Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage
| dc.contributor.author | Chopera, Denis R | en_ZA |
| dc.contributor.author | Woodman, Zenda | en_ZA |
| dc.contributor.author | Mlisana, Koleka | en_ZA |
| dc.contributor.author | Mlotshwa, Mandla | en_ZA |
| dc.contributor.author | Martin, Darren P | en_ZA |
| dc.contributor.author | Seoighe, Cathal | en_ZA |
| dc.contributor.author | Treurnicht, Florette | en_ZA |
| dc.contributor.author | Rosa, Debra Assis de | en_ZA |
| dc.contributor.author | Hide, Winston | en_ZA |
| dc.contributor.author | Karim, Salim Abdool | en_ZA |
| dc.date.accessioned | 2016-01-02T05:05:45Z | |
| dc.date.available | 2016-01-02T05:05:45Z | |
| dc.date.issued | 2008 | en_ZA |
| dc.description.abstract | Author Summary Following infection with HIV, it is well established that a person's genetic makeup is a major determinant of how quickly they will progress to AIDS. Particularly important is the class I Human leukocyte antigen (HLA) gene that is responsible for alerting the immune system to HIV's presence. One of the reasons our immune systems are unable to beat HIV is that the virus can mutate to forms that our HLA genes no longer recognise. However, some people have versions of the HLA gene (for example HLA-B*57 and HLA-B*5801) that are known to force HIV to tolerate mutations that damage its ability to reproduce. Slower HIV reproduction is thought to be one reason that HLA-B*57 and HLA-B*5801 positive people progress to AIDS more slowly than most other HIV infected persons. We report here on a study of HLA-B*57 and HLA-B*5801 negative women in which better control of disease tended to be associated with their being infected with viruses carrying mutations that have been previously shown to reduce replication. These mutations characterise viruses found infecting HLA-B*57 and HLA-B*5801 positive people. This indicates for the first time that HLA-B*57 or HLA-B*5801 negative people that are infected by such reproductively compromised viruses may also experience better survival prospects. | en_ZA |
| dc.identifier.apacitation | Chopera, D. R., Woodman, Z., Mlisana, K., Mlotshwa, M., Martin, D. P., Seoighe, C., ... Karim, S. A. (2008). Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage. <i>PLoS One</i>, http://hdl.handle.net/11427/16158 | en_ZA |
| dc.identifier.chicagocitation | Chopera, Denis R, Zenda Woodman, Koleka Mlisana, Mandla Mlotshwa, Darren P Martin, Cathal Seoighe, Florette Treurnicht, Debra Assis de Rosa, Winston Hide, and Salim Abdool Karim "Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage." <i>PLoS One</i> (2008) http://hdl.handle.net/11427/16158 | en_ZA |
| dc.identifier.citation | Chopera, D. R., Woodman, Z., Mlisana, K., Mlotshwa, M., Martin, D. P., Seoighe, C., ... & Gray, C. M. (2008). Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage. PLoS pathogens, 4(3), e1000033. doi:10.1371/journal.ppat.1000033 | en_ZA |
| dc.identifier.ris | TY - Journal Article AU - Chopera, Denis R AU - Woodman, Zenda AU - Mlisana, Koleka AU - Mlotshwa, Mandla AU - Martin, Darren P AU - Seoighe, Cathal AU - Treurnicht, Florette AU - Rosa, Debra Assis de AU - Hide, Winston AU - Karim, Salim Abdool AB - Author Summary Following infection with HIV, it is well established that a person's genetic makeup is a major determinant of how quickly they will progress to AIDS. Particularly important is the class I Human leukocyte antigen (HLA) gene that is responsible for alerting the immune system to HIV's presence. One of the reasons our immune systems are unable to beat HIV is that the virus can mutate to forms that our HLA genes no longer recognise. However, some people have versions of the HLA gene (for example HLA-B*57 and HLA-B*5801) that are known to force HIV to tolerate mutations that damage its ability to reproduce. Slower HIV reproduction is thought to be one reason that HLA-B*57 and HLA-B*5801 positive people progress to AIDS more slowly than most other HIV infected persons. We report here on a study of HLA-B*57 and HLA-B*5801 negative women in which better control of disease tended to be associated with their being infected with viruses carrying mutations that have been previously shown to reduce replication. These mutations characterise viruses found infecting HLA-B*57 and HLA-B*5801 positive people. This indicates for the first time that HLA-B*57 or HLA-B*5801 negative people that are infected by such reproductively compromised viruses may also experience better survival prospects. DA - 2008 DB - OpenUCT DO - 10.1371/journal.ppat.1000033 DP - University of Cape Town J1 - PLoS One LK - https://open.uct.ac.za PB - University of Cape Town PY - 2008 T1 - Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage TI - Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage UR - http://hdl.handle.net/11427/16158 ER - | en_ZA |
| dc.identifier.uri | http://hdl.handle.net/11427/16158 | |
| dc.identifier.uri | http://dx.doi.org/10.1371/journal.ppat.1000033 | |
| dc.identifier.vancouvercitation | Chopera DR, Woodman Z, Mlisana K, Mlotshwa M, Martin DP, Seoighe C, et al. Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage. PLoS One. 2008; http://hdl.handle.net/11427/16158. | en_ZA |
| dc.language.iso | eng | en_ZA |
| dc.publisher | Public Library of Science | en_ZA |
| dc.publisher.department | Institute of Infectious Disease and Molecular Medicine | en_ZA |
| dc.publisher.faculty | Faculty of Health Sciences | en_ZA |
| dc.publisher.institution | University of Cape Town | |
| dc.rights | This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | en_ZA |
| dc.rights.holder | © 2008 Chopera et al | en_ZA |
| dc.rights.uri | http://creativecommons.org/licenses/by/4.0 | en_ZA |
| dc.source | PLoS One | en_ZA |
| dc.source.uri | http://journals.plos.org/plospathogens | en_ZA |
| dc.subject.other | Microbial mutation | en_ZA |
| dc.subject.other | Viral load | en_ZA |
| dc.subject.other | Mutation detection | en_ZA |
| dc.subject.other | Mutation | en_ZA |
| dc.subject.other | HIV | en_ZA |
| dc.subject.other | HIV-1 | en_ZA |
| dc.subject.other | Viral replication | en_ZA |
| dc.subject.other | Enzyme-linked immunoassays | en_ZA |
| dc.title | Transmission of HIV-1 CTL escape variants provides HLA-mismatched recipients with a survival advantage | en_ZA |
| dc.type | Journal Article | en_ZA |
| uct.type.filetype | Text | |
| uct.type.filetype | Image | |
| uct.type.publication | Research | en_ZA |
| uct.type.resource | Article | en_ZA |
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