Surveillance of hepatitis delta virus infection in Colombia, South America.
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Adolescent↗
Biomedical subjects
J E Maynard
Publications and source records attributed to J E Maynard.
Hepatitis B: global importance and need for control.
Hepatitis B is a disease of global importance, with greater than 300 million carriers of the virus world-wide. Hepatitis B virus (HBV) is the cause of up to 80% of cases of primary liver cancer, the single most important cause of mortality globally. In countries where HBV carrier rates reach 10%, HBV infection may account for 3% of total mortality, a level which exceeds polio-related mortality before the introduction of polio vaccine. The only means by which hepatitis B can be eventually eliminated is mass vaccination of infants with hepatitis B vaccine as part of the Expanded Programme on Immunization (EPI) in areas of the world where the HBV carrier rate exceeds 2.5%. With recent dramatic increases in hepatitis B vaccine production and decreases in per-dose price, there are grounds for optimism that global HBV infection rates may be reduced by as much as 90% over the next 10 years.
Global Health↗
Recovery of hepatitis A virus from a water supply responsible for a common source outbreak of hepatitis A.
An outbreak of hepatitis A occurred in a north Georgia trailer park served by a private well. Of 18 residents who were serosusceptible to hepatitis A virus (HAV), 16 (89%) developed hepatitis A. Well water samples were collected 3 months after illness onset in the index case and 28 days after illness onset in the last trailer park resident. Hepatitis A virus antigen (HAVAg) was detected in the samples by enzyme immunoassay from three of the five cell lines following two 30-day passages and from a fourth cell line following a third passage of 21 days.
Adult↗
A common-source outbreak of fulminant hepatitis B in a hospital.
A nosocomial outbreak of fulminant hepatitis B infection at a medical center in Haifa, Israel, between 7 and 26 June 1986, involved five patients who had been hospitalized previously in the medical ward in late April and early May (first generation). This outbreak had an unusual clinical course, with fulminant hepatic failure associated with acute renal failure from acute glomerulonephritis, leading to death within a few days. The onset dates of hepatitis were tightly clustered temporally and incubation periods were short. Extensive laboratory and epidemiologic evaluation showed that the probable common-source vehicle of transmission was a multiple-dose vial of heparin and normal saline flush solution that may have been contaminated by blood of a known HBsAg carrier, who was positive for anti-HBe, hospitalized at the same time. A sixth patient died in August 1986 (second generation), after his initial admission in June that coincided with the terminal hospitalizations of three first-generation patients. Those patients had marked coagulopathies, and transmission to the sixth patient most probably occurred through environmental contamination by patients or through cross-contamination between patients through staff. The unusually high mortality rate (5 of 6) in this outbreak has not been definitely explained.
Aged↗
Hepatitis A in Mauritius: an apparent transition from endemic to epidemic transmission patterns.
Between January 1984 and December 1985 a large outbreak of viral hepatitis occurred in the island nation of Mauritius (population 986,000). No hepatitis epidemics had occurred there since the 1930s. The outbreak involved 2428 reported cases; however, reporting levels were thought to be extremely low. All of the island's nine geographical districts were affected, but cases were concentrated in five districts mostly in the central and northern parts of the island. The highest attack rate occurred in children aged five to nine; persons above age 14 were almost unaffected. The male:female ratio of cases was 1.1:1. Evidence to support hepatitis A virus (HAV) as the infecting agent included; (1) clinical illness was compatible with hepatitis A; (2) the age profile of cases was typical for community-wide hepatitis A outbreaks; (3) the rate of positive tests for hepatitis B surface antigen in suspected hepatitis patients did not increase during the outbreak; and (4) nine of nine clinically ill children tested were serum-positive for IgM anti-hepatitis A virus antibody. Transmission was probably by the person-to-person route; no common source was implicated. The outbreak appears to represent a transition from a 40-year pattern of endemic HAV transmission on the island to an epidemic pattern.
Adolescent↗
Appearance of immune complexes during experimental hepatitis A infection in chimpanzees.
Circulating immune complexes (CICs) were detected during the course of experimental hepatitis A virus (HAV) infection in 8 of 9 chimpanzees. In all cases, the predominant class of antibody detected in the CIC was IgM. The appearance of IgM-CIC usually preceded the onset of liver enzyme elevations, and in all instances, the appearance of IgM-CIC correlated with the presence of IgM anti-HAV. Six of 8 animals tested had significant depression of C3 concentrations during the course of infection, and this depression occurred at the peak of CIC activity. Immunohistologic studies demonstrated granular deposits of IgM localized in sinusoidal cells during peak of IgM-CIC activity. IgM-CICs appear to be a fairly consistent finding during HAV infection and probably represent the viremic phase of the disease. However, they do not appear to mediate hepatocellular injury by direct action on hepatocytes.
Animals↗
Enterically transmitted non-A, non-B hepatitis: serial passage of disease in cynomolgus macaques and tamarins and recovery of disease-associated 27- to 34-nm viruslike particles.
