Biomedical subjects
Publications and source records attributed to K R Berquist.
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.
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.
HBc Ag was detected by fluorescent antibody in liver biopsies taken from chronic hepatitis B surface antigen (HBs Ag) carriers having e antigen in their sera. HBc Ag could not be detected in liver biopsies from similar individuals having e antibody in their sera.
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.
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We performed a prospective study to assess the risk of patients acquiring infection following routine professional contact with two dentists incubating type B viral hepatitis. Serum samples from patients exposed during the six weeks before onset of hepatitis in the dentists were tested for hepatitis B surface antigen and for antibody to the antigen shortly after illness developed and again six months later. Household members of exposed patients served as a control group. None of the exposed patients or controls became ill with hepititis, and none developed antigen. Three of the 237 exposed patients developed antibody, as did four of the 245 controls. The difference between exposed patients and controls was not significant. These results do not support the hypothesis that these two dentists transmitted infection to their patients.
An epidemic of Coxsackie B4 virus infection in an isolated group of islands in the Bering Sea in 1967 provided an opportunity to test the suggestion that infection with this virus might be associated with an increased incidence of diabetes. In 1973 islanders were tested by glucose-tolerance tests and their two-hour plasma glucose levels were analysed in the light of serological evidence of CB4 infection five years earlier. There was no evidence of any increased prevalence of diabetes in those who had been infected in 1967.
Thirty-four chimpanzees were inoculated with sera containing the adw, ayw, adr, or ayr subtype of hepatitis B surface antigen (HBs Ag). Twenty-nine of the animals became infected with hepatitis B virus, and in every instance the subtype of HBs Ag in the infected animal was the same as the subtype in the inoculum. Infectivity titers were established for the adw and ayw inocula. The patterns of serologic events varied in the infected animals but included most of the typical patterns of serologic change seen in human cases of type B hepatitis. Mild disease, manifested by elevated concentrations of serum enzymes and changes detected by liver biopsy, occurred in 23 of the 29 infected animals.
We report the temporal patterns of various immunohistological and serological parameters of acute self-limited hepatitis B virus infection of two chimpanzees, and we provide evidence that the synthesis of hepatitis B core antigen precedes that of hepatitis B surface antigen. Our data suggest that existence of a biphasic hepatitis B virus infection involving a hematogenous reinfection of the liver and indicate that recruitment of liver cells to produce hepatitis B virus may occur in a pattern consistent with a replicative cycle of about 8 days.
We have induced hepatitis A in marmosets of the subspecies Saguinus mystax following primary inoculation with human serum containing the MS-1 strain of hepatitis A virus (HAV) and in 3 further marmoset subpassages using infective marmoset serum from each preceding passage. In each passage acquisition of serum antibody against 17 nm virus-like particles recovered from acute illness stools of human volunteers who developed hepatitis following inoculation with the MS-1 strain of HAV, as well as from acute illness stools of hepatitis A cases from a common source epidemic of heaptitis A in Arizona could be demonstrated by immune electron microscopy (IEM). Particle-containing stool filtrates from the latter epidemic also induced hepatitis in chimpanzees after intravenous inoculation. Inoculation of partially purified particles from a single banding in CsCl2 has further resulted in the induction of hepatitis in S. mystax marmosets. We have successfully induced hepatitis in a series of chimpanzees inoculated with sera containing hepatitis B surface antigen (HBsAg) of varying subspecificities. Susceptibility appears universal in animals who are initially lacking in serum antibody (anti-HBs) and antibody induced following experimental infection is homologous in subspecificity to the subspecificities of the antigenic coat components of the HBsAg in the inoculum. Results of cross challenge experiments indicate that animals developing hepatitis following inoculation of HBsAg of one subspecificity set in the d/y-w/r system do not again develop hepatitis following inoculation with HBsAg of the alternate subspecificity set.
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Transformed chimpanzee lymphocytes were examined to determine whether they would support the replication of hepatitis B virus. After 5 months, no hepatitis B virus, hepatitis B surface antigen, or antibody to hepatitis B surface antigen was detected.
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