In the univariate analysis, there were no associations between anti-HEV-positive status and chronic liver disease, route of HIV infection, nadir or current CD4 cell count, HBV or HCV serological markers, age, sex, or ALT levels. Interestingly, liver cirrhosis was the only factor associated with anti-HEV detection: seroprevalence was 23% in patients with cirrhosis versus 6% in patients without cirrhosis (P = 0.002). In multivariate analysis including nadir CD4 cell count, route of HIV transmission, and HBV and HCV serological markers as covariables, liver cirrhosis was again the only variable independently associated with anti-HEV antibodies [OR 5.77; 95% confidence interval

(CI) 1.14-22.98; P = 0.013] (Table 2). It was determined whether HEV RNA was present in all anti-HEV-positive patients. Two individuals with HCV-associated liver cirrhosis and Cell Cycle inhibitor one without chronic liver disease were HEV RNA-positive (genotype 3); none of them presented clinical symptoms or biochemical

data suggestive of acute hepatitis. Two of these patients had preserved CD4 counts and the other had a CD4 count <200 cells/μL. In this cross-sectional cohort analysis, overall HEV seroprevalence among HIV-infected patients was 9%, a value consistent with the reported rate in a similar study in the south of France (8), but higher than that observed in Germany (5%) [7]. Studies assessing whether HIV-infected individuals are at higher risk of HEV infection are scarce Y-27632 order and the results are discordant [7, 13, 14]. Several epidemiological factors may explain these differences. In some endemic areas, an association has been observed between higher anti-HEV seroprevalence and lower CD4 cell count [15]. In nonendemic areas, the prevalence is uneven, which seems to indicate geographical differences, even between HIV-infected patients in two neighbouring regions [8]. Furthermore, higher prevalence rates were reported in an

Italian study among HIV-infected homosexual men [13]. In contrast to data for the general population [16], but consistent with the results of the French study, we found that HEV-positive status was not related to the specific route of HIV infection, there was no correlation with the patients’ clinical or immunological status, as evaluated Ribonucleotide reductase using the current and nadir CD4 cell counts, and there was no correlation with HCV or HBV chronic infection. The most striking finding of our study is the high HEV seroprevalence observed in patients with cirrhosis (23%) as compared with patients without cirrhosis (6%; OR 5.77). This observation is in agreement with reported data in non-HIV-infected patients, and suggests that individuals with cirrhosis are at a high risk of acquiring HEV infection [17]. An explanation for this finding could be the immune dysfunction observed in patients with cirrhosis, who present decreased innate immune system activity with a reduction in natural killer cell activity [18].