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In 1985, the authors studied the epidemiology of hepatitis B virus (HBV) in a healthy Middle Eastern population. Residents of three remote villages and urban areas of Jordan were assessed for seroprevalence of hepatitis B surface antigen (HBsAg) and HBV infection. Infection was defined as the presence of antibody to hepatitis B core antigen (total) and/or antibody to hepatitis B surface antigen, with or without HBsAg. The overall HBsAg prevalence was 9.9% and was not age-related, although significant differences were noted between the villages (range, 5.7%-12.8%). The prevalence of HBV infection was 36% and increased with age. In addition, there were differences between the villages in patterns of age-specific infection. A newly constructed socioeconomic index showed greater HBsAg prevalence in lower (14.4%) than in upper (2.4%) socioeconomic groups. A history of contact with a jaundiced person and socioeconomic status were independent risk factors for HBsAg-positive status, while contact with a jaundiced person, rural background, and age were independently related to HBV infection. There was evidence of familial clustering of HBV in two of the villages, with HBV carriers and infected children particularly aggregating around HBsAg-positive siblings. There was also a trend toward an association of HBsAg-positive children with HbsAg-positive mothers. HBV carrier prevalence correlated with family size, and HBV infection in the household increased proportionately with the number of carriers in the family. Hepatitis B e antigen was detected most frequently in children and antibody to hepatitis B e antigen in adults. Postnatal early childhood transmission through contact among children of poorer and larger families probably accounts for the high endemicity of HBV in this region.

In 1982, the Centers for Disease Control, the Food and Drug Administration, and the manufacturer created a surveillance system to monitor spontaneous reports of adverse events occurring after inoculation with the new plasma-derived hepatitis B vaccine (Heptavax-B, Merck Sharp and Dohme, West Point, PA). In the three years between June 1, 1982 and May 31, 1985, an estimated 850,000 persons received the vaccine. During that period, a total of 41 reports were received for one of the following neurologic adverse events: convulsions (five cases), Bell's palsy (10 cases), Guillain-Barré syndrome (nine cases), lumbar radiculopathy (five cases), brachial plexus neuropathy (three cases), optic neuritis (five cases), and transverse myelitis (four cases). Half of these occurred after the first of three required vaccine doses. There were no deaths. Calculation of the relative risks of these illnesses after hepatitis B vaccination was highly dependent on diagnostic classification of the cases, estimates of the size of the vaccinated population, background incidence of the diseases, and the length and distribution of the hypothetical at-risk interval used in the analysis. Other factors important in judging the results of the study could not be measured, including underreporting. In some analyses, Guillain-Barré syndrome was reported significantly more often than expected (p less than 0.05, Poisson probability distribution). However, no conclusive epidemiologic association could be made between any neurologic adverse event and the vaccine. Even if such an association did exist, the preventive benefits of the vaccine in persons at high risk for hepatitis B would unequivocally outweigh the risk of any neurologic adverse event.

To define better the epidemiology and clinical impact of hepatitis delta virus (HDV) infection among hepatitis B virus (HBV) carriers in less developed countries, the authors prospectively studied a cohort of 216 Yucpa Indian HBV carriers in Venezuela. HBV carriers were followed regularly between 1983 and 1988 by physical examination, laboratory testing for liver enzymes and HBV and HDV markers, and epidemiologic history. Among the cohort, 74 (34%) were initially positive for HDV infection, and 35 additional persons became infected during the study. Risk factors for new HDV infection included living in southern Yucpa villages; being young adults (15-19 years) or young children (1-9 years), and living in a household with a person with acute HDV infection. Persons with HDV infection were at high risk of developing chronic liver disease; 56% of HDV-infected persons had moderate-to-severe chronic liver disease at the end of the study compared with none of the HBV carriers without HDV infection. Mortality rates were 6.9% and 8.8% per year, respectively, among initially HDV-positive HBV carriers and those with new HDV infection, because of rapidly progressive chronic liver disease and fulminant hepatitis; mortality was significantly lower in HBV carriers without HDV infection and in non-HBV carriers. HDV superinfection is a devastating disease in HBV carriers in tropical South America. Prevention of HBV infection with hepatitis B vaccine is the best available tool to reduce the impact of this problem.

