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Biomedical subjects

E Tabor

Publications and source records attributed to E Tabor.

At least 145 records · Page 8Linked to original sources
PubMed1980

Hepatitis B e antigen and antibody: detection by radioimmunoassay in chimpanzees during experimental hepatitis B.

Hepatitis B e antigen (HBeAg) and its antibody (anti-HBe) were evaluated using a sensitive radioimmunoassay (RIA) in weekly serum samples obtained from nine chimpanzees experimentally infected with hepatitis B virus (HBV). In two chimpanzees with HBV infection with detectable hepatitis B surface antigen (HBsAG) for less than five weeks, and in one chimpanzee with documented HBV infection with no detectable HBsAg, HBeAg was not detected; in all three, anti-HBe became detectable early in the infection. In six chimpanzees in which HGsAg was detected for 16 weeks or longer, HBeAg was detected early in the infection; in five, anti-HBe became detectable and HBeAg undetectable prior to the clearance of HBsAg. The sixth remained HGsAg-positive and HBeAg-positive for more than two years and never developed anti-HBe. These results confirmed the sensitivity of this RIA and its value in predicting the course of HBV infections.

Animals↗
PubMed1980

Hepatitis B virus, hepatitis A virus and persistently elevated aminotransferases in hemophiliacs.

To determine the exposure to hepatitis A and hepatitis B viruses (HAV, HBV) following intravenous replacement therapy in patients with classic hemophilia and to assess the role of these viruses in persistently elevated aminotransferases, sera were studied from 136 patients from 9 months to 67 years of age were transfused with either single-donor cryoprecipitate (CRYO) or Antihemophilic Factor Concentrate (AHF) for periods ranging from a few months to 15 years. Serologic evidence of past or present infection with HBV was detected in 90% of all 136 patients and in 85% of those 34 patients 10 years of age or younger. Sixty-four percent of those with serologic markers of hepatitis B had high titers of antibody to the hepatitis B surface antigen and low titers of antibody to the hepatitis B core antigen. These findings are consistent with the known high frequency of early exposure to HBV in hemophiliacs receiving replacement therapy and with recovery from these hepatitis B infections. Sixteen percent of these patients had persistently elevated aminotransferase levels; HBV could not be implicated as the cause of the enzyme elevations in most of these cases.

Adolescent↗
PubMed1980

Absence of an association between past infection with hepatitis A virus and primary hepatocellular carcinoma.

Serum samples from 77 caucasians of Greek origin with primary hepatocellular carcinoma (PHC) and 77 age- and sex-matched controls were tested for antibody to the hepatitis A virus (anti-HAV). Anti-HAV was detected in 63 patients with PHC (82%) and in 70 controls (91%). These data suggest that past infection with hepatitis A virus is not related to the development of PHC, in marked contrast to the strong association between PHC and HBV.

Adult↗
PubMed1980

Hepatitis B e antigen in the absence of hepatitis B surface antigen.

Hepatitis B e antigen (HBeAg) was detected by agar gel diffusion in the serum of four Ugandan adults (three patients with tropical splenomegaly syndrome and one healthy adult) who did not have detectable hepatitis B surface antigen (HBsAg) by radioimmunoassay. Two of them had antibody to hepatitis B core antigen, and the other two had antibody to HBsAg. Detection of HBeAg by a relatively insensitive immunodiffusion test in the absence of HBsAg detectable by a sensitive radioimmunoassay suggested that production or removal of these two antigens may occur independently.

Adult↗
PubMed1980

Inactivation of an agent of human non-A, non-B hepatitis by formalin.

Samples of serum (0.1 ml each) containing an agent of human non-A, non-B hepatitis of documented infectivity were incubated with formalin in a concentration of 1:1,000 at 37 C for 96 hr. Three colony-born infant chimpanzees were then inoculated with this formalin-treated serum; one received a single intravenous inoculation, and two received two subcutaneous inoculations one month apart. A fourth uninoculated chimpanzee served as a control. None developed recognizable non-A, non-B hepatitis during seven months of observation, as judged by normal aminotransferase levels in weekly serum samples, normal liver histology in liver biopsy specimens, and the absence of non-A, non-B hepatitis-associated antigen and antibody in their sera. All four chimpanzees were subsequently shown to be susceptible to non-A, non-B hepatitis when challenged with 0.1 ml of the untreated infectious serum 31 weeks after the initial inoculations.

