Transmission of hepatitis B by immune serum globulin.
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Animals↗
Biomedical subjects
R J Gerety
Publications and source records attributed to R J Gerety.
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↗
Acute non-A, non-B hepatitis: specific ultrastructural alterations in endoplasmic reticulum of infected hepatocytes.
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Acute Disease↗
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↗
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↗
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↗
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↗
Summary of an international workshop on hepatitis B vaccines.
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Congresses as Topic↗
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↗
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↗
Electron and immunoelectron microscopic study on liver tissues of marmosets infected with hepatitis A virus.
Electron and immunoelectron microscopic studies were carried out on liver tissues from three marmosets, experimentally infected with hepatitis A virus and sacrificed during the acute phase of illness. Ultrastructurally, the liver cells demonstrated marked cisternal dilation of endoplasmic reticulum and vesicular transformation and contortion of endoplasmic reticulum profiles. Clusters of virus-like particles of 24 to 27 nm. in diameter, both "solid" and "empty" forms, were found in membrane-bound cytoplasmic vesicles. In one animal, the virus-like particles were significantly smaller, measuring 17 to 22 nm. in size, and almost all were solid forms embedded in an amorphous matrix. Clusters of virus-like particles were found in the bile canaliculi of liver cell cords and in lysosomal structures of monocytes or Kupffer cells in the hepatic sinusoids. The latter correlated with the immunofluorescent microscopic finding. Indirect immunoferritin staining was carried out on fresh and formalin-fixed liver tissues, using convalescent phase serum from patients recovered from hepatitis A virus infection as the primary antibody, and the ferritin-labeled rabbit anti-human IgG or ferritin-labeled staphylococcal protein A as the secondary antibody. Specific stainings were observed with the virus-like particles, indicating that the particles were probably antigenically related to hepatitis A virus. Our findings are in agreement with the immunofluorescent and immunoelectron microscopic studies reported by others and support the concept that hepatitis A virus is produced in the liver. The infection seems to produce cytopathic effect especially to the endoplasmic reticulum organelle of hepatocytes.
Animals↗
Hepatitis A infection and primary hepatocellular carcinoma.
The prevalence of antibody to the hepatitis A antigen (anti-HAV) has been studied in Senegal, among patients suffering from primary hepatocellular carcinoma (PHC) and among healthy blood donors. Anti-HAV was found in 62.5% of 64 cases of PHC as compared to 64% of 50 blood donors. Anti-HAV was as prevalent among PHC patients who evidenced chronic hepatitis B infection as among those without markers of chronic hepatitis B infection. These data suggest that hepatitis A infection is not associated with PHC in Senegal.
Adult↗
Acute non-A, non-B hepatitis. Prolonged presence of the infectious agent in blood.
Non-A, non-B hepatitis, previously transmitted to chimpanzees by inoculation of human serum, was serially transmitted through a second and third passage to additional chimpanzees using serum drawn during acute non-A, non-B hepatitis. Sera obtained at weeks 4 and 5 after inoculation from two different chimpanzees, and from one chimpanzee at week 13 after inoculation, were shown to cause elevation of serum aminotransferase levels and abnormal liver biopsies in recipient chimpanzees, with no serologic evidence of hepatitis A or B, cytomegalovirus, or Epstein-Barr virus infection. Serum obtained 3 wk after inoculation did not cause elevation of aminotransferase levels in the recipient chimpanzee, although a single abnormal biopsy was obtained. Thus, the non-A, non-B hepatitis agent was present in serum during acute disease near the time of the first aminotransferase elevation (week 4; perhaps also week 3), and persisted at least until 1 week after the peak aminotransferase level (week 13).
Alanine Transaminase↗
Hepatitis B and primary hepatocellular carcinoma in a European population.
The prevalence of serological markers of active of past hepatitis-B virus (H.B.V.) infection was determined in 80 Greek patients with primary hepatocellular carcinoma (P.H.C.), 160 age and sex matched controls and 40 patients with metastatic liver cancer (M.L.C.). The relative risk of the various patterns of H.B.V. serological markers for P.H.C. was calculated. Active H.B.V. infection, as indicated by positive tests for hepatitis-B surface antigen (HBsAg), or antibody to hepatitis-B core antigen (anti-HBc) without antibody to HBsAg) (anti-HBs), was associated with P.H.C. (relative risk 10.4) but not with M.L.C. (relative risk 1.2). Patients without markers and those who had recovered from hepatitis B (anti-HBs-positive) had approximately the same low risk for P.H.C. (relative risk 0.8). Active infection was more common in P.H.C. patients with co-existing cirrhosis than in those without cirrhosis (67% versus 26%). Thus the relationship between active hepatitis B and P.H.C. seen in African and Asian populations is now seen in a European Caucasian population with different racial, environmental, and dietary circumstances.
