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This study describes the influence of hepatitis C virus (HCV) and hepatitis G virus (HGV) co-infection on CD4 cell count decline and plasma human immunodeficiency virus (HIV) viral load in HIV-infected patients during a 1-year period following interruption of highly active anti-retroviral therapy (HAART) guided by CD4 count. CD4 cell count decline and plasma HIV viral load did not differ between HIV mono-infected patients and those patients co-infected with HCV and HGV. HCV genotype 1 had no apparent influence on the cellular and viral dynamics in HIV-infected patients compared with other HCV genotypes, although the unbalanced groups make larger studies desirable.

The aims of this study were to analyze the mortality directly attributable to chronic viral hepatitis in HIV-1 infected patients and to investigate the influence of hepatitis virus infections on the survival of this population. A cohort of 328 HIV-1 infected, antiretroviral-treated patients, followed up from 1989 to 1996, was investigated in the study. The median follow-up period of the cohort was 120 weeks. The median baseline CD4 + cell count of the cohort was 303 cells/mm3. Hepatitis C virus, hepatitis B virus and hepatitis D virus infections were present in 214 (65%), 16 (4.9%) and 9 (2.7%) patients, respectively. Sixty-seven (20.4%) subjects died but there was no information on the vital status of 36 patients (11%). The causes of mortality were AIDS in 49 (73%), liver failure in 3 (4.5%) and other causes in 15 (22.4%). The cohort was divided into two groups for survival analysis, the groups consisting of persons infected by a hepatitis virus and persons without hepatitis virus infection. There was no difference in survival between the two groups (p = 0.31, log-rank). It is concluded that mortality among HIV-1/hepatitis virus coinfected patients with moderate to severe immunosuppression is mostly due to AIDS, and that the survival of these subjects is not influenced by the presence of hepatitis virus infections, particularly hepatitis C virus.

Background/aims: A unusually high rate of HCV-infected individuals in whom the HCV genotype cannot be ascertained by means of single PCR and LIPA procedures has recently been reported in our area. The aim of the present study was to investigate the epidemiological, clinical and molecular characteristics of these patients., Methods: Cross-sectional study. Eighty anti-HCV-positive patients with chronic liver disease, 45 (56.25%) of them intravenous drug users, were included. HCV genotyping was carried out in all patients using commercial single PCR and LIPA procedures. Samples where no HCV RNA amplification and/or indeterminate HCV genotype were found were also tested by means of a nested PCR. HCV viral load was measured in all patients., Results: HCV genotyping was not achieved in 23 (28.75%) individuals. No amplification of HCV RNA was found in 19 of them, and in four other cases the LIPA procedure did not allow identification of a distinct HCV genotype. After the use of nested PCR+LIPA, it was found that the HCV genotype 4 was found in 11 of those 23 individuals (47.82%). Ten of these 11 HCV genotype 4-harboring individuals were intravenous drug users. The HCV viral load was lower in HCV genotype 4-harboring individuals than in those whom the genotypes 1, 2 or 3 were found (p<0.001)., Conclusions: A high rate of HCV genotype 4-harboring cases has been found among HCV-infected individuals in Southern Spain. Had only single PCR been used, these individuals could have been wrongly regarded as non-viremic.

Background/aims: To investigate the possible role of HIV infection in the natural history of chronic parenterally-acquired hepatitis C., Methods: A multicenter cross-sectional study was performed in 547 patients with chronic parenterally-acquired hepatitis C with or without HIV infection (116 HIV-positive and 431 HIV-negative). Approximate duration of HCV infection was estimated in all patients included, and histologic diagnoses made at different time intervals following HCV infection were analyzed in both groups. Factors related to serum HCV-RNA levels were also investigated., Results: Histologic findings were similar in liver biopsies from both HIV-infected and noninfected patients. However, in the first 10 years, 13 out of 87 (14.9%) HIV-positive subjects developed cirrhosis, in comparison with 7 out of 272 (2.6%) in the HIV-negative group (p < 0.01). Similar results were found in the first 5 and 15 years, respectively, and most of the HIV-negative patients with cirrhosis (42 out of 56) developed cirrhosis in a time interval longer than 15 years. Consequently, mean interval from estimated time of HCV infection to cirrhosis was significantly longer in HIV-negative than HIV-positive patients (23.2 vs. 6.9 years; p < 0.001). Chronic active hepatitis (with and without cirrhosis) and long duration of HCV infection were significantly associated with higher HCV load (p < 0.05). Finally, HIV-positive patients with CD4+ cell counts > 500 cells/ml showed a lower HCV load than those with < 500 cells/ml (p < 0.05)., Conclusions: HIV infection modifies the natural history of chronic parenterally-acquired hepatitis C with an unusually rapid progression to cirrhosis. HIV-related immunodeficiency may be a determinant of higher hepatitis C viremia levels and more severe liver damage.

