Abstract
To assess the level of intra-patient diversity and evolution of HIV-1C non-structural genes in primary infection, viral quasispecies obtained by single genome amplification (SGA) at multiple sampling timepoints up to 500 days post-seroconversion (p/s) were analyzed. The mean intra-patient diversity was 0.11% (95% CI; 0.02 to 0.20) for vif, 0.23% (95% CI; 0.08 to 0.38) for vpr, 0.35% (95% CI; −0.05 to 0.75) for vpu, 0.18% (95% CI; 0.01 to 0.35) for tat exon 1 and 0.30% (95% CI; 0.02 to 0.58) for rev exon 1 during the time period 0 to 90 days p/s. The intra-patient diversity increased gradually in all non-structural genes over the first year of HIV-1 infection, which was evident from the vif mean intra-patient diversity of 0.46% (95% CI; 0.28 to 0.64), vpr 0.44% (95% CI; 0.24 to 0.64), vpu 0.84% (95% CI; 0.55 to 1.13), tat exon 1 0.35% (95% CI; 0.14 to 0.56 ) and rev exon 1 0.42% (95% CI; 0.18 to 0.66) during the time period of 181 to 500 days p/s. There was a statistically significant increase in viral diversity for vif (p = 0.013) and vpu (p = 0.002). No associations between levels of viral diversity within the non-structural genes and HIV-1 RNA load during primary infection were found. The study details the dynamics of the non-structural viral genes during the early stages of HIV-1C infection.
Highlights
The majority of HIV infections in the world, those in sub-Saharan Africa, are attributable to subtype C cementing its status as a major public health concern
We addressed the following questions: (1) What are the phylogenetic relationships of HIV-1 nonstructural genes during primary HIV-1 infection? (2) What is the level of intra-patient diversity during primary infection? (3) How does viral diversity in non-structural HIV-1 genes change over time? and (4) Is HIV-1 RNA load in plasma associated with diversity of HIV-1 nonstructural genes during primary HIV-1 infection?
This is the first report on the extent and dynamics of viral diversity within HIV-1C non-structural genes during primary HIV-1C infection
Summary
The majority of HIV infections in the world, those in sub-Saharan Africa, are attributable to subtype C cementing its status as a major public health concern. Numerous studies have linked viral diversity in HIV-1 structural genes with disease progression [2,3,4,5,6,7,8]. To our best knowledge no published reports to date have pertained to diversity and/or divergence of viral non-structural genes during primary HIV-1 subtype C infection. SalazarGonzales et al showed that the transmitted/founder full length sequences from 12 subjects (9 infected with HIV subtype B and 3 subtype C) contained intact non-structural genes [9]. Michael et al reported defective accessory genes (HXB2 sequence positions 4,961 to 6,346) in longitudinal HIV-1 subtype B infection [10]. A longitudinal study on twins infected with HIV-1 subtype B perinatally showed discordant disease progression rates with a dramatic increase in tat gene sequence diversity in the sicker child over time [12]
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