An experimental model of enterically transmitted non-A, non-B hepatitis (ET-NANBH) was established in tamarins (Saguinus mystax mystax) and cynomolgus macaques (Macaca fascicularis). First-passage animals were inoculated with two different stool suspensions obtained from human patients with well-defined ET-NANBH that originated from Burma and Pakistan, where epidemics of ET-NANBH occur. Both inocula contained 27- ato 34-nm-diameter viruslike particles (VLPs) that were specifically aggregated by acute-phase ET-NANBH sera. ET-NANBH was subpassaged in both tamarins and cynomolgus macaques by using pools of stool suspensions from first-passage animals. One additional passage of disease in cynomolgus macaques resulted in a significantly shortened incubation period and increased severity of disease. VLPs similar to those found in the human inocula were observed in stool specimens of first-, second-, and third-passage cynomolgus macaques and in first- and second-passage tamarins. Our findings indicate that cynomolgus macaques are particularly suitable experimental models for studies of human ET-NANBH. The 27- to 34-nm VLPs found in infected human and primate stools appear to be etiologically linked to disease.
Animals↗
The effect of underreporting on the apparent incidence and epidemiology of acute viral hepatitis.
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.
Adult↗
Epidemic non-A, non-B hepatitis in patients from Pakistan.
Epidemic non-A, non-B hepatitis was diagnosed in three young Pakistani men during a 10-month period at the Los Angeles County-University of Southern California Medical Center. All three patients had recently visited or lived in Karachi, Pakistan. None had serologic markers of hepatitis B virus infection or IgM antibody (acute-phase) to hepatitis A virus. A liver biopsy from one patient showed marked cholestasis and cholangiolar transformation of hepatocytes, a pattern previously described in patients with epidemic non-A, non-B hepatitis. Immune electron microscopy of a stool specimen obtained from this patient 10 days after the onset of symptoms showed virus-like particles, 27 nm in diameter, that were specifically aggregated by antibody contained in acute-phase sera from the three Pakistani patients, from patients with non-A, non-B hepatitis in Burma and Nepal, and from an experimentally infected marmoset. Recognition of three separate cases of probable epidemic-type non-A, non-B hepatitis in patients at one institution during such a short time suggests that Pakistan is endemic for this infection and that the disease may be more commonly spread to the United States than is now presumed.
Adult↗
[Hepatitis in the Americas: report of the PAHO Collaborating Group].
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Americas↗
Long-term immunogenicity and efficacy of hepatitis B vaccine in homosexual men.
To study the duration of antibody persistence and protection provided by the hepatitis B vaccine, we followed 773 homosexual men for five years after completion of vaccination. Among the 635 participants in whom antibody levels above 9.9 sample ratio units (SRU) developed after vaccination, 15 percent lost antibody altogether, and in another 27 percent, antibody levels declined below 10 SRU within five years. The extent of the maximal antibody response strongly predicted the persistence of protective antibody. Hepatitis B infection occurred in 55 men; 8 of these infections were clinically important (characterized by the presence of the hepatitis B surface antigen and elevation of liver-enzyme levels), and two of the patients became hepatitis B virus carriers. The long-term risk of hepatitis B infection was inversely related to the maximal antibody response to vaccine. Most severe infections occurred among those who responded poorly or had no response to the vaccination. The risk of late infection with hepatitis B in those with an initially adequate vaccine response increased markedly when antibody levels decreased below 10 SRU, but only 1 of 34 late infections resulted in viremia and liver inflammation. A second series of vaccinations induced a moderate antibody response in 50 percent of the subjects who initially had no response or a poor response; however, the persistence of antibody was poor. Both antibody loss and the risk of severe disease should be considered when booster-dose strategies for the hepatitis B vaccine are being designed.
Carrier State↗
Lethal outbreak of hepatitis B in a dental practice.
Between April 1, 1984, and Feb 1, 1985, nine cases of hepatitis B occurred in the patients of a dentist practicing in a rural Indiana county (population, 35,000). This was over 20 times the mean annual incidence for the county in the previous decade. All of the patients had been treated by the dentist two to five months before illness. Although the dentist had never had hepatitis symptoms, his serum was positive for hepatitis B surface antigen and hepatitis B e antigen and negative for anti-hepatitis B core IgM antibody, indicating that he was probably a hepatitis B carrier. Two patients (22%) died of fulminant hepatitis; the case-fatality ratio was over ten times the reported US mean for hepatitis B. Using a case definition based on anti-hepatitis B core IgM antibody positivity and exposure to the dentist during a defined time period, a serosurvey of the dentist's patients identified 15 asymptomatic cases (overall attack rate, 3.2%). Infection risk was related to the amount of trauma involved in the cases' dental procedures. No cause was found for the unusual lethality of the outbreak.
Adult↗
Etiology and natural history of post-transfusion and enterically-transmitted non-A, non-B hepatitis.
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Animals↗
Adsorption, purification, and growth characteristics of hepatitis A virus strain HAS-15 propagated in fetal rhesus monkey kidney cells.