The aim of the present study was to investigate the possible role of human immunodeficiency virus (HIV) infection in the natural course of chronic hepatitis C. Seventy-six adult patients with chronic parenterally acquired hepatitis C virus (HCV) infection examined from 1989 to 1993 were enrolled; of these 32 (42.1%) were HIV positive and 44 (57.9%) were HIV negative. Serum HCV RNA quantitation was carried out by polymerase chain reaction in a well-characterized group (n = 20; 11 HIV positive and 9 HIV negative). Distribution of histological findings in liver biopsies from both HIV-infected and noninfected patients was similar. However, within 15 years after initial HCV infection, 8 of 32 (25%) HIV-positive patients developed cirrhosis, in comparison with only 2 of 31 (6.5%) patients in the HIV-negative group (p < 0.05); similar incidences of cirrhosis were found in both patient groups within 5 and 10 years after HCV infection. Most of the HIV-negative cirrhotic patients (9 of 11) developed cirrhosis in a time interval longer than 15 years. Finally, HCV load was almost ten times higher (1 10-fold dilution) in the HIV-positive group, but this difference did not reach statistical significance in this small study population. These results suggest that HIV infection can alter the natural course of chronic parenterally acquired hepatitis C, causing an unusually rapid progression to cirrhosis.

To determine the predictive value of IgM anti-hepatitis C virus (HCV) testing in patients with chronic hepatitis C infections undergoing interferon-alpha (IFN-alpha) therapy, IgM anti-HCV reactivity was analysed by two different methods (non-commercial and commercial) in 19 patients and monitored at times 0 (pretreatment), 3, 6, 12, and 24 months during follow-up. Eight patients were non-responders, five remained in sustained response 1 year after stopping treatment, and six had a relapse. No correlation between alanine transaminase (ALT) levels and IgM anti-HCV reactivity was found by either method in baseline samples. In addition, neither the presence nor absence of IgM anti-HCV in baseline samples, nor the loss of specific IgM reactivity during treatment, had any predictive value. Finally, no other parameters analysed (age, sex, risk group and histological diagnosis), were significantly associated with IgM anti-HCV reactivity in our study. In summary, these results suggest that baseline detection and monitoring of IgM anti-HCV reactivity are not useful in predicting the sustained response to IFN-alpha therapy in chronic hepatitis C infection.

To define the role of sexual transmission in the spread of hepatitis C virus (HCV) infection, a seroprevalence study of antibodies against HCV was performed in populations at high risk for sexually transmitted diseases. Subjects included 310 female prostitutes, 88 clients of prostitutes, 168 homosexual men and 147 stable heterosexual partners of index cases reactive for anti-HCV (98 of whom were partners of drug addicts coinfected with HCV and human immunodeficiency virus [HIV]). All subjects denied prior transfusion or intravenous drug use. Controls were 400 voluntary blood donors selected randomly from first-time donors. The prevalence of anti-HCV by enzyme immunoassay, confirmed by a second-generation recombinant immunoblot assay, was 6.4% in prostitutes, 6.8% in clients of prostitutes, 4.2% in homosexual men, 7.4% in heterosexual partners of index cases and 1.2% in random donors. However, the anti-HCV prevalence in stable heterosexual partners of HCV-positive/HIV-positive index cases was 2.2 times higher than in stable heterosexual partners of index cases reactive for anti-HCV only (9.2% vs. 4.1%), and sexual partners of index cases coinfected with HCV and HIV were almost three times more likely to be infected with HIV than with HCV (25.5% vs. 9.2%). These data suggest that HCV infection may be sexually transmitted but with low efficiency and that this efficiency could be increased in the presence of coexistent HIV infection in the index case.