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Published on: August 15, 2012
SEN Virus infection in HIV/HCV coinfected patients
1Klinik für Gastroenterologie, Hepatologie und Infektiologie, Universitätsklinik Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany. sagir@med.uni-duesseldorf.de
Insights
Hepatitis C Virus (HCV) coinfection in HIV patients does not affect treatment outcomes. SEN Virus (SENV) replication is lower in HIV/HCV coinfected individuals, but SENV presence does not alter HCV therapy effectiveness.
Area of Science:
- Virology
- Infectious Diseases
- Immunology
Background:
- Chronic Hepatitis C Virus (HCV) infection is a significant coinfection in HIV-positive individuals.
- The impact of SEN Virus (SENV) on HCV treatment outcomes in coinfected patients is not well understood.
Purpose of the Study:
- To investigate the prevalence of SENV DNA in different patient groups.
- To determine the influence of SENV on HCV treatment response in HIV/HCV coinfected patients receiving combination therapy.
Main Methods:
- Polymerase chain reaction (PCR) was used to detect SENV DNA in 67 HIV/HCV coinfected patients, 77 HIV monoinfected patients, 95 HCV monoinfected patients, and 122 healthy donors.
- Quantitative analysis of SENV H DNA levels was performed.
Main Results:
- SENV DNA was detected in 12% of HIV/HCV coinfected patients, 11.7% of HIV monoinfected patients, 22% of HCV monoinfected patients, and 9.8% of healthy donors.
- Mean SENV H DNA levels were significantly lower in HIV/HCV coinfected patients compared to other groups.
- Sustained virological response rates to HCV therapy did not differ between SENV-positive and SENV-negative HIV/HCV coinfected patients (62.5% vs. 47.5%).
Conclusions:
- Hepatitis C Virus (HCV) coinfection may suppress SEN Virus (SENV) replication in HIV-positive individuals, leading to lower SENV H DNA levels.
- SEN Virus (SENV) infection does not appear to influence the outcome of combination therapy for Hepatitis C Virus (HCV) in coinfected patients.
Background:
Chronic Hepatitis C Virus (HCV) infection is currently one of the most relevant coinfections in HIV positive patients. The influence of SEN Virus (SENV) on the outcome of HCV therapy in HIV/HCV coinfected patients who underwent combination therapy with pegylated interferon (PEG-IFN) and ribavirin is unclear.
Methods:
SENV DNA was determined by polymerase chain reaction in 67 HIV/HCV coinfected patients, 77 HIV monoinfected patients, 95 treatment naive HCV monoinfetcted patients, and 122 healthy blood donors. Quantitative analysis was done for SENV H DNA.
Results:
SENV DNA was detected in 8 of 67 (12%) HIV/HCV coinfected patients, in 9 of 77 (11.7%) HIV monoinfected patients, in 21 of 95 (22%) HCV monoinfected patients, and 12 of 122 (9.8%) healthy blood donors. HIV monoinfected patients showed the highest mean SENV H DNA level. The mean SENV H DNA was significantly lower in HIV/HCV coinfected patients compared to all other groups. The sustained virological response rates to combination therapy of HCV in HIV/HCV coinfected patients did not differ between patients with detectable SENV 5/8 (62.5%) and without SENV 28/59 (47.5%; p = 0.47). We found no significant difference in SENV H DNA pretreatment levels between nonresponders and responders to combination therapy (112 +/- 144 copies vs. 8 +/- 7 copies/ml; p = 0.27).
Conclusion:
Coinfection with HCV may reduce SENV H replication in HIV positive patients and results in significantly lower SENV H DNA levels in HIV/HCV coinfected patients. SENV infection has no influence on the outcome of HCV combination therapy in HIV/HCV coinfected patients.
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