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Published on: January 5, 2016
Effects of Well-Controlled HIV Infection on Complement Activation and Function.
Alexandria E-B Rossheim1, Tina D Cunningham, Pamela S Hair
1*Division of Infectious Diseases, Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA; †Center for Health Analytics and Discovery, Office of Research, Eastern Virginia Medical School, Norfolk, VA; ‡Department of Pediatrics, Eastern Virginia Medical School, Norfolk, VA; §Children's Specialty Group, Norfolk, VA; and ‖Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA.
Even with controlled HIV infection, complement activation persists, contributing to chronic inflammation. Hepatitis C coinfection further elevates this inflammatory response, indicating a heightened proinflammatory state.
Area of Science:
- Immunology
- Virology
- Inflammation Research
Background:
- Uncontrolled Human Immunodeficiency Virus (HIV) infection activates the complement system, increasing chronic inflammation.
- The persistence of complement activation and its contribution to chronic inflammation in well-controlled HIV infection remain unstudied.
Purpose of the Study:
- To investigate complement activation markers in adults with well-controlled HIV infection.
- To assess the impact of well-controlled HIV infection and Hepatitis C virus (HCV) coinfection on complement activation and inflammatory markers.
Main Methods:
- Observational, cross-sectional study of 305 adults with well-controlled HIV and 30 healthy controls.
- Sera analyzed for complement activation (C3a, C5a), complement function (CH50), and immunoglobulin levels (IgG1-IgG4).
- Statistical analyses controlled for age, sex, race, comorbidities (including HCV), smoking, and statin use.
Main Results:
- Well-controlled HIV infection showed a 54% increase in complement activation (C3a levels) versus healthy controls (P < 0.0001).
- Hepatitis C coinfection was associated with an additional 52% increase in complement activation (C3a) compared to HIV alone (P = 0.003).
Conclusions:
- Complement activation may contribute to a proinflammatory state in well-controlled HIV infection.
- Hepatitis C virus coinfection exacerbates the proinflammatory state through increased complement activation compared to HIV infection alone.
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