL, Carrington, M, and Yu, XG

Abstract

Natural progression of HIV-1 infection depends on genetic variation in the human major histocompatibility complex (MHC) class I locus, and the CD8+ T cell response is thought to be a primary mechanism of this effect. However, polymorphism within the MHC may also alter innate immune activity against human immunodeficiency virus type 1 (HIV-1) by changing interactions of human leukocyte antigen (HLA) class I molecules with leukocyte immunoglobulin-like receptors (LILR), a group of immunoregulatory receptors mainly expressed on myelomonocytic cells including dendritic cells (DCs). We used previously characterized HLA allotype-specific binding capacities of LILRB1 and LILRB2 as well as data from a large cohort of HIV-1-infected individuals (N = 5126) to test whether LILR-HLA class I interactions influence viral load in HIV-1 infection. Our analyses in persons of European descent, the largest ethnic group examined, show that the effect of HLA-B alleles on HIV-1 control correlates with the binding strength between corresponding HLA-B allotypes and LILRB2 (p = 10-2). Moreover, overall binding strength of LILRB2 to classical HLA class I allotypes, defined by the HLA-A/B/C genotypes in each patient, positively associates with viral replication in the absence of therapy in patients of both European (p = 10-11-10-9) and African (p = 10-5-10-3) descent. This effect appears to be driven by variations in LILRB2 binding affinities to HLA-B and is independent of individual class I allelic effects that are not related to the LILRB2 function. Correspondingly, in vitro experiments suggest that strong LILRB2-HLA binding negatively affects antigen-presenting properties of DCs. Thus, we propose an impact of LILRB2 on HIV-1 disease outcomes through altered regulation of DCs by LILRB2-HLA engagement.

Published
2014

24. Association study of common genetic variants and HIV-1 acquisition in 6,300 infected cases and 7,200 controls

Author

Balloux, F., McLaren, P.J., Coulonges, C., Ripke, S., van den Berg, L., Buchbinder, S., Carrington, M., Cossarizza, A., Dalmau, J., Deeks, S.G., Delaneau, O., De Luca, A., Goedert, J.J., Haas, D., Herbeck, J.T., Kathiresan, S., Kirk, G.D., Lambotte, O., Luo, M., Mallal, S., van Manen, D., Martinez-Picado, J., Meyer, L., Miro, J.M., Mullins, J.I., Obel, N., O'Brien, S.J., Pereyra, F., Plummer, F.A., Poli, G., Qi, Y., Rucart, P., Sandhu, M.S., Shea, P.R., Schuitemaker, H., Theodorou, I., Vannberg, F., Veldink, J., Walker, B.D., Weintrob, A., Winkler, C.A., Wolinsky, S., Telenti, A., Goldstein, D.B., de Bakker, P.I.W., Zagury, J-F, Fellay, J., Balloux, F., McLaren, P.J., Coulonges, C., Ripke, S., van den Berg, L., Buchbinder, S., Carrington, M., Cossarizza, A., Dalmau, J., Deeks, S.G., Delaneau, O., De Luca, A., Goedert, J.J., Haas, D., Herbeck, J.T., Kathiresan, S., Kirk, G.D., Lambotte, O., Luo, M., Mallal, S., van Manen, D., Martinez-Picado, J., Meyer, L., Miro, J.M., Mullins, J.I., Obel, N., O'Brien, S.J., Pereyra, F., Plummer, F.A., Poli, G., Qi, Y., Rucart, P., Sandhu, M.S., Shea, P.R., Schuitemaker, H., Theodorou, I., Vannberg, F., Veldink, J., Walker, B.D., Weintrob, A., Winkler, C.A., Wolinsky, S., Telenti, A., Goldstein, D.B., de Bakker, P.I.W., Zagury, J-F, and Fellay, J.

