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Published on: December 3, 2019
Downregulation of CD38 activation markers by atorvastatin in HIV patients with undetectable viral load
Stéphane De Wit1, Marc Delforge, Coca Valentina Necsoi
1Division of Infectious Diseases, Saint-Pierre University Hospital, Brussels, Belgium.
Insights
Atorvastatin significantly reduced immune activation, measured by CD38, in HIV patients with undetectable viral loads. This study suggests a potential benefit of statins in managing chronic inflammation during HIV disease.
Area of Science:
- Immunology
- Virology
- Pharmacology
Background:
- Chronic inflammation and immune activation persist in HIV patients even with suppressed viral loads.
- These factors contribute to the long-term complications of HIV disease.
- CD38 activation is a marker of immune activation relevant to HIV pathogenesis.
Purpose of the Study:
- To investigate the impact of atorvastatin on CD38 activation in HIV patients with undetectable viral loads.
- To assess whether atorvastatin influences other markers of inflammation and immune status.
Main Methods:
- A case-control study was conducted with 133 cases and 266 controls.
- Patients had undetectable viral loads.
- CD38 activation, high-sensitivity C-reactive protein (hsCRP), and CD4 counts were measured at week 48.
Main Results:
- CD38 activation levels were significantly lower in the atorvastatin group (cases) compared to the control group at week 48.
- No significant differences were observed in high-sensitivity C-reactive protein (hsCRP) or CD4+ T-cell counts between the groups.
- The findings indicate a specific reduction in immune activation.
Conclusions:
- Atorvastatin effectively reduces immune activation, as indicated by lower CD38 expression, in HIV patients with suppressed viremia.
- The drug did not significantly alter hsCRP or CD4 counts in this cohort.
- These results suggest atorvastatin may be a valuable therapeutic option for managing immune activation in HIV.
Abstract:
Immune activation and chronic inflammation are recognized as major component of HIV disease even in patients with undetectable viral load. We evaluated the effect of atorvastatin on CD38 activation in such patients, in a case-control study (133 cases - 266 controls). At week 48, CD38 activation was significantly lower in cases vs. controls, with no difference in high-sensitivity C-reactive protein (hsCRP) and CD4. These results suggest that atorvastatin reduces the level of immune activation in patients with undetectable viral load.
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