HIV-1 clade B pol evolution following primary infection

Characterize intra-individual HIV-1 subtype B pol evolution in antiretroviral naive individuals. Longitudinal cohort study of individuals enrolled during primary infection. Eligible individuals were antiretroviral naïve participants enrolled in the cohort from December 1997-December 2005 and having...

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Bibliographic Details
Published in:PloS one 2013-06, Vol.8 (6), p.e68188-e68188
Main Authors: Hightower, George K, May, Susanne J, Pérez-Santiago, Josué, Pacold, Mary E, Wagner, Gabriel A, Little, Susan J, Richman, Douglas D, Mehta, Sanjay R, Smith, Davey M, Pond, Sergei L Kosakovsky
Format: Article
Language:English
Subjects:
Acquired immune deficiency syndrome
Adult
AIDS
Algorithms
Antiretroviral agents
Antiretroviral Therapy, Highly Active - methods
Bioinformatics
Biology
Blood
CD4 antigen
CD4 Lymphocyte Count - methods
Cohort Studies
Disease transmission
Divergence
Drug resistance
Evolution
Evolution, Molecular
Evolutionary design method
Female
Gene sequencing
Genes, pol - genetics
Genes, Viral - genetics
Genetic Variation - genetics
Genomes
Haplotypes
Histocompatibility antigen HLA
HIV
HIV Infections - drug therapy
HIV Infections - genetics
HIV-1 - genetics
HLA Antigens - genetics
Human immunodeficiency virus
Humans
Hypothesis testing
Infections
Longitudinal Studies
Medicine
Middle Aged
Mitochondrial DNA
Mutation
Phylogenetics
Substitutes
Viral Load - methods
Young Adult
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Summary:Characterize intra-individual HIV-1 subtype B pol evolution in antiretroviral naive individuals. Longitudinal cohort study of individuals enrolled during primary infection. Eligible individuals were antiretroviral naïve participants enrolled in the cohort from December 1997-December 2005 and having at least two blood samples available with the first one collected within a year of their estimated date of infection. Population-based pol sequences were generated from collected blood samples and analyzed for genetic divergence over time in respect to dual infection status, HLA, CD4 count and viral load. 93 participants were observed for a median of 1.8 years (Mean = 2.2 years, SD =1.9 years). All participants classified as mono-infected had less than 0.7% divergence between any two of their pol sequences using the Tamura-Nei model (TN93), while individuals with dual infection had up to 7.0% divergence. The global substitution rates (substitutions/nucleotide/year) for mono and dually infected individuals were significantly different (p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0068188