Abstract

Multiple genome-wide association studies (GWAS) have been performed in HIV-1 infected individuals, identifying common genetic influences on viral control and disease course. Similarly, common genetic correlates of acquisition of HIV-1 after exposure have been interrogated using GWAS, although in generally small samples. Under the auspices of the International Collaboration for the Genomics of HIV, we have combined the genome-wide single nucleotide polymorphism (SNP) data collected by 25 cohorts, studies, or institutions on HIV-1 infected individuals and compared them to carefully matched population-level data sets (a list of all collaborators appears in Note S1 in Text S1). After imputation using the 1,000 Genomes Project reference panel, we tested approximately 8 million common DNA variants (SNPs and indels) for association with HIV-1 acquisition in 6,334 infected patients and 7,247 population samples of European ancestry. Initial association testing identified the SNP rs4418214, the C allele of which is known to tag the HLA-B*57:01 and B*27:05 alleles, as genome-wide significant (p = 3.6×10−11). However, restricting analysis to individuals with a known date of seroconversion suggested that this association was due to the frailty bias in studies of lethal diseases. Further analyses including testing recessive genetic models, testing for bulk effects of non-genome-wide significant variants, stratifying by sexual or parenteral transmission risk and testing previously reported associations showed no evidence for genetic influence on HIV-1 acquisition (with the exception of CCR5Δ32 homozygosity). Thus, these data suggest that genetic influences on HIV acquisition are either rare or have smaller effects than can be detected by this sample size.

Published
2013

25. Influence of HLA-C expression level on HIV control

Author

Apps, R., Qi, Y., Carlson, J.M., Chen, H., Gao, X., Thomas, R., Yuki, Y., Del Prete, G.Q., Goulder, P., Brumme, Z.L., Brumme, C.J., John, M., Mallal, S., Nelson, G., Bosch, R., Heckerman, D., Stein, J.L., Soderberg, K.A., Moody, M.A., Denny, T.N., Zeng, X., Fang, J., Moffett, A., Lifson, J.D., Goedert, J.J., Buchbinder, S., Kirk, G.D., Fellay, J., McLaren, P., Deeks, S.G., Pereyra, F., Walker, B., Michael, N.L., Weintrob, A., Wolinsky, S., Liao, W., Carrington, M., Apps, R., Qi, Y., Carlson, J.M., Chen, H., Gao, X., Thomas, R., Yuki, Y., Del Prete, G.Q., Goulder, P., Brumme, Z.L., Brumme, C.J., John, M., Mallal, S., Nelson, G., Bosch, R., Heckerman, D., Stein, J.L., Soderberg, K.A., Moody, M.A., Denny, T.N., Zeng, X., Fang, J., Moffett, A., Lifson, J.D., Goedert, J.J., Buchbinder, S., Kirk, G.D., Fellay, J., McLaren, P., Deeks, S.G., Pereyra, F., Walker, B., Michael, N.L., Weintrob, A., Wolinsky, S., Liao, W., and Carrington, M.

Abstract

A variant upstream of human leukocyte antigen C (HLA-C) shows the most significant genome-wide effect on HIV control in European Americans and is also associated with the level of HLA-C expression. We characterized the differential cell surface expression levels of all common HLA-C allotypes and tested directly for effects of HLA-C expression on outcomes of HIV infection in 5243 individuals. Increasing HLA-C expression was associated with protection against multiple outcomes independently of individual HLA allelic effects in both African and European Americans, regardless of their distinct HLA-C frequencies and linkage relationships with HLA-B and HLA-A. Higher HLA-C expression was correlated with increased likelihood of cytotoxic T lymphocyte responses and frequency of viral escape mutation. In contrast, high HLA-C expression had a deleterious effect in Crohn’s disease, suggesting a broader influence of HLA expression levels in human disease.

Published
2013

26. Tat-Specific CTL Exert Strong Selective Pressure During Acute SIV Infection

Author

O'Connor, D., Allen, T. M., Jing, P., Dzuris, J. L., Dunphy, E., Mothé, B. R., Liebl, M. E., Vogel, T. U., Mortara, Lorenzo, Dodds, E., Emerson, C., Kunstman, K. J., Wang, X., Hughes, A. L., Desrosiers, R. C., Altman, J. D., Wolinsky, S. M., Sette, A., and Watkins, D. I.

