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HIV-1 protease-induced apoptosis.

Michaela Rumlová1, Ivana Křížová, Alena Keprová

  • 1Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, v,v,i,, IOCB & Gilead Research Center, Flemingovo nám, 2, 166 10 Prague, Czech Republic. rumlova@uochb.cas.cz.

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Summary

Active HIV-1 protease (PR) induces apoptosis through the mitochondrial pathway. HIV-1 PR directly targets mitochondria, disrupts membrane potential, and interacts with BCA3 to promote cell death, explaining its role in HIV pathogenesis.

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Area of Science:

  • Molecular Biology
  • Virology
  • Cell Biology

Background:

  • Apoptosis contributes to CD4+ T cell depletion in HIV/AIDS.
  • The exact mechanism of HIV-1-induced apoptosis is unclear.
  • HIV-1 protease (PR) is a potential, yet unproven, factor in this process.

Purpose of the Study:

  • To investigate the direct role and mechanism of HIV-1 protease (PR) in inducing apoptosis.
  • To establish a link between HIV-1 PR enzymatic activity and cellular death pathways.

Main Methods:

  • Cellular expression of active HIV-1 PR in HeLa and HEK-293 cells.
  • Mitochondrial localization studies and membrane potential assays.
  • Analysis of caspase activation, PARP cleavage, and DNA fragmentation.
  • In vitro cleavage assays of mitochondrial proteins.
  • Yeast two-hybrid screening to identify interaction partners.

Main Results:

  • Active HIV-1 PR localizes to mitochondria and induces apoptosis via the mitochondrial pathway.
  • HIV-1 PR causes a concentration-dependent decrease in mitochondrial membrane potential.
  • HIV-1 PR activates caspase 9, cleaves PARP, and induces DNA fragmentation.
  • HIV-1 PR cleaves mitochondrial proteins (Tom22, VDAC, ANT), releasing AIF and Hsp60.
  • BCA3 identified as a novel HIV-1 PR interaction partner, enhancing p53 activity on the BAX promoter.

Conclusions:

  • HIV-1 PR directly induces apoptosis by affecting mitochondrial membrane integrity.
  • HIV-1 PR interacts with BCA3, further contributing to apoptosis.
  • These findings elucidate a mechanism for HIV-1-induced cell death relevant to AIDS pathogenesis.