Animals↗
PubMed1980

Negative serology for hepatitis A and B viruses in 18 cases of neonatal cholestasis.

Serologic evidence of hepatitis A virus (HAV) or hepatitis B virus (HBV) infection was sought in 14 patients with biliary atresia and in four patients with neonatal hepatitis; maternal serum was also analyzed. Specific sensitive radioimmunoassays were used to detect HBV surface antigen (HBsAg) and antibody (anti-HBs); complement fixation was used to detect antibody to HBV core antigen (anti-HBc). Antibody to HAV (anti-HAV) was assayed by radioimmunoassay, as well as by immune adherence hemagglutination. There was no evidence of active or past HBV infection in any infant or mother studied. All three infants with detectable anti-HAV were born to mothers similarly anti-HAV positive; serial testing of sera from two of these infants documented disappearance of detectable anti-HAV by 9 months of age. It is unlikely, therefore, that either HAV or HBV had an etiologic role in neonatal cholestasis in these patients. The role of other (non-A, non-B) hepatitis viruses or nonviral etiologies must be investigated.

Antibodies, Viral↗
PubMed1979

Antigen-antibody system associated with non-A, non-B hepatitis detected by indirect immunofluorescence.

Ten chimpanzees were infected with non-A, non-B hepatitis by inoculation of patient serum or serum from a chimpanzee previously inoculated with patient serum. Convalescent serum from one of them reacted, in indirect immunofluorescent tests, with some of the hepatocyte nuclei in sections of autologous liver biopsy specimens and specimens from eight of the other chimpanzees. Serum from a convalescent patient reacted in the same way. These positive sera did not react with liver sections from uninfected chimpanzees. No reaction with positive liver sections was given by serum from chimpanzees which were uninfected or had antibodies to hepatitis A or B antigens. These control results suggest that the antigen-antibody system detected has specificity for non-A, non-B hepatitis.

Animals↗
PubMed1979

Serologic response in human hepatitis A: detection of antibody by radioimmunoassay and immune adherence hemagglutination.

An indirect solid-phase radioimmunoassay (RIA) for detection of antibody to the hepatitis A antigen (anti-HAV) was developed using polystyrene pearls as the solid phase and hepatitis A antigen (HAAg) extracted from marmoset livers. This RIA was compared to an immune adherence hemagglutination assay (IAHA) which employed HAAg derived from the stools of chimpanzees collected during acute hepatitis A. Anti-HAV was detected in the sera of 15 humans with naturally acquired hepatitis A infection. Sensitivity and specificity were greater using the RIA, permitting the detection of anti-HAV as early as the time of onset of jaundice. Either seroconversion or a significant increase in the titer of anti-HAV was demonstrated following hepatitis A exposure in paired sera from six patients by both techniques. No significant difference in anti-HAV responses was noted between patients with icteric compared to anicteric hepatitis A or between children and adults with hepatitis A.

Adolescent↗
PubMed1979

Detection of an antigen-antibody system in serum associated with human non-A, non-B hepatitis.

An antigen was detected by counterelectrophoresis in serum samples from six of seven chimpanzees during the acute phase of experimentally induced non-A, non-B hepatitis using antiserum from a chimpanzee convalescent from human non-A, non-B hepatitis. This antigen could not be detected in 35 preinoculation serum samples from these chimpanzees, or in 94 weekly bleedings from three chimpanzees with hepatitis A and three chimpanzees with hepatitis B. The antigen was detected in serum samples obtained from three humans with chronic non-A, non-B hepatitis whose blood had transmitted non-A, non-B hepatitis to other humans (including a nurse by accidental needlestick) and to chimpanzees by experimental inoculation. In addition, the antigen was detected in serum obtained retrospectively from 11 to 31 former blood donors whose blood had transmitted posttransfusion non-A, non-B hepatitis several years previously to recipients of a single unit of their blood. Antibody to this antigen was detected in convalescent serum samples from all seven chimpanzees studied, in convalescent serum from the nurse infected by accidental needlestick, and in serum from a hemodialysis patient convalescent from non-A, non-B hepatitis.