Published
2000

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

Author

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

Abstract

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

Published
2000

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

Author

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

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

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

Published
1999

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

Author

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

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

30. Common genetic variation and the control of HIV-1 in humans

Author

Fellay, J, Ge, D, Shianna, K V, Colombo, S, Ledergerber, B, Cirulli, E T, Urban, T J, Zhang, K, Gumbs, C E, Smith, J P, Castagna, A, Cozzi-Lepri, A, De Luca, A, Easterbrook, P, Günthard, H F, Mallal, S, Mussini, C, Dalmau, J, Martinez-Picado, J, Miro, J M, Obel, N, Wolinsky, S M, Martinson, J J, Detels, R, Margolick, J B, Jacobson, L P, Descombes, P, Antonarakis, S E, Beckmann, J S, O'Brien, S J, Letvin, N L, McMichael, A J, Haynes, B F, Carrington, M, Feng, S, Telenti, A, Goldstein, D B, Fellay, J, Ge, D, Shianna, K V, Colombo, S, Ledergerber, B, Cirulli, E T, Urban, T J, Zhang, K, Gumbs, C E, Smith, J P, Castagna, A, Cozzi-Lepri, A, De Luca, A, Easterbrook, P, Günthard, H F, Mallal, S, Mussini, C, Dalmau, J, Martinez-Picado, J, Miro, J M, Obel, N, Wolinsky, S M, Martinson, J J, Detels, R, Margolick, J B, Jacobson, L P, Descombes, P, Antonarakis, S E, Beckmann, J S, O'Brien, S J, Letvin, N L, McMichael, A J, Haynes, B F, Carrington, M, Feng, S, Telenti, A, and Goldstein, D B

Abstract

To extend the understanding of host genetic determinants of HIV-1 control, we performed a genome-wide association study in a cohort of 2,554 infected Caucasian subjects. The study was powered to detect common genetic variants explaining down to 1.3% of the variability in viral load at set point. We provide overwhelming confirmation of three associations previously reported in a genome-wide study and show further independent effects of both common and rare variants in the Major Histocompatibility Complex region (MHC). We also examined the polymorphisms reported in previous candidate gene studies and fail to support a role for any variant outside of the MHC or the chemokine receptor cluster on chromosome 3. In addition, we evaluated functional variants, copy-number polymorphisms, epistatic interactions, and biological pathways. This study thus represents a comprehensive assessment of common human genetic variation in HIV-1 control in Caucasians.

Published
2009

31. Increased sequence diversity coverage improves detection of HIV-Specific T cell responses

Author

Frahm, N., Kaufmann, D.E., Yusim, K., Muldoon, M., Kesmir, Can, Linde, C.H., Fischer, W., Allen, T.M., Li, B., McMahon, B.H., Faircloth, K.L., Hewitt, H.S., Mackey, E.W., Miura, T., Khatri, A., Wolinsky, S., McMichael, A., Funkhouser, R.K., Walker, B.D., Brander, C., Korber, B.T., Frahm, N., Kaufmann, D.E., Yusim, K., Muldoon, M., Kesmir, Can, Linde, C.H., Fischer, W., Allen, T.M., Li, B., McMahon, B.H., Faircloth, K.L., Hewitt, H.S., Mackey, E.W., Miura, T., Khatri, A., Wolinsky, S., McMichael, A., Funkhouser, R.K., Walker, B.D., Brander, C., and Korber, B.T.

Abstract

The accurate identification of HIV-specific T cell responses is important for determining the relationship between immune response, viral control, and disease progression. HIV-specific immune responses are usually measured using peptide sets based on consensus sequences, which frequently miss responses to regions where test set and infecting virus differ. In this study, we report the design of a peptide test set with significantly increased coverage of HIV sequence diversity by including alternative amino acids at variable positions during the peptide synthesis step. In an IFN-gamma ELISpot assay, these "toggled" peptides detected HIV-specific CD4(+) and CD8(+) T cell responses of significantly higher breadth and magnitude than matched consensus peptides. The observed increases were explained by a closer match of the toggled peptides to the autologous viral sequence. Toggled peptides therefore afford a cost-effective and significantly more complete view of the host immune response to HIV and are directly applicable to other variable pathogens.

