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Atorvastatin restricts HIV replication in CD4+ T cells by upregulation of p21

Shokrollah Elahi1, Robert H Weiss, Shahzma Merani

  • 1aDepartment of Dentistry bDepartment of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada cDivision of Nephrology and Cancer Center, University of California, Davis dSacramento VA Medical Center, Sacramento, California, USA.

AIDS (London, England)
|December 10, 2015
PubMed

Insights

Atorvastatin reduces immune activation and HIV replication in CD4 T cells by upregulating p21. This lipid-lowering drug may offer new treatment avenues for HIV patients, potentially reducing cardiovascular disease risk.

Area of Science:

  • Immunology
  • Virology
  • Pharmacology

Background:

  • HIV persistence causes inflammation and immune activation, accelerating aging and increasing comorbidity risk.
  • Reducing immune activation is crucial for managing HIV and preventing non-AIDS-defining conditions.

Purpose of the Study:

  • To investigate the anti-inflammatory and anti-viral effects of atorvastatin on HIV-infected CD4 T cells.
  • To elucidate the molecular mechanisms underlying atorvastatin's action against HIV-1 infection.

Main Methods:

  • CD4 T cells were infected with HIV-1 in vitro with or without atorvastatin.
  • Measurements included immune activation markers, viral replication, regulatory T cell expansion, and p21 expression.

Main Results:

  • Atorvastatin reduced T-cell immune activation markers and HIV-1 co-receptor CCR-5 expression.
  • It expanded regulatory T cells (Tregs) and upregulated T-cell immunoglobulin and ITIM domain (TIGIT).
  • Atorvastatin increased p21 expression in CD4 T cells, conferring resistance to HIV-1 infection and replication.

Conclusions:

  • Atorvastatin confers CD4 T cell resistance to HIV-1 infection through p21 upregulation.
  • Statins show promise as a therapeutic strategy for HIV-infected individuals, potentially mitigating accelerated aging and comorbidities.
Abstract

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