A human fecal isolate of hepatitis A virus strain HAS-15 was adapted to rapid growth in FRhK-4 cells by more than 20 7-day passages. A cell culture-derived inoculum of strain HAS-15 was used at a multiplicity of infection of 80 radioimmunofocus-forming units per cell, and a one-step growth curve was determined. Both intracellular production and supernatant release of infectious virions were evaluated. Detection of virus release into the medium directly corresponded to intracellular production of infectious virions. A classical eclipse period was not observed during the growth curve determinations; however, detectable infectious virion production was absent for approximately 20 h after infection. This 20-h period was immediately followed by a 4-day logarithmic phase of virus production. A maximum intracellular virus titer of 10(9) radioimmunofocus-forming units per ml was achieved, and this level remained essentially constant for up to 14 days after infection. The infectious virus and viral antigen produced during the growth cycle were ascertained by a radioimmunofocus assay and by a radioimmunoassay, respectively. Cell culture supernatants were negative for viral antigen as determined by the radioimmunoassay, even though as many as 10(8) hepatitis A virus radioimmunofocus-forming units per ml were found. An adsorption study was also performed with strain HAS-15 by using FRhK-4 cells. More than 99.9% of the infectious virus was adsorbed at 25 degrees C in less than 20 min.
Adsorption↗
Hepatitis B vaccine use in chronic hemodialysis centers in the United States.
The Centers for Disease Control surveyed 1,255 chronic hemodialysis centers in the United States in 1983 to assess the use of hepatitis B vaccine as well as the risk of acquiring hepatitis B among both patients and staff. The response rate to a mailed questionnaire was 90%. Seventy-one percent of the centers reported that they gave vaccine, but only an estimated 6% of susceptible patients and 32% of susceptible staff received all three doses of vaccine. Centers more likely to give vaccine included those that provided dialysis to large patient populations and those that provided dialysis for hepatitis B surface antigen-positive patients. As a result of vaccine administration, the overall prevalence of antibody to hepatitis B surface antigen increased significantly, to 18% for patients and 39% for staff. Extensive use of the vaccine in the future, combined with infection control practices, could virtually eliminate the risk of acquiring hepatitis B virus infection in hemodialysis centers.
Ambulatory Care Facilities↗
The control of hepatitis B virus infection with vaccine in Yupik Eskimos. Demonstration of safety, immunogenicity, and efficacy under field conditions.
In 1981, a hepatitis B vaccine demonstration project was initiated among Yupik Eskimos of southwest Alaska to demonstrate that, under field conditions, the vaccine was safe, immunogenic, and efficacious. Laboratory tests for serologic markers of hepatitis B virus infection (HBsAg, anti-HBs, and anti-HBc) performed on sera collected in May 1981 from 3,988 residents of 17 remote Eskimo villages revealed that 2,645 (66.3%) had no evidence of hepatitis B virus infection. Because of a limited supply of vaccine, specific criteria for selection were used so that those at highest risk of infection would be immunized first. In November 1981, the first dose of vaccine was administered to 1,693 carefully selected individuals. The second dose was administered to 1,678 (99.1%) of those who received the first dose, and the final dose was administered to 1,630 persons (96.3%). Serologic follow-up showed the vaccine to be safe (0.4% experienced minor adverse reactions) and immunogenic (97.4% developed antibody). Vaccine-induced antibody levels were significantly higher for persons less than 30 years of age (p less than 0.001) and for females (p less than 0.001). Vaccine recipients were also protected from hepatitis B virus infection (p = 0.002). This public health measure proved to be feasible and effective in this remote arctic population despite difficult conditions for delivery and administration of this temperature-sensitive vaccine. This strategy for immunization is now being applied on a larger scale in Alaska as part of a program for the primary prevention of this infection and its sequelae.
Adolescent↗
Antibody to hepatitis B surface antigen and screening before hepatitis B vaccination.
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Costs and Cost Analysis↗
Posttransfusion non-A, non-B hepatitis in chimpanzees. Physicochemical evidence that the tubule-forming agent is a small, enveloped virus.
Posttransfusion non-A, non-B hepatitis associated with the formation of hepatocyte cytoplasmic tubules was experimentally transmitted to chimpanzees by intravenous inoculation of a proven-infectious plasma that had been pelleted and microfiltrated, or purified by a combination of pelleting and rate-zonal banding. The results of these studies indicate that a factor VIII-derived non-A, non-B tubule-forming agent will pass through an 80-nm membrane filter and that it can be recovered from infected plasma by use of a purification procedure that assumes the non-A, non-B tubule-forming agent is a small, enveloped virus. Our findings, in combination with the known sensitivity of the non-A, non-B tubule-forming agent to chloroform and its apparent lack of nucleic acid homology with hepatitis B virus, further suggest that at least one etiologic agent of human posttransfusion non-A, non-B hepatitis may be a small, enveloped RNA virus.
Animals↗