To determine the significance of certain serological test results commonly encountered in hepatitis B virus testing, we reviewed serological test data from nine studies of hepatitis B conducted between 1980 and 1982. Three tests, for hepatitis B surface antigen and for antibodies to hepatitis B surface antigen and hepatitis B core antigen (anti-HBs and anti-HBc), were used to measure hepatitis B virus infection risk in various populations. Two results, low levels of anti-HBs alone and low levels of anti-HBc alone, occurred at constant frequencies (2.72 and 0.4%, respectively), regardless of the prevalence of HBV infection in the population. Positivity for low levels of anti-HBs alone persisted for 1 year in less than one-half of those studied; in addition, response to hepatitis B virus vaccine was augmented in only one-third of this group. Positivity for low levels of anti-HBc alone did not persist in any of 11 persons studied. These findings indicate that presently available tests for anti-HBs and anti-HBc at low levels are often nonspecific and should be interpreted with caution.

To determine if passively reported cases of acute viral hepatitis are representative of the affected population, an active surveillance system was set up that identified all persons in Pierce County, Washington, who had been diagnosed by a physician as having acute viral hepatitis in the period March 1 through August 31, 1984. In this county, this was part of an ongoing epidemiologic study of viral hepatitis that had previously included some stimulation of reporting. The active surveillance system covered all primary sources of medical care, including all private physicians who were most likely to see persons with hepatitis. Secondary sources, those that did not provide direct medical care but might be aware of new cases, were also surveyed. The results of active surveillance showed that passive reporting was about 65% complete in Pierce County. No change occurred in the number of hepatitis A cases reported, but hepatitis B cases increased by 50%, and non-A, non-B hepatitis cases increased by 138%. Most of the increase was a result of enhanced reporting from private physicians. The two risk groups most affected by underreporting were homosexual men with hepatitis B and blood transfusion recipients with non-A, non-B hepatitis. During active surveillance, the proportion of persons with hepatitis B who reported homosexual activity was 52% compared with 20% from passive surveillance. Transfusion recipients represented 24% of the non-A, non-B hepatitis reported from active surveillance compared with 9% reported from passive surveillance. Although Pierce County may not be representative of all counties in the United States, persons responsible for public health prevention programs should recognize that data acquired through passive surveillance may not accurately reflect the magnitude of the risk for specific populations or the amount of disease that can be prevented.

Between June 1, 1983 and August 30, 1984, an epidemic involving 313 cases of hepatitis A occurred in Muskingum County, Ohio. One hundred ninety-seven cases occurred in the city of Zanesville, with 34.7% of cases concentrated in two neighborhoods in the eastern part of the city. Case characteristics were similar to those reported in previous community-wide outbreaks, including a maximum attack rate among 5-9-year-olds and a very low attack rate in adults over 30 years. Case households were larger, and their members were less educated than the mean for households in the city. Forty-eight per cent of the cases reported exposures to other cases which temporally could have been the source of infection. A case-control study failed to show differences in several behavioral factors between case and control households, but did confirm that lower socioeconomic status was a risk factor for the disease. Broad use of immunoglobulin was effective in preventing clinical disease among family contacts, but did not stop the outbreak. This outbreak typifies a genre of hepatitis A epidemic transmitted from person to person in which exact routes of spread are poorly understood and control is difficult. Lower socioeconomic status may be a marker for some unidentified behaviors that promote hepatitis A transmission.

Hepatitis delta virus, discovered in 1977, requires the help of hepatitis B virus to replicate in hepatocytes and is an important cause of acute, fulminant, and chronic liver disease in many regions of the world. Because of the helper function of hepatitis delta virus, infection with it occurs either as a coinfection with hepatitis B or as a superinfection of a carrier of hepatitis B surface antigen. Although the mechanisms of transmission are similar to those of hepatitis B virus, the patterns of transmission of delta virus vary widely around the world. In regions of the world in which hepatitis delta virus infection is not endemic, the disease is confined to groups at high risk of acquiring hepatitis B infection and high-risk hepatitis B carriers. Because of the propensity of this viral infection to cause fulminant as well as chronic liver disease, continued incursion of hepatitis delta virus into areas of the world where persistent hepatitis B infection is endemic will have serious implications. Prevention depends on the widespread use of hepatitis B vaccine. This review focuses on the molecular biology and the clinical and epidemiologic features of this important viral infection.

Serological markers for hepatitis B virus in male homosexuals demonstrated a high prevalence of past and present infection. Seropositivity of 91% for hepatitis B e antigen or antibody was demonstrated by radioimmunoassay in hepatitis B surface antigen-positive specimens.

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.