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Subtype-associated differences in HIV-1 reverse transcription affect the viral replication.

Sergey Iordanskiy1, Mackenzie Waltke, Yanjun Feng

  • 1Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, 4240 Fair Street, East Campus, Lincoln, NE 68583-0900 USA. mtmsxi@gwumc.edu

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Subtype C HIV-1 reverse transcriptase (RT) significantly reduces viral replication by impairing reverse transcript accumulation. This study clarifies the molecular basis for lower replication capacity in subtype C HIV-1 strains compared to subtype B.

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Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Subtype B HIV-1 reverse transcriptase (RT) impact on replication is well-known, but less is understood for subtype C, responsible for most global infections.
  • Subtype C HIV-1 isolates exhibit lower replication capacity than subtype B, with the underlying reasons remaining unclear.

Purpose of the Study:

  • To investigate the impact of HIV-1 subtype C pol gene products, particularly RT, on viral replication, reverse transcription, and DNA integration.
  • To elucidate the molecular basis for differences in replication capacity between HIV-1 subtypes B and C.

Main Methods:

  • Recombinant HIV-1 viruses of subtypes B and C with varying pol gene fragments (protease, integrase, RT) were constructed.
  • Infected cells expressing CXCR4 or CCR5 co-receptors were analyzed for Gag/GagPol processing, viral RNA incorporation, reverse transcription product accumulation, and viral DNA integration.
  • Single viral genome assays assessed point mutation frequencies.

Main Results:

  • No significant differences in Gag/GagPol processing or viral RNA incorporation were observed between subtypes.
  • HIV-1 subtype C RT, or its polymerase and connection-RNase H domains, significantly slowed viral replication.
  • Viruses with subtype C RT showed reduced accumulation of reverse transcription products and lower viral DNA integration.

Conclusions:

  • The whole RT, and specific domains (polymerase, connection-RNase H), from subtype C HIV-1 contribute to lower reverse transcript accumulation.
  • This reduced accumulation in virions and reverse transcription complexes results in significantly lower overall HIV-1 replication for subtype C.