Rationale:

• Frequent hepatitis A outbreaks have occurred among men who have sex with men.
• Hepatitis A outbreaks have been reported among illicit drug users.
• HAV transmission from solvent-detergent-treated clotting factor concentrates has been documented.
• It is generally accepted that persons who work with HAV in laboratory settings receive hepatitis A vaccine.
• HAV transmission to humans from nonhuman primates susceptible to HAV has been documented.

Evidence:

• Two prospective studies of 129 and 399 homosexual men, respectively, conducted before the availability of hepatitis A vaccine suggest that men who have sex with men are at substantial risk for HAV infection (38; 39).
• A seroprevalence study of 411 homosexual and bisexual men in San Francisco determined that hepatitis A was common in this population (40).
• Outbreaks of hepatitis A among men who have sex with men have been documented in Sweden, Canada, the U.S., and Australia (41; 42; 43; 44; 45).
• A case-control study conducted during an outbreak of hepatitis A among men who have sex with men suggests that high-risk sexual practices or other modifiable behaviors are not always associated with infection (46).
• Case investigations, case-control studies, outbreak investigations, and analysis of national viral hepatitis surveillance data have been used to determine that illicit drug users are at increased risk for hepatitis A (47; 48; 49; 50; 51; 52; 53).
• Serum samples from 300 injection drug users, 300 homosexual men, and 300 blood donors in one U.S. city determined that injection drug users are at increased risk for HAV infection (54).
• A case-control study among 28 methamphetamine users with confirmed hepatitis A identified during an outbreak in 1997 and 18 susceptible control subjects suggested multiple modes of HAV transmission among methamphetamine users (47).
• Transmission of hepatitis A to recipients of solvent-detergent-treated factor VIII concentrates has occurred in Europe, Africa, and the U.S. (55; 56; 57).
• A seroprevalence study among 252 hemophiliac patients in the southwestern U.S. suggests that there is a strong association between hepatitis A seroprevalence and lifetime cumulative doses of clotting factor concentrates (58).
• Outbreaks of hepatitis A have been reported among persons working with nonhuman primates (59; 60).

Comments:

• Hepatitis A vaccine is well tolerated in HIV-infected persons and has no effect on the course of HIV infection or plasma HIV RNA load (61).
• HIV-positive individuals respond less well to the two-dose series of hepatitis A vaccine compared with immunocompetent individuals. Available studies suggest that 50% of HIV-infected individuals have an immune response that is considered protective. However, factors associated with protection vary among the following three studies.
• A study of 214 HIV-infected individuals found that the response to hepatitis A vaccine was directly related to the CD4 count at vaccination. Higher CD4 counts were associated with higher vaccine response rates, independent of the nadir CD4 count and the viral load level (26).
• A retrospective study of 138 HIV-infected persons who completed the two-dose hepatitis A vaccine series and had post-vaccine titers evaluated determined that 48% of study participants responded to vaccine. Multivariate analyses determined that female sex and higher CD4 counts were independent predictors of response (27).
• A serologic study of 238 HIV-infected individuals determined that 50% developed immunity after the two-dose series. Factors associated with a protective response were HIV plasma RNA level <1,000 copies/mL and male gender (28).
• A recent survey from the 1999 to 2002 NHANES database showed that 8% of adult Americans were at high risk for hepatitis A but only 13% reported receiving hepatitis A vaccine, suggesting that efforts to identify and vaccinate high-risk groups need to be improved (62).
• A review of the available literature on vaccine immunogenicity among injection drug users suggests that that there is a tendency towards decreased antibody responses after immunization; however, there is no conclusive evidence suggesting a decrease in clinical protection from infection (63).