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for superinfection with delta agent (hepatitis D virus, or HDV) occurs in 25% of HIV-infected
persons with HBV, and liver injury is worsened, with greater viral replication of both HBV and
HDV. Persons with HIV infection should be vaccinated against HBV, but they also respond
poorly to hepatitis B immunizations, and more poorly with lower CD4 cells counts, with lower
antibody titers, and frequently lose this antibody protection.[871,878]
Treatment of HBV with HIV is considered when hepatitis B e antigen (HBeAg) is
present, HBV–DNA is >20,000 IU/ml (>2000 if HBeAg negative). Since therapy is suppressive
and not curative, treatment may continue indefinitely. Treatment is most likely to be successful
when the serum HBV–DNA level is low, HBeAg is positive, and serum ALT is elevated. Drugs
employed include interferon-alpha, lamivudine, adefovir, entecavir, telbivudine, emcitrabine, and
tenofovir. Use of the antiretroviral agent tenofovir has been shown to be particularly effective in
suppressing HBV replication in persons with HIV, with improvement indicated by tests of
hepatic function. Such therapy has the potential to slow or reverse chronic liver disease in these
patients. Resistance to nucleoside analogues may develop, and is inversely proportional to the
degree of initial HBV suppression.[879]

HEPATITIS C.-- In Western Europe and the U.S., hepatitis C virus (HCV) infection has
been found in 25-30% of HIV-positive persons overall, and by risk factor 72-95% of those who
are injection drug users, 1-12% of men having sex with men, and 9-27% of heterosexuals.[876]
Vertical transmission is a function of the incidence of congenital HIV infection. Recently
infected persons tend to be asymptomatic, and disease progression occurs over years. Persons
with HCV co-infected with HIV are less likely to clear HCV, and 80% go on to chronic disease.
HIV co-infection is associated with increased HCV RNA levels, increased hepatic inflammation
and fibrosis, and more rapid progression to cirrhosis and end-stage liver disease. The decreased
number of CD4 lymphocytes, and a relative increase in CD8 cells, promotes fibrogenesis
through activation of hepatic stellate cells. In addition, there is a greater prevalence of diabetes
mellitus in these persons.[871,872,877,878]
Liver biopsy is required to determine the extent of liver disease. Transaminase levels
may be in the normal range even when fibrosis is present. Genomic testing for detection of
single nucleotide polymorphisms predicting virologic response is useful. Response rates to
ribavirin therapy are lower than in immunocompetent persons. Treatment with pegylated
interferon plus ribavirin results in a treatment response from 29% to 62% and a sustained HCV
clearance of 17 to 53% in HIV–HCV co-infected patients.[877,879]
As survival increases with antiretroviral therapy for HIV, increasing numbers of cases of
hepatocellular carcinoma occur in patients who have viral hepatitis, mainly hepatitis C. The
course is more aggressive, with shorter survival, than in persons not infected with HIV.[880]

HEPATITIS, NON B or C.-- There is no significant effect of HIV infection upon the
clinical course of hepatitis A virus (HAV) infection. However, the duration of hepatitis A
viremia may be prolonged in persons infected with HIV, with a higher viral load of HAV. [881]
Hepatitis G virus (GBV-C) is not associated with a known disease. However, coinfection
with GBV-C has been shown to be associated with reduced mortality in persons with HIV. The
rate of HIV replication in vitro in peripheral blood mononuclear cells has been shown to be
inhibited by GBV-C. Approximately 40% of HIV infected persons can have coinfection with
GBV-C.[219]