Hepatitis B in homosexual men: prevalence of infection and factors related to transmission.

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.

Delayed development of antibody to hepatitis B surface antigen after symptomatic infection with hepatitis B virus.

During a 2-year period, 38 patients with clinical hepatitis B virus infection were seen at the Public Health Service Alaska Native Hospital in Bethel. This hospital serves an area in southwest Alaska that is hyperendemic for hepatitis B virus. The patients came to the hospital at various times from 15 scattered villages, and 92% were Eskimo. None of the patients had a recent history of hypodermic injection or blood transfusions. Twenty-five patients, all originally positive for hepatitis B surface antigen (HBsAg), were followed for up to 5 years after onset of illness, and 15 were either slow to develop, or never developed, antibody to HBsAg (anti-HBs), although only one patient became a chronic carrier of HBsAg. Six patients had a prolonged "window phase" between the disappearance of HBsAg and the appearance of anti-HBs which lasted for more than 1 year. Three patients had only transient anti-HBs after HBsAg disappeared, and five never developed measurable anti-HBs at all. All patients had antibody to hepatitis B core when both HBsAg and anti-HBs were absent. In contrast to studies in other populations, only 42% had anti-HBs 1 year after onset of illness, 63% had it at 18 months, 70% had it at 2 years, and 80% had it at 5 years. Factors related to ethnicity might account for the differences in the development of anti-HBs after acute symptomatic hepatitis B virus infection seen in Eskimos when compared with whites.

Vasculitis in Eskimos living in an area hyperendemic for hepatitis B.

Six cases of hepatitis B-associated vasculitis occurred during a four-year period in Eskimos living in southwest Alaska, an area hyperendemic for hepatitis B. All showed positive results in tests for hepatitis B surface antigen (HBsAg), and all five patients tested for hepatitis B e antigen (HBeAg) showed positive values. Two patients died of the disease. Of three who recovered, two had positive values for HBsAg and HBeAg when tested two years later. In the villages of four patients, the prevalence of hepatitis B virus (HBV) infection ranged from 18.2% to 73.1%. Serological evidence of HBsAg was found in 22% and antibody to HBsAg (anti-HBs) in 30% of close relatives of the patients. Two patients had no previous serological evidence of infection with HBV, indicating that vasculitis followed recent infection. The results provide epidemiologic evidence of the clinical association between HBV infection and vasculitis.

Prevalence of HBsAg and anti-HBs in the Czech Socialist Republic (CSR).

A sample of 1 000 individuals of the urban and rural population of CSR covering all age groups was tested for the presence of HBsAg and anti-HBs. The rates for antigenaemia and antibody prevalence as determined by the RIA method were 1.5% and 12.5%, respectively. The antigen subtype adw was identified. HBsAg findings were significantly more frequent among the urban population, while the prevalence of antibody was comparable in both population types and both sexes. HBeAg was not detected in any case, anti HBe in one.

Hepatitis B e-antigen and its correlation with other serological markers in chimpanzees.

Three chimpanzees experimentally infected with hepatitis B virus, and another three chimpanzees that were hepatitis surface antigen carriers, were studied for the presence of viral antigens and humoral immune responses. Quantitative analyses of hepatitis B surface and e-antigens in sequential serum samples at early acute stages revealed cyclic oscillations of these two antigens following a synchronous pattern. Similar analyses of anti-e-antigen and anti-hepatitis B core antigen antibodies from the three experimentally infected primates indicated that peak titers of these two antibodies occurred as surface antigen decreased to undetectable levels. Of the three surface-antigen carriers, two were positive for e-antigen and one was positive for e-antigen antibody for the entire course of surveillance (8, 9, and 22 months, respectively).

Stability of a reference panel of lyophilized hepatitis B antigens and antibodies.

A lyophilized hepatitis B working/reference panel has been prepared for use in standardization tests. This panel includes HBsAg, anti-HBs, HBeAg/anti-HBe and subtype reagents. Quantitative analysis of the HBsAg reagents indicates that at a storage temperature of -20 degrees C, only 1 log at maximum of RIA counts per minute would be lost in 95 years. After storage at -20 degrees C for 1 year, there has been no loss of reactivity in any of the tests used to detect HBsAg, anti-HBs, HBeAg/anti-HBe or subtypes.

Evaluation of a finger prick blood collection method for the seroepidemiology of hepatitis B.

