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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since 1961, viral hepatitis has been recognized as an occupational hazard among handlers of newly imported chimpanzees and other nonhuman primates. To determine whether previously reported cases were caused by human viral hepatitis type A, we tested paired serum samples from two outbreaks for antibody to hepatitis A antigen (anti-HA) by immune adherence hemagglutination (IAHA), recently available test. In both outbreaks, one of hepatitis transmitted from chimpanzee to man (Michigan, 1964), the second from chimpanzee to chimpanzee, man, and woolly monkey (Connecticut, 1971), serologic data documented recent hepatitis A virus infection among contacts-human and nonhuman primate-of implicated chimpanzees. This confirms serologically a previously noted epidemiologic association between nonhuman primate-associated hepatitis and human viral hepatitis, type A.
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PMID:Nonhuman primate-associated viral hepatitis type A. Serologic evidence of hepatitis A virus infection. 18 Mar 3

Serum samples from different groups of adults were tested for HBsAg and IHxAg, using a complement-fixation microtest and the Indian-ink immune reaction, respectively. (i) In healthy men 18-24 years of age, living in camps in closed communities, HBsAg was demonstrated in 1.5%, IHxAg in 12.2%, and both antigens in 0.7%. The incidence of HBsAg positivity seems to be age-dependent and influenced by environmental factors. (ii) For patients hospitalized with liver and/or biliary-tract diseases other than hepatitis, the respective percentages were 10, 13.5 and 4.5%. (iii) Of the cases clinically diagnosed as infectious hepatitis (IH, hepatitis A) or serum hepatitis (SH, hepatitis B), 14% were positive for both antigens whereas 10% were double-negative; 76% were positive for either HBsAg or IHxAg. In two-thirds of the single-positive cases the demonstrated antigen agreed with the clinical diagnosis, in one-third the unexpected antigen was present. (iv) SGPT and thymol turbidity values agreed better with the serological findings that with the clinical diagnosis. The number of days in hospital appeared to be related to both the serological findings and the clinical diagnosis. The clinical course was the most severe for those having both antigens in blood. (v) IHxantibodies from early convalescence were sensitive, those from a later stage were resistant, to 2-mercaptoethanol. (vi) No correlation was found between the presence of IHxAg and that of the rheumatoid factor. (vii) The IHx Indian-ink reaction is disturbed by the presence of labile serum proteins while the essentially similar reverse passive haemagglutination reaction was not affected by them. (viii) Testing for IHxAg seems to be a procedure valuable in the differential diagnosis of IH and SH, though the results are less convincing in adult age than in childhood.
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PMID:Serological differential diagnosis of viral hepatitis in adults. 18 Jul 57

Virus-like particles, acute hepatitis, hepatitis type C. Intranuclear virus-like particles were found by electron microscopy in liver cells of a woman suffering from mild HBsAG- and IHxAG negative acute hepatitis. The particles encountered were morphologically different from those found in hepatitis B and hepatitis A respectively. Futher studies are required to clarify whether the structures represent an incidental finding of a new human (passenger) virus or they may be related to the aetiological agent of the supposed hepatitis type C.
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PMID:Intranuclear virus-like particles in HBsAG- and IHxAG-negative acute hepatitis (type C?) (Preliminary report). 18 Jul 61

Virus-like hepatitis A antigen (HA Ag) particles, presumably hepatitis A virus, were isolated from the liver, bile, and stool of three chimpanzees that had been infected with stool filtrates containing HA Ag particles. Specimens of serum, stool, liver biopsy material, and bile were obtained at selected intervals during the experiment. The animals developed mild hepatitis 19-21 days after inoculation, and antibody to HA Ag appeared de novo in their convalescent-phase serum. During acute illness, virus-like particles similar to the HA Ag particle were seen in liver cell cytoplasm by electron microscopy. HA Ag particles were detected by immune electron microscopy and a new radioimmunoassay in isopycnically banded samples of liver, bile, and stool. HA Ag particles were found at densities of 1.29-1.39 g/cm3, but the major peak density for antigen particles in samples of liver, bile, and stool was approximately 1.34 g/cm3. The fact that HA Ag particles can be recovered from chimpanzee liver, bile, and stool makes these potentially important sources of infectious and antigenic materials.
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PMID:Hepatitis A antigen particles in liver, bile, and stool of chimpanzees. 18

