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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
medicine
HIV type 1 polymerase gene polymorphisms are associated with phenotypic differences in replication capacity and disease progression
Journal of Infectious Diseases, Volume 209, No. 1, Year 2014
Notification
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Description
Background. Determinants of intersubtype differences in human immunodeficiency virus type 1 (HIV-1) clinical disease progression remain unknown.Methods. HIV-1 subtype was independently determined for 5 separate genomic regions in 396 HIV-1 seroconverters from Rakai, Uganda, using a multiregion hybridization assay. Replication capacities (RC) in samples from a subset of 145 of these subjects were determined. HIV-1 genomic regions and pol RC were examined for association with disease progression. Amino acid polymorphisms were examined for association with pol RC.Results. In multivariate analyses, the hazard for progression to the composite end point (defined as a CD4+ T-cell count <250 cells/mm3, antiretroviral therapy initiation, or death) among patients with subtype D pol infection was 2.4 times the hazard for those infected with subtype A pol infection (P =. 001). Compared with subtype A pol (the reference group), the hazard for progression to the composite end point for subtype D pol infection with a pol RC >67% (ie, the median pol RC) was significantly greater (HR, 4.6; 95% confidence interval [CI], 1.9-11.0; P =. 001), whereas the hazard for progression to the composite end point for subtype D pol infection with a pol RC ≤67% was not significantly different (HR, 2.2; 95% CI, 1.0-4.9; P =. 051). Amino acid substitutions at protease positions 62 and 64 and at reverse transcriptase position 272 were associated with significant differences in pol RC.Conclusions. HIV-1 pol gene intersubtype and RC differences are associated with disease progression and may be influenced by amino acid polymorphisms. © 2013 Published by Oxford University Press.
Available Materials
https://efashare.b-cdn.net/share/pmc/articles/PMC3864385/bin/supp_209_1_66__index.html
https://efashare.b-cdn.net/share/pmc/articles/PMC3864385/bin/supp_jit425_jit425supp_fig1.pdf
https://efashare.b-cdn.net/share/pmc/articles/PMC3864385/bin/supp_jit425_jit425supp.docx
Authors & Co-Authors
Ng, Oon Tek
United States, Baltimore
Johns Hopkins University
Singapore, Singapore City
Tan Tock Seng Hospital
Laeyendecker, Oliver B.
United States, Baltimore
Johns Hopkins University
United States, Bethesda
National Institute of Allergy and Infectious Diseases Niaid
Redd, Andrew D.
United States, Bethesda
National Institute of Allergy and Infectious Diseases Niaid
Munshaw, Supriya
United States, Baltimore
Johns Hopkins University
Grabowski, Mary Kate
United States, Baltimore
Johns Hopkins Bloomberg School of Public Health
Paquet, Agnes C.
United States, San Francisco
Monogram Biosciences
Evans, Mark C.
United States, San Francisco
Monogram Biosciences
Haddad, Mojgan
United States, San Francisco
Monogram Biosciences
Huang, Wei
United States, San Francisco
Monogram Biosciences
Robb, Merlin Lee
United States, Rockville
Hjf
Reynolds, Steven James
United States, Baltimore
Johns Hopkins University
United States, Bethesda
National Institute of Allergy and Infectious Diseases Niaid
Gray, Ronald H.
United States, Baltimore
Johns Hopkins Bloomberg School of Public Health
Wawer, Maria J.
United States, Baltimore
Johns Hopkins Bloomberg School of Public Health
Serwadda, David Musoke
Uganda, Kampala
Makerere University
Eshleman, Susan H.
United States, Baltimore
Johns Hopkins School of Medicine
Quinn, Thomas Charles
United States, Baltimore
Johns Hopkins University
United States, Bethesda
National Institute of Allergy and Infectious Diseases Niaid
Statistics
Citations: 19
Authors: 16
Affiliations: 8
Identifiers
Doi:
10.1093/infdis/jit425
ISSN:
00221899
Research Areas
Environmental
Genetics And Genomics
Infectious Diseases
Study Locations
Uganda