Published
2007

33. Prevalence of XMRV Nucleic Acid and Antibody in HIV-1-Infected Men and in Men at Risk for HIV-1 Infection

Author

Spindler, J., primary, Hackett, J., additional, Qiu, X., additional, Wiegand, A., additional, Boltz, V. F., additional, Swanson, P., additional, Bream, J. H., additional, Jacobson, L. P., additional, Li, X., additional, Rinaldo, C. R., additional, Wolinsky, S. M., additional, Coffin, J. M., additional, Kearney, M. F., additional, and Mellors, J. W., additional

Published
2011
Full Text
View/download PDF

35. Measuring recent thymic emigrants in blood of normal and HIV-1-infected individuals before and after effective therapy

Author

Zhang, LQ, Lewin, SR, Markowitz, M, Lin, HH, Skulsky, E, Karanicolas, R, He, YX, Jin, X, Tuttleton, S, Vesanen, M, Spiegel, H, Kost, R, van Lunzen, J, Stellbrink, HJ, Wolinsky, S, Borkowsky, W, Palumbo, P, Kostrikis, LG, Ho, DD, Zhang, LQ, Lewin, SR, Markowitz, M, Lin, HH, Skulsky, E, Karanicolas, R, He, YX, Jin, X, Tuttleton, S, Vesanen, M, Spiegel, H, Kost, R, van Lunzen, J, Stellbrink, HJ, Wolinsky, S, Borkowsky, W, Palumbo, P, Kostrikis, LG, and Ho, DD

Abstract

The role of the thymus in HIV-1 pathogenesis remains unclear. We developed an assay to quantify the number of recent thymic emigrants in blood based on the detection of a major excisional DNA byproduct (termed alpha1 circle) of T cell receptor rearrangement. By studying 532 normal individuals, we found that alpha1 circle numbers in blood remain high for the first 10-15 yr of life, a sharp drop is seen in the late teen years, and a gradual decline occurs thereafter. Compared with age-matched uninfected control individuals, alpha1 circle numbers in HIV-1-infected adults were significantly reduced; however, there were many individuals with normal alpha1 circle numbers. In 74 individuals receiving highly active antiretroviral therapy, we found no appreciable effect on alpha1 circle numbers in those whose baseline values were already within the normal range, but significant increases were observed in those with a preexisting impairment. The increases in alpha1 circle numbers were, however, numerically insufficient to account for the rise in levels of naive T lymphocytes. Overall, it is difficult to invoke thymic regenerative failure as a generalized mechanism for CD4 lymphocyte depletion in HIV-1 infection, as alpha1 circle numbers are normal in a substantial subset of HIV-1-infected individuals.

Published
1999

36. A Plea for Justice for Jailed Medical Workers

Author

Ahuja, S. K., primary, Aiuti, F., additional, Berkhout, B., additional, Biberfeld, P., additional, Burton, D. R., additional, Colizzi, V., additional, Deeks, S. G., additional, Desrosiers, R. C., additional, Dierich, M. P., additional, Doms, R. W., additional, Emerman, M., additional, Gallo, R. C., additional, Girard, M., additional, Greene, W. C., additional, Hoxie, J. A., additional, Hunter, E., additional, Klein, G., additional, Korber, B., additional, Kuritzkes, D. R., additional, Lederman, M. M., additional, Malim, M. H., additional, Marx, P. A., additional, McCune, J. M., additional, McMichael, A., additional, Miller, C., additional, Miller, V., additional, Montagnier, L., additional, Montefiori, D. C., additional, Moore, J. P., additional, Nixon, D. F., additional, Overbaugh, J., additional, Pauza, C. D., additional, Richman, D. D., additional, Saag, M. S., additional, Sattentau, Q., additional, Schooley, R. T., additional, Shattock, R., additional, Shaw, G. M., additional, Stevenson, M., additional, Trkola, A., additional, Wainberg, M. A., additional, Weiss, R. A., additional, Wolinsky, S., additional, and Zack, J. A., additional

