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A Combination of M50I and V151I Polymorphic Mutations in HIV-1 Subtype B Integrase Results in Defects in

Jun Yang1, Ming Hao1, Muhammad A Khan2

  • 1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory, Frederick, MD 21702, USA.

Viruses
|November 27, 2021
PubMed

Insights

A specific mutation in HIV integrase (IN:M50I) impairs virus release and replication. However, a second mutation (IN:V151I) is required for this defect, revealing a dual-mutation requirement for defective HIV production.

Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • A prior study identified an HIV-1 integrase (IN) mutation (IN:M50I) that severely impairs viral release and replication.
  • Compensatory mutations in IN or RNaseH (RH) were found to restore infectivity, suggesting IN and RH involvement in HIV infectability.

Purpose of the Study:

  • To investigate the prevalence of these HIV mutations in patients undergoing antiretroviral therapy.
  • To understand the specific mutational combinations leading to defective HIV replication.

Main Methods:

  • Population analysis of 529 plasma virus RNA sequences using MiSeq.
  • Sequence comparison between defective and recombinant viruses.
  • Western Blotting assays to assess viral protein processing.

Main Results:

  • Fourteen HIV plasma samples harbored the IN:M50I mutation without compensatory changes.
  • The IN:V151I mutation was identified in these viruses, known to be polymorphic.
  • Reversion of IN:V151I to wild-type restored viral replication and Gag/GagPol processing.

Conclusions:

  • The IN:M50I mutation alone does not produce replication-defective HIV.
  • A combination of IN:M50I and IN:V151I mutations is necessary to generate defective HIV particles.
  • This finding clarifies the specific genetic requirements for impaired HIV production and infectivity.
Keywords:
M50IV151Iautoprocessingintegrasematurationpolymorphismsviral replication

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