Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
immunology and microbiology
Rare HLA drive additional HIV evolution compared to more frequent alleles
AIDS Research and Human Retroviruses, Volume 25, No. 3, Year 2009
Notification
URL copied to clipboard!
Description
HIV-1 can evolve HLA-specific escape variants in response to HLA-mediated cellular immunity. HLA alleles that are common in the host population may increase the frequency of such escape variants at the population level. When loss of viral fitness is caused by immune escape variation, these variants may revert upon infection of a new host who does not have the corresponding HLA allele. Furthermore, additional escape variants may appear in response to the nonconcordant HLA alleles. Because individuals with rare HLA alleles are less likely to be infected by a partner with concordant HLA alleles, viral populations infecting hosts with rare HLA alleles may undergo a greater amount of evolution than those infecting hosts with common alleles due to the loss of preexisting escape variants followed by new immune escape. This hypothesis was evaluated using maximum likelihood phylogenetic trees of each gene from 272 full-length HIV-1 sequences. Recent viral evolution, as measured by the external branch length, was found to be inversely associated with HLA frequency in nef (p<0.02), env (p<0.03), and pol (p≤0.05), suggesting that rare HLA alleles provide a disproportionate force driving viral evolution compared to common alleles, likely due to the loss of preexisting escape variants during early stages postinfection. © Mary Ann Liebert, Inc.
Authors & Co-Authors
Rousseau, Christine M.
United States, Seattle
University of Washington
United States, Seattle
Northwest Sustainability Institute
Lockhart, David W.
United States, Seattle
University of Washington
Listgarten, Jennifer
United States, Redmond
Microsoft Research
Maley, Stephen N.
United States, Seattle
University of Washington
Kadie, Carl M.
United States, Redmond
Microsoft Research
Learn, Gerald H.
United States, Seattle
University of Washington
Nickle, David C.
United States, Seattle
University of Washington
Heckerman, David E.
United States, Redmond
Microsoft Research
Deng, Wenjie
United States, Seattle
University of Washington
Brander, Christian
United States, Boston
Massachusetts General Hospital
Ndung'u, Thumbi P.
United States, Boston
Massachusetts General Hospital
South Africa, Durban
The Nelson R. Mandela Medical School
Coovadia, Hoosen Mahomed
South Africa, Durban
The Nelson R. Mandela Medical School
Goulder, Philip Jeremy Renshaw
United States, Boston
Massachusetts General Hospital
South Africa, Durban
The Nelson R. Mandela Medical School
United Kingdom, Oxford
Nuffield Department of Medicine
Korber, Bette T.
United States, Los Alamos
Los Alamos National Laboratory
United States, Santa fe
Santa fe Institute
Walker, Bruce D.
United States, Boston
Massachusetts General Hospital
South Africa, Durban
The Nelson R. Mandela Medical School
United States, Chevy Chase
Howard Hughes Medical Institute
Mullins, James I.
United States, Seattle
University of Washington
Statistics
Citations: 16
Authors: 16
Affiliations: 9
Identifiers
Doi:
10.1089/aid.2008.0208
ISSN:
08892229
Research Areas
Genetics And Genomics
Infectious Diseases
Study Design
Cross Sectional Study