Published
2006
Full Text
View/download PDF

38. Genetic Composition of Human Immunodeficiency Virus Type 1 in Cerebrospinal Fluid and Blood without Treatment and during Failing Antiretroviral Therapy

Author

Strain, M. C., primary, Letendre, S., additional, Pillai, S. K., additional, Russell, T., additional, Ignacio, C. C., additional, Günthard, H. F., additional, Good, B., additional, Smith, D. M., additional, Wolinsky, S. M., additional, Furtado, M., additional, Marquie-Beck, J., additional, Durelle, J., additional, Grant, I., additional, Richman, D. D., additional, Marcotte, T., additional, McCutchan, J. A., additional, Ellis, R. J., additional, and Wong, J. K., additional

Published
2005
Full Text
View/download PDF

40. Sexual Transmission and Propagation of SIV and HIV in Resting and Activated CD4 + T Cells

Author

Zhang, Z.-Q., primary, Schuler, T., additional, Zupancic, M., additional, Wietgrefe, S., additional, Staskus, K. A., additional, Reimann, K. A., additional, Reinhart, T. A., additional, Rogan, M., additional, Cavert, W., additional, Miller, C. J., additional, Veazey, R. S., additional, Notermans, D., additional, Little, S., additional, Danner, S. A., additional, Richman, D. D., additional, Havlir, D., additional, Wong, J., additional, Jordan, H. L., additional, Schacker, T. W., additional, Racz, P., additional, Tenner-Racz, K., additional, Letvin, N. L., additional, Wolinsky, S., additional, and Haase, A. T., additional

Published
1999
Full Text
View/download PDF

41. Lack of strong immune selection pressure by the immunodominant, HLA-A*0201-restricted cytotoxic T lymphocyte response in chronic human immunodeficiency virus-1 infection.

Author

Brander, C, primary, Hartman, K E, additional, Trocha, A K, additional, Jones, N G, additional, Johnson, R P, additional, Korber, B, additional, Wentworth, P, additional, Buchbinder, S P, additional, Wolinsky, S, additional, Walker, B D, additional, and Kalams, S A, additional

Published
1998
Full Text
View/download PDF

42. Immunological and Virological Analyses of Persons Infected by Human Immunodeficiency Virus Type 1 while Participating in Trials of Recombinant gp120 Subunit Vaccines

Author

Connor, R. I., primary, Korber, B. T. M., additional, Graham, B. S., additional, Hahn, B. H., additional, Ho, D. D., additional, Walker, B. D., additional, Neumann, A. U., additional, Vermund, S. H., additional, Mestecky, J., additional, Jackson, S., additional, Fenamore, E., additional, Cao, Y., additional, Gao, F., additional, Kalams, S., additional, Kunstman, K. J., additional, McDonald, D., additional, McWilliams, N., additional, Trkola, A., additional, Moore, J. P., additional, and Wolinsky, S. M., additional

Published
1998
Full Text
View/download PDF

43. Overlapping epitopes in human immunodeficiency virus type 1 gp120 presented by HLA A, B, and C molecules: effects of viral variation on cytotoxic T-lymphocyte recognition

Author

Wilson, C C, primary, Kalams, S A, additional, Wilkes, B M, additional, Ruhl, D J, additional, Gao, F, additional, Hahn, B H, additional, Hanson, I C, additional, Luzuriaga, K, additional, Wolinsky, S, additional, Koup, R, additional, Buchbinder, S P, additional, Johnson, R P, additional, and Walker, B D, additional

Published
1997
Full Text
View/download PDF

45. HIV-1 Evolution and Disease Progression

Author

Nowak, M. A., primary, Anderson, R. M., additional, Boerlijst, M. C., additional, Bonhoeffer, S., additional, May, R. M., additional, McMichael, A. J., additional, Wolinsky, S. M., additional, Kunstman, K. J., additional, Safrit, J. T., additional, Koup, R. A., additional, Neumann, A. U., additional, and Korber, B. T. M., additional

Published
1996
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results