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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Hepatitis C virus infection is associated with endothelial dysfunction in HIV/hepatitis C virus coinfected patients
Isabel Fernández de Castro1, Dariela Micheloud, Juan Berenguer
1Laboratory of Molecular Epidemiology of Infectious Diseases, National Centre of Microbiology, Instituto de Salud Carlos III, Majadahonda,Madrid, Spain.
Insights
HIV and HCV coinfection elevates adhesion molecules, particularly with HCV genotype 1 and advanced fibrosis. Treatment with interferon-alpha and ribavirin may reduce these markers, indicating potential cardiovascular benefits.
Area of Science:
- Immunology
- Virology
- Cardiovascular Medicine
Background:
- HIV/HCV coinfection is a significant global health issue.
- Adhesion molecules like sICAM-1 and sVCAM-1 are implicated in cardiovascular disease.
- Understanding their role in coinfection is crucial for risk assessment.
Purpose of the Study:
- To quantify serum levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in HIV/HCV coinfected patients.
- To examine the association of these markers with clinical and epidemiological characteristics.
- To assess their relationship with therapeutic response to interferon-alpha and ribavirin therapy.
Main Methods:
- Retrospective cross-sectional study design.
- Inclusion of 183 treatment-naive HIV/HCV coinfected patients on HAART and 24 healthy controls.
- Analysis of 30 patients undergoing 48-week interferon-alpha + ribavirin therapy.
Main Results:
- Elevated sICAM-1 and sVCAM-1 levels were observed in HIV/HCV coinfected patients compared to controls.
- Higher levels correlated significantly with HCV genotype 1, advanced fibrosis (F≥3), and elevated liver enzymes.
- Non-responders to therapy exhibited higher adhesion molecule levels, while sustained responders showed significantly lower levels.
Conclusions:
- HIV/HCV coinfection alters serum levels of sICAM-1 and sVCAM-1, particularly in patients with HCV genotype 1 and advanced liver disease.
- Therapeutic response to interferon-alpha + ribavirin may lead to a reduction in these cardiovascular risk markers.
- These findings highlight the potential of treatment to mitigate cardiovascular risks in coinfected individuals.
Objective:
To quantify serum levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in HIV/HCV coinfected patients to examine their association with several clinical and epidemiological characteristics and the therapeutic responsiveness to interferon (IFN)-alpha and ribavirin therapy (IFN-alpha + RBV).
Design:
Retrospective study.
Methods:
We carried out a cross-sectional study with 183 IFN-alpha-naive patients on HAART, and 24 healthy controls. We also analyzed 30 out of 183 patients on IFN-alpha + RBV for the duration of 48 weeks.
Results:
HIV/HCV coinfected patients had higher levels of sICAM-1 and sVCAM-1 than the healthy control group (P < 0.05). Patients with HCV-genotype 1, advanced fibrosis (F>or=3) or moderate to severe activity grade (A>or=2) had the highest values of sICAM-1 and sVCAM-1. When we carried out a multivariate analysis, we found a significant positive relationship between both HCV-genotype 1 and advanced fibrosis (F>or=3) with sICAM-1 (R = 0.549; P < 0.001); and a significant positive relationship between HCV-genotype 1 and advanced fibrosis (F>or=3) with sVCAM-1 (R = 0.624; P < 0.001). We also found a positive relationship of sICAM-1 or sVCAM-1 levels with transaminases and alkaline phosphatase circulation levels (P < 0.05). Nonresponder patients had higher sICAM-1 and sVCAM-1 serum levels, and patients with sustained virologic response had significantly lower levels of sICAM-1 (P = 0.001) and sVCAM-1 (P = 0.019).
Conclusion:
HIV and HCV coinfection induces alterations in sICAM-1 and sVCAM-1 serum levels, which were higher in patients with HCV-genotype 1 and advanced stage of HCV infection. However, response to IFN-alpha + RBV may reduce these cardiovascular risk markers.
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