A finger prick-swab method of blood specimen collection was qualitatively and quantitatively compared with the conventional venipuncture method for HBsAg and anti-HBs determinations by radioimmunoassay (RIA). The new method consisted of pricking the finger, collecting 0.1-0.2 ml of blood with a cotton-wool swab, and eluting the swab in 1 ml of 1% bovine albumin in saline containing 0.1% sodium azide. Using chimpanzees seropositive for HBsAg or anti-HBs, comparisons were made of RIA results of: (a) whole blood, haemolysed blood, serum, and plasma; (b) paired finger prick samples and serum; (c) dilutions of finger prick samples and serum; and (d) different volumes of blood on swabs. Field studies were carried out at two institutions where hepatitis B was hyperendemic to compare results from paired finger prick and serum specimens assayed by the RIA and haemagglutination techniques. The laboratory studies showed that swab RIA values for anti-HBs were significantly lower than serum values and that for HBsAg, swab values were significantly higher than serum values. In HBsAg tests, the field studies showed 100% agreement between the two methods; in anti-HBs tests, the finger prick method showed 85% agreement with positive sera. Because of the logistics of collecting and processing blood serum, the finger prick-swab technique may be a valuable aid in large-scale seroepidemiological surveys for hepatitis B.

Hepatitis B infection in physicians. Results of a nationwide seroepidemiologic survey.

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.

Simultaneous infection with type A and B hepatitis viruses.

The occurrence of a common source hepatitis A epidemic among the residents of a New England state mental institution where hepatitis B is hyperendemic provided an opportunity to observe concurrent infections with both agents. Nine HBsAg-positive individuals developed hepatitis A infections documented by hepatitis A antibody seroconversion in eight. The incidence of hepatitis A infections in susceptible HBsAg-positive persons (67%) did not differ from that in HBsAg-negative individuals (63%). The icteric to anicteric infection ratio in the HBsAG-positives (1:1.7) was similar to that in the negatives (1:2.1), and the clinical course in the antigen positives did not differ significantly from that of the antigen negatives. In addition to confirming previous reports that the viruses of hepatitis A and B are immunologically distinct, these results document that infection with either is independent of the other, and that the morbidity from simultaneous infection is no greater than that caused by either alone.

Epidemiology of hepatitis B in two Alaska communities.

In 1973, epidemiologic and serologic data related to hepatitis B infection were collected from the residents of two remote Alaskan Eskimo villages located in an area of high hepatitis incidence. A total of 418 sera were tested by solid-phase radioimmunoassay for heaptitis B surface antigen (HBsAg) and antibody to that antigen (anti-HBs). The overall infection prevalence of 54.8% in the two villages included a 13.9% prevalence of HBsAg and a 40.9% prevalence of anti-HBs. Families containing an individual with HBsAg had significantly higher infection prevalence than those without an antigen carrier. Larger households had higher proportions of infected members than smaller households. The data suggest that efficient transmission of hepatitis B virus occurs within the household setting in these villages by other than classically established parenteral routes.

Hepatitis B surface antigen in saliva, impetiginous lesions, and the environment in two remote Alaskan villages.

A study was conducted in an area of hepatitis B hyperendemicity to determin whether contact with infective bodily secretions or contaminated environmental surfaces could be involved in the transmission of the hepatitis B virus. Hepatitis B surface antigen was detected in gingival swab, saliva, and impetiginous lesion exudate samples from children. Hepatitis B surface antigen also was found in swab samples of surfaces frequently touched or placed in the mouth. In the absence of classical exposure to infectious blood or blood products, these findings suggested that, in a crowded home environment, saliva and cutaneous exudates containing hepatitis B virus may play a role in the transmission of hepatitis B.

Experimental studies on the transmission of hepatitis B by mosquitoes.

Culex tarsalis and Aedes aegypti mosquitoes were fed on chimpanzees carrying hepatitis B surface antigen (HBS Ag) of known infectivity and pools were tested by radioimmunoassay daily for the presence of HBS Ag. HBS Ag continued to be detected at low levels in mosquito tissue after digestion of the blood meal. Inoculation of susceptible chimpanzees with macerated pools of A. aegypti mosquitoes at two intervals after digestion of the blood meal did not produce hepatitis or serologic evidence of hepatitis B virus infection. Mechanical transmission studies by interrupting feeding of A aegypti from HBS Ag-carrier chimpanzees and transferring them to susceptible chimpanzees did not produce hepatitis. These findings do not support the hypothesis that mosquitoes are involved in either biological or mechanical transmission of hepatitis B.

Antiviral effects of virazole in chronic hepatitis B surface antigen-seropositive chimpanzees.

Virazole (Ribavirin, ICN 1229), a broad-spectrum, antiviral chemotherapeutic agent was used to treat two adult chronically hepatitis B surface antigen (HB(s) Ag)-seropositive chimpanzees. No significant change in serum hepatitis B surface antigen was noted and no adverse reactions were observed. The role of viral replication in the chronic carrier state of hepatitis B is discussed.