Adult↗
Transmission of hepatitis B virus infection by transfusion of frozen-deglycerolized red blood cells.
Chimpanzees were used to determine the ability of prior freezing of red blood cells to prevent the transmission of Type B post-transfusion hepatitis. Four units of human whole blood were each inoculated with 10(6) infectious doses of hepatitis B virus. Although all units became HBsAg negative after freezing and deglycerolization, hepatitis B virus infection developed in all four chimpanzees when these units were transfused. Two of these chimpanzees had only serologic evidence of infection, including the development of HBsAg and antibody to both the hepatitis B surface and core antigens; in these animals, the incubation periods were prolonged (24 to 25 weeks). In contrast, the other two animals also had elevated serum glutamic pyruvic transaminase (peaks of 190 and 461 IU per liter) and had a more rapid onset. There was no hepatitis B virus infection in two nontransfused controls. Our results do not support the use of frozen red blood cells for the prevention of post-transfusion hepatitis.
Alanine Transaminase↗
Transmission of non-A, non-B hepatitis from man to chimpanzee.
Non-A, non-B hepatitis was transmitted to four colony-born chimpanzees by intravenous inoculation of human sera. Two chimpanzees were inoculated with serum from a patient with a clinical and serological diagnosis of chronic non-A, non-B hepatitis whose blood appeared to transmit this disease to a nurse following accidental needle-stick, and the other two chimpanzees were inoculated with serum from either of two former blood-donors whose HBsAg-negative blood appeared to transmit clinically recognisable hepatitis, and who were found to have raised serum-aminotransferase levels 1 1/2 and 5 years later. Serum-aminotransferase levels rose in all four chimpanzees, beginning 2--4 weeks after inoculation: peak alanine-aminotransferase values were 210 to 328 I.U./l. Evidence of hepatitis was present in liver biopsy specimens from all four chimpanzees, beginning 8--10 weeks after inoculation. None showed serological evidence of infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, or Epstein-Barr virus.
Alanine Transaminase↗
Effect of ethanol during hepatitis B virus infection in chimpanzees.
To determine whether the use of ethyl alcohol (ethanol, C2H5OH) may increase the liver damage caused by hepatitis B virus infection, ethanol was infused into four chimpanzees on one or two occasions during the course of natural or experimentally induced hepatitis B virus infections. A fifth chimpanzee, without active hepatitis B virus infection, served as a control. Moderate elevations of serum aspartate or alanine aminotransferases occurred in four of the five chimpanzees, including the control chimpanzee, in direct association with ethanol infusion; pre-existing enzyme elevations persisted in a fifth chimpanzee. No alteration occurred in the titers of hepatitis B surface antigen or of antibody to hepatitis B core antigen in three of the four infected chimpanzees. There was no significant alteration in the course of hepatitis B virus infection by ethanol infusion in these chimpanzees.
Acute Disease↗
The role of the hepatitis B virus infection in patients with chronic hepatitis in Argentina.
Over a seven-year period, we monitored 221 patients with chronic hepatitis from two medical centers. By using the counterlectrophoresis (CEP) test to detect the presence of HBsAg and anti-HBc, or both, we established that 87.7% of them had hepatitis B infection. Serum specimens originally found negative for HBsAg by CEP were further tested by reversed passive hemagglutination (RPH), and those originally found negative for anti-HBc by CEP were further tested by radioimmunoassay (RIA). Five patients were anti-HBc-positive and HBs-Ag-negative. No sex predominance was observed, but HBsAg incidence increased with increasing age. The HBeAg antigen was detected in 46.8% of the 161 cases tested for it; the most frequent subtype found was adw (63.7%). The present findings indicate that HBV infection largely contributes to the development of chronic hepatitis in Argentinian patients.
Adolescent↗