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Updated: Jul 18, 2026

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis
Published on: April 17, 2017
Mitigation of antiretroviral-induced hyperlipidemia by hepatitis C virus co-infection
Curtis L Cooper1, Edward Mills, Jonathan B Angel
1Division of Infectious Diseases, The Ottawa Hospital, University of Ottawa, Ottawa, Ontario, Canada. ccooper@ottawahospital.on.ca
Insights
Hepatitis C virus (HCV) co-infection may protect against high cholesterol caused by HIV treatment. Further research is needed to understand this effect and its impact on cardiovascular disease risk.
Area of Science:
- Infectious Diseases
- Hepatology
- Cardiology
Background:
- Hyperlipidemia is a known complication of HIV antiretroviral therapy.
- The interplay between HIV, hepatitis C virus (HCV), antiretroviral drugs, and lipid metabolism is not fully understood.
Purpose of the Study:
- To evaluate the impact of HIV/HCV co-infection on lipid profiles in patients undergoing antiretroviral therapy.
- To compare lipid complications between HIV-mono-infected and HIV/HCV-co-infected individuals.
Main Methods:
- Retrospective analysis of lipid data from patients at the Ottawa Hospital Immunodeficiency Clinic (1996-2005).
- Inclusion of 357 HIV-mono-infected and 115 HIV/HCV-co-infected patients.
- Evaluation of lipid changes and metabolic complications during highly active antiretroviral therapy (HAART).
Main Results:
- HIV/HCV co-infected patients showed significantly smaller increases in total cholesterol compared to HIV-mono-infected patients.
- Metabolic complications led to HAART interruption in 8% of HIV-mono-infected patients, versus less than 1% in co-infected patients.
- Total cholesterol increased in co-infected patients receiving interferon-based HCV treatment with sustained virological response (SVR).
Conclusions:
- HCV co-infection appears to offer protection against HAART-related lipid abnormalities.
- The underlying mechanisms for this protective effect require further investigation.
- The long-term implications for cardiovascular disease risk in co-infected patients warrant attention.
Background:
Hyperlipidemia is a recognized complication of HIV antiretroviral therapy. The interactions between HIV, hepatitis C virus (HCV), antiretroviral agents and lipids are not well understood.
Methods:
We evaluated the lipid data of patients receiving antiretroviral therapy at the Ottawa Hospital Immunodeficiency Clinic between January 1996 and June 2005 using a clinic database.
Results:
A total of 357 HIV-mono-infected and 115 HIV/HCV-co-infected patients were evaluated. The mean changes in total cholesterol (mmol/l) from baseline to months 6 and 12 were 1.00 and 1.24 in HIV mono-infection, and 0.19 (P < 0.001) and 0.01 (P < 0.001) in HIV/HCV, respectively. Metabolic complications including hypercholesterolemia resulted in the interruption of HAART in HIV mono-infection (8%), but not in those with HIV/HCV (< 1%; P < 0.001). Eight per cent of HIV-mono-infected and no co-infected patients initiated lipid-lowering therapy while on their initial course of HAART (P < 0.001). Total cholesterol increased by 0.85 mmol/l in HIV/HCV-co-infected recipients of interferon-based HCV treatment achieving a sustained virological response (SVR), but did not change in those who did not achieve a SVR.
Conclusion:
HCV co-infection appears to confer a degree of protection from HAART-related lipid complications. The mechanism of this finding deserves evaluation. The implications of this observation for long-term cardiovascular disease risk remains a pressing issue.
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