Seroepidemiological investigation of patients and family contacts in an epidemic of hepatitis A

Abstract

Serial blood and faecal samples were collected from patients and family contacts during an outbreak of hepatitis A in a village and tested by a solid-phase competitive type radioimmunoassay for hepatitis A antigen and hepatitis A antibody. The amount and duration of excretion of hepatitis A antigen was correlated with the severity of the illness. In 2 severe clinical cases, hepatitis A antigen was demonstrated in faecal extracts 11 days before the onset of jaundice and continuing for 10 days thereafter, with maximum shedding during the late incubation period. Faecal antigen was demonstrated in low concentrations for only 2 days in a patient with mild disease and in a person with subclinical infection. There was an inverse correlation between the incidence of infection and prevalence of hepatitis A antibody and age. Of 24 infections, 19 (79%) occurred in persons in the age group 0 to 20 years, a group in which only 6% of individuals had pre-existing antibody. Hepatitis A antibody was present in the serum of 3 persons in low titres of 1:20 to 1:40 on the day jaundice developed. The antibody titres increased very rapidly during the following 2 weeks of illness and slowly during the following months, reaching titres of 1:900 to 1:3500. In a separate study, a mean antibody titre of 1:591 was found in 13 patients, 12 years after clinical hepatitis A with jaundice.

Prolonged Fecal Excretion of Hepatitis A Virus in Adult Patients With Hepatitis A As Determined by Polymerase Chain Reaction

“…[2][3][4][5][6][7][8][9][10] In neonates, fecal excretion of HAV RNA may continue for as long as 6 Sensitivity of RT-PCR. Substances normally found in stool can inhibit the PCR reaction.…”

Propagation of hepatitis A virus in human embryo fibroblasts

“…The cells were either of malignant origin [Frosner et al, 1979;Locarnini et al, 1981;Deinhardt et al, 19811, and some of them contained the hepatitis B virus genome [Frosner et al, 1979;Deinhardt et al, 19811, or were available in only limited quantities [Provost and Hilleman, 1979;Flehmig, 19801, thus preventing the production of larger amounts of HAV for use in research and preparation of antigens for diagnostic tests or vaccine development. Therefore, we tested other cell types, including human diploid fibroblasts, for susceptibility to infection with HAV.…”

“…After inoculation of PLC/PRF/5 cells with HAV-containing human stool, hepatitis A antigen (HAAg) appeared only after more than 7 weeks of incubation, and the infectivity titer in tissue culture reached about 100-1,000 [Frosner et al, 1979;Deinhardt et al, 19811 . During serial passage of the virus in tissue culture, the infectivity titer increased and the time of first appearance of HAAg shortened to 1-2 weeks.…”

“…Hepatitis A virus (HAV) has been propagated recently in tissue culture; it was grown in two lines derived from human primary hepatocellular carcinoma cells (PLC/PRF/5 and Hep 3 B) [Frosner et al, 1979;Deinhardt et al, 19811 and in marmoset liver and rhesus monkey kidney cells [Provost and Hilleman, 1979;Flehmig, 19801. After inoculation of PLC/PRF/5 cells with HAV-containing human stool, hepatitis A antigen (HAAg) appeared only after more than 7 weeks of incubation, and the infectivity titer in tissue culture reached about 100-1,000 [Frosner et al, 1979;Deinhardt et al, 19811 .…”

Progression of hepatitis non-A, non-B to chronic active hepatitis: a histological follow-up of two cases.

“…Also analyses for antibodies to the hepatitis B core antigen (anti-HBc) by immunoelectro-osmophoresis (Hansson and Johnsson, 1971) and hepatitis Be antigen (HBeAg) and its antibody by immunodiffusion (Magnius et al, 1975) were found to be negative. Analyses for antibodies against hepatitis A virus (anti-HAV) by radioimmunoassay (Frosner et al, 1977) A liver biopsy one year later revealed progression to chronic active hepatitis with signs of cirrhosis (Fig. 6) (Fig.…”