Skip to content

Advertisement

Volume 9 Supplement 2

AIDS Vaccine 2012

  • Poster presentation
  • Open Access

Evolutionary dynamics of HIV-1 subtype C accessory and regulatory genes in primary infection

  • 1,
  • 2,
  • 3,
  • 4,
  • 3 and
  • 2
Retrovirology20129 (Suppl 2) :P142

https://doi.org/10.1186/1742-4690-9-S2-P142

  • Published:

Keywords

  • Primary Infection
  • Viral Diversity
  • Sampling Time Point
  • Vaccine Research
  • Differential Diversity

Background

Studies addressing the dynamics of accessory and regulatory viral gene diversity and selection during early stage of HIV-1 infection are limited but crucial for progress towards vaccine research.

Methods

Intra-patient diversity and evolution was assessed during primary HIV-1C infection, viral quasispecies were obtained by single genome amplification (SGA) at multiple sampling time points up to one year post-seroconversion (p/s).

Results

The mean intra-patient diversity was found to be 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 0.42% (95%CI; 0.18 to 0.66) for rev exon 1 during the time period of 181 to 500 days p/s. Statistically significant increases in viral diversity were observed for vif (p=0.013) and vpu (p=0.002). Weak and sporadic associations between levels of viral diversity within the non-structural genes and HIV-1 RNA load during primary infection were found. Positive and negative selection patterns over the first year post-seroconversion were assessed in each of these genes, providing insight into the selection pressures on these genes which are crucial for viral replication in-vivo.

Conclusion

Our study highlights differential diversity and slower diversification across these HIV-1 genes. The most likely cause is different selection pressure imposed by host immune response to the encoded viral gene products that may result in different evolutionary rates.

Authors’ Affiliations

(1)
HSPH/UB/BHP, Boston, MA, Botswana
(2)
Harvard School of Public Health (HSPH)/ BHP, Boston, MA, USA
(3)
University of Botswana (UB), Gaborone, Botswana
(4)
Botswana Harvard AIDS Institute Partnership (BHP), Gaborone, Botswana

Copyright

© Rossenkhan et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Advertisement