HCV serostatus did not affect the risk of HIV-1 disease progression, but the risk of liver disease-related deaths was markedly increased in HCV-seropositive patients. The overall virologic and immunologic responses to HAART were not affected by HCV serostatus.

This is the first report that the 983T>C genotype (part of the CYP2B6*18 haplotype) impacts on nevirapine plasma concentrations and the first study to assess the impact of 983C homozygosity on efavirenz concentrations. These data have implications for administration of non-nucleoside reverse transcriptase inhibitors to Black patients.

HCV serostatus did not influence the CD4 recovery in patients with HIV with maximum virologic suppression after starting combination antiretroviral therapy. Furthermore, no difference in CD4 gain was found when comparing distinct HCV genotypes in HCV-RNA+ patients or when comparing HCV viremic vs. aviremic HCV-seropositive patients.

Various clinical studies indicated a lower prevalence of HP infection in HIV patients. The present study was initiated to determine whether the decreased frequency of HP infections in HIV patients might be associated with the stage of the underlying HIV disease or concomitant drug regimens the patients had received. 60 randomly selected HIV outpatients were stratified according to the stage of their HIV infection (CDC classification), their CD4 cell count and to the drug regimens they were given. Within these subgroups of patients, HP infection prevalence was separately investigated by serological and C13 breath testing. Data were compared to a reference population of 30 healthy volunteers. No difference in HP infection prevalence was found between the HIV infected patients in general and the reference cohort. A significantly lower proportion of HP infected individuals was observed among those HIV patients who had AIDS-defining diseases. Furthermore, a substantial but insignificant decrease of HP infection prevalence was noted in HIV patients with an extensive decline of CD4 cell count (< 100/microl). HIV patients who had received antimicrobial or H2-antagonizing drugs within 12 months prior to the study commencement also were found to have a remarkably decreased frequency of HP infections independently of their CD4 cell count. No association between HP infection prevalence and patients age, sex, risk group and the type of their antiretroviral treatment was found.We concluded from these results that the decreased HP infection prevalence in HIV patients may, apart from frequent antibiotic treatment, be correlated to the stage of HIV-mediated immune suppression.

Morbidity and mortality from co-morbid hepatitis B (HBV) and hepatitis C (HCV) infection in HIV co-infected patients are increasing; hence, the management of HIV and HBV or HCV co-infected individuals is now one of the most challenging clinical management issues. Less than 10% of all HIV-infected patients show markers of chronic HBV infection. Hepatitis B in HIV co-infected patients is characterized by high levels of HBV replication and a high risk for cirrhosis. Treatment of HBV with lamivudine (3TC) remains the best treatment option at this time. Initial results of studies of adefovir or tenofovir, however, demonstrate good antiretroviral efficacy, even in patients with 3TC-resistant HBV. In Europe, it is estimated that approximately 30% of HIV-infected individuals are co-infected with HCV. HIV accelerates HCV liver disease especially when HIV-associated immune deficiency progresses. Within 10-15 years of initial HCV infection, 15-25% of patients who are co-infected with HIV develop cirrhosis compared with 2-6% of patients without HIV infection. With the introduction of pegylated interferon in combination with ribavirin, promising treatment options have become available for HIV/HCV co-infected patients leading to early virological response rates of approximately 50%. The high number of HIV/HCV and HIV/HBV co-infections, as well as the much more unfavorable course of HBV and HCV in these patients, underlines the need to establish treatment strategies for HBV and HCV in HIV co-infected individuals.