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J Clin Virol. 2005 Jul;33(3):183-7. Epub 2004 Dec 10.

SEN virus seroprevalence in HIV positive patients: association with immunosuppression and HIV-replication.

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Klinik für Gastroenterologie, Hepatologie und Infektiologie, der Universitätsklinik Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany.



Patients infected with HIV are often co-infected with other viruses. SEN virus (SENV) was isolated from a HIV positive patient with intravenous drug use and post-transfusion hepatitis. SENV strains D and H seem to be relevant for the development of post-transfusion hepatitis. We compared the prevalence of SENV strains D and H and the viral load of SENV H in HIV-infected patients with healthy blood donors. The results were correlated with clinical markers such as HIV stage, CD4 cell count, HIV-RNA positivity, HAART or the transmission mode in HIV infected individuals.


Blood samples of 143 HIV-positive patients were analysed and compared with a control group of 122 healthy blood donors. SENV D and -H was detected by PCR.


SENV was detectable in 15.4% (22/143) of HIV-positive patients compared to 10.4% (12/122) in the control group (P=0.18). SENV H DNA-levels were significantly higher in HIV-positive patients (P=0.01). The prevalence in patients with CD4 cells less than 200/mm(3) was 31% (13/42), compared to 12.3% (8/65) in cases with CD4 cells between 200 and 500/mm(3), and 2.8% in cases with CD4 cells above 500/mm(3) (P=0.002 for CD4 cells <200 versus CD4 cells >200, P=0.031 for CD4 cells <500 versus CD4 cells >500). Prevalence of these strains was not significantly influenced by CDC stages. SENV was detected significantly more frequent in patients with detectable HIV-RNA (P=0.005). Patients undergoing HAART were significantly less frequent positive for SENV D or -H (P=0.029) than patients without HAART. In a multivariate analysis using a logistic regression model HIV-RNA positivity and CD4 cell count were identified as independent factors for SENV prevalence.


SENV (D and H) prevalence is not significantly higher in HIV-positive patients in comparison to healthy blood donors. SENV prevalence depends on CD4 cell count and HIV-RNA.

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