Animals↗
PubMed1979

Hepatitis B virus infection in infants and toddlers in Nigeria: the need for early intervention.

One or more serologic markers of hepatitis B were detected in serum samples from 29 of 61 (48%) Nigerian children between ages 6 months and 2 years who were followed for three months. Eight (13%) had acute infections, nine (15%) had chronic infections, and 12 (20%) had transplacentally acquired maternal antibody. Of 17 with active hepatitis B, 13 had been infected prior to the first serum sample (76% of infections) and four were infected during the three months of this study (24% of infections). These data indicate that effective intervention at an early age would have prevented 24% of the HBV infections which occurred in these infants, and intervention soon after birth might have prevented all of the cases.

Age Factors↗
PubMed1979

Simultaneous acute infections with hepatitis A and hepatitis B viruses in a chimpanzee.

The unexpected occurrence of a hepatitis B virus (HBV) infection in a chimpanzee experimentally inoculated with hepatitis A virus (HAV) provided an opportunity to examine the course of simultaneous acute infections with both agents. A chimpanzee inoculated intravenously with HAV developed elevated levels of aminotransferases in serum, detectable excretion of hepatitis A antigen in feces, and a marked antibody response to HAV. During the acute phase of this experimentally induced infection with HAV, the chimpanzee simultaneously developed an HBV infection. The latter was characterized by jaundice, a second increase in levels of aminotransferases in serum, and the appearance in serum of hepatitis B surface antigen (HBsAg), hepatitis B e antigen, antibody to hepatitis B core antigen, and, later, antibody to HBsAg. During the acute phase of both HAV and HBV infections, marked histopathologic inflammatory changes were observed in serial liver biopsy specimens. In this chimpanzee, the concurrent acute infection with both HAV and HBV occurred in association with marked liver damage.

Acute Disease↗
PubMed1979

Acquired immunity to human non-A, non-B hepatitis: cross-challenge of chimpanzees with three infectious human sera.

Chimpanzees that had recovered from non-A, non-B hepatitis transmitted by inoculation of serum from each of three chronically infected humans were challenged by inoculation with a second of the three infectious sera to determine whether recovery from infection caused by one serum afforded protection against later infection by another. None of the challenge inoculations caused recognizable non-A, non-B hepatitis in any of the chimpanzees, a finding suggesting that either one agent or several agents sharing a common or similar antigen were responsible for the original non-A, non-B hepatitis in fections in these chimpanzees. Although circumstantial evidence in the literature suggests the existence of more than one agent of non-A, non-B hepatitis, the fact that the three inocula were obtained from humans residing in different geographic areas of the eastern United States suggests that one agent or a group of related agents may be the cause of many cases of non-A, non-B hepatitis in the United States.

Alanine Transaminase↗
PubMed1979

Lack of susceptibility of marmosets to human non-A, non-B hepatitis.

Infectious sera from three humans with chronic non-A, non-B hepatitis, whose blood or serum had transmitted non-A, non-B hepatitis both to other humans and to experimentally inoculated chimpanzees, were inoculated into five marmosets. A sixth uninoculated marmoset served as a control. No elevations in levels of serum alanine aminotransferase or isocitric dehydrogenase occurred in serum samples obtained weekly from any of the marmosets during three months following inoculation. This study indicates that certain species of marmoset, which are susceptible to and provide well-documented animal models for hepatitis A and GB-agent hepatitis, do not appear to be susceptible to the agent(s) of human non-A, non-B hepatitis. In addition, this study suggests that the agent(s) of human non-A, non-B hepatitis and the GB agent are probably different.

Alanine Transaminase↗