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Blood samples from 154 asymptomatic carriers of HBsAg were studied for the presence of HbeAg and anti-HBe using techniques of rheophoresis and a micro solid phase radioimmunoassay (micro-SPRIA). The level of HBsAg in each sample was determined by titration using reverse passive hemagglutination (RPHA) test. The significance of relationship between the titer of HBsAg, HBeAg, anti-HBe, and anti-HBc were statistically analyzed. Micro-SPRIA detected almost twice as many reactives for HBeAg and anti-HBe as were found by rheophoresis; the difference in sensitivity was significant (P less than 0.001). The mean HBsAg titer of 41 samples reactive for HBeAg was 11,181, while it was 3,032 for 92 samples reactive for anti-HBe. The remaining 23 samples with no detectable HBeAg or anti-HBe had a mean HBsAg titer of 1,018. The differences in the distribution of HBsAg among the three categories is statistically significant (P less than 0.005). HBeAg was most likely to be found in samples with higher concentrations of HBsAg.

To estimate the risk of hepatitis B virus (HBV) infection among hospital workers, we measured the prevalence of HBV infection in employees in five hospitals in different parts of the country and examined the effect of occupational and non-occupational factors on HBV prevalence. Among 5,697 persons studied, serologic markers of HBV infection were found in 807 (14%). Prevalence of infection was strongly related to race (Asian greater than Black greater than White), sex (male greater than female) and increasing age. Risk related to health occupation, studied by examining the change in HBV prevalence with duration in occupational group, was most strongly correlated with frequency of contact with blood during work. Workers having frequent blood contact had the highest estimated infection rate (1.05 per 100 person-years) and those with moderate contact an intermediate infection rate, compared to a negligible infection rate in workers with no blood contact. Frequency of needle accidents had an independent, positive effect on HBV infection rates, while degree of patient contact had no effect. Infection risk was uniform among all hospitals for groups with frequent blood contact. Among different occupation groups, risk of HBV infection also correlated closely with degree of blood-needle contact during daily work. This study provides a general approach to assessing risk of HBV infection in hospital personnel, and indicates that risk may be most easily estimated by quantitating degree of blood-needle contact during daily work.

Of 3,816 homosexual men examined in five sexually transmitted disease clinics in the United States, 6.1% had hepatitis B surface antigen, 52.4% had antibody to hepatitis B surface antigen, and 3.0% of the men who had no other indicator of infection with hepatitis B virus (HBV) had antibody to hepatitis B core antigen. The rate of seropositivity for HBV indicated by the presence of one or more of these serologic markers was 61.5%; seropositivity was significantly related to the duration of regular homosexual activity and to the number of nonsteady male sexual contacts in the four months before the patients were interviewed. Anal-genital intercourse, oral-anal intercourse, and rectal douching were significantly related to evidence of HBV infection, but oral-oral contact and oral-genital contact were not. Trauma to the rectal mucosa is a feature common to the practices that were significantly related to seropositivity for HBV.

A randomized, double-blind, vaccine/placebo trial of the Merck 20-micrograms hepatitis B virus (HBV) vaccine was done among 1402 homosexual men attending venereal disease clinics in five American cities. Vaccination was followed by only minimal side effects. Two doses of vaccine induced antibody in 80% of vaccine recipients. A booster dose 6 months after the first dose induced antibody in 85% of recipients and markedly increased the proportion of recipients who produced high antibody titers. The incidence of HBV events was markedly less in the vaccine recipients compared to that in the placebo recipients (p = 0.0004). Between month 3 and 15 after the first dose, 56 more significant HBV events (hepatitis, or hepatitis B surface antigen positive, or both) occurred in the placebo group while only 11 occurred in the vaccine group. Ten of the 11 HBV events in the vaccine recipients occurred in hypo- or nonresponders to the vaccine. This vaccine appears to be safe, immunogenic, and efficacious in preventing infection with hepatitis B virus.

To define the epidemiologic features of occupationally acquired hepatitis B infection among physicians, we conducted a seroepidemiologic survey of physicians attending three American Medical Association conventions in 1975 and 1976. Of 1,192 participating physicians, 220 (18.5%) had serologic evidence of prior hepatitis B virus infection (positive hepatitis B surface antibody). The infection rate was higher among those practicing in urban communities; it increased with the number of years in practice; and among specialties, it was highest in pathologists (27%) and surgeons (28%). The serologic data demonstrated a changing pattern of viral hepatitis related to entry into the medical profession, with hepatitis B accounting for a majority of clinical hepatitis experienced after beginning medical practice.

Experimental hepatitis A virus (HAV) infection was studied in marmosets after enteral (intragastric) inoculation with special reference to the primary sites of HAV replication and immunopathology of the disease. The experiment was carried out using 28 Saguinus mystax negative for antibody to HAV (anti-HAV) and with statistically uniform baseline values of serum isocitrate dehydrogenase (SICD) activity. Each animal was infected with 1 ml of a 15% w/v stool suspension that was derived from marmosets infected with the third or fourth passage of the MS-1 strain of HAV. The incubation period measured by the first significant SICD elevation was 32 days in 11 of 13 marmosets. The animals were sacrificed 2, 4, 7, 11, 14, 18, 23, 28, and 32 days after inoculation and 1, 4, 8, 14, 21, 28, and 35 days after SICD elevation. HAV antigen, immunoglobulins, complement, and fibrin were identified in the liver, eight segments of the gastrointestinal tract, lymphoid system, and kidneys. HAV antigen was found only in the cytoplasm of hepatocytes and in gallbladder bile. These findings indicated that the liver was the sole and primary site of virus replication. Combined immunomorphologic and histopathologic observations also revealed that HAV antigen localization was associated with the sites of hepatocellular damage. There was no immunomorphologic evidence for humoral immune clearance of HAV antigen in the liver, lymphoid system, or kidneys.