No acute cases of clinical or anicteric hepatitis were in observed in 75% of 161 patients who had been exposed to hepatitis A by an oral surgeon during the contagious period. Three cases of liver dysfunction of indeterminate cause did occur, although at least two could be attributed to multiple abuses of drugs 3-5 and not to exposure to hepatitis. The fact that hepatitis A did not spread in this instance suggests that oral surgeons who are ill with acute hepatitis A do not necessarily transmit the disease to their patients. Epidemiologic investigations of similar situations will undoubtedly augment this preliminary data.
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PMID:Hepatitis type A in an oral surgeon: a prospective study of contacts. 18 49

Morphologically similar hepatitis A antigen particles (HA Ag)3 have been detected in the stools of patients with type A hepatitis and in the livers of marmosets experimentally infected with hepatitis A virus. To investigate the humoral antibody responses to these antigens and to compare the immunologic properties of HA Ag from these two sources, we immunized guinea pigs with either marmoset liver-derived HA Ag or with human stool-derived HA Ag in complete Freund's adjuvant and measured their antibody responses by immune electron microscopy (IEM) and immune adherence hemagglutination (IAHA). Antibodies reacting with both hepatitis A antigens were elicited in both groups. As determined by IEM, no distinction was seen between the reaction of guinea pig antiserum to each HA Ag tested under code when reacted against either liver-derived or stool-derived HA Ag. Antibodies elicited to marmoset liver-derived HA Ag and human stool-derived HA Ag had similar end point dilution titers by IAHA when tested against either "light" density (1.34 g/cm3) or "heavy" density (1.40 g/cm3) stool-derived HA Ag or liver-derived HA Ag. Low levels of antibody to normal liver or stool control antigens were observed transiently but did not obscure the specific response to HA Ag. These data suggest that morphologically similar HA Ag particles from different sources and with different densities are immunologically similar and may be identical. In contrast to the heterogeneity of surface antigens of hepatitis B virus, the comparable immunogenicity and apparent antigenic homogeneity of HA Ags derived from various sources may simplify the approach to development of a vaccine against viral hepatitis, type A.
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PMID:Hepatitis A antigen isolated from liver and stool: immunologic comparison of antisera prepared in guinea pigs. 18 82

To investigate the prevalence and distribution of antibody to hepatitis A antigen we tested 947 randomly selected people in the Greater New York City area; 45 per cent were antigen positive, as determined by the immune adherence method. Antibody was detected two to three times more frequently in lower social classes (72 to 80 per cent) than in middle and upper-middle classes (18 to 30 per cent). The rate of antibody detection was strongly correlated with age; the prevalence gradually increased throughout adulthood and reached its peak level in people 50 years of age and older. Those with serologic evidence of past exposure to hepatitis B virus were significantly more often antibody positive than those without such evidence (61 vs. 40 per cent; P less than 0.001). Very few of the positive subjects had had hepatitis. The prevalence of this antibody varies among different population groups, increases with age, decreases with rise in socioeconomic status, is independent on sex and race, and correlates with serologic evidence of hepatitis B virus infections.
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PMID:Distribution of antibody to hepatitis a antigen in urban adult populations. 18 13

Hepatitis A is a disease of worldwide distribution which occurs in endemic and epidemic form and is transmitted primarily by person-to-person contact through the fecal-oral route. Common source epidemics due to contamination of food are relatively common, and water-borne epidemics have been described less frequently. The presumed etiologic agent of hepatitis A has now been visualized by immune electron microscopic (IEM) techniques in early acute-illness-phase stools of humans with hepatitis A as well as in chimpanzees experimentally infected with material known to contain hepatitis A virus. In addition, several new serologic tests for the detection of antibody against hepatitis A virus have been described. These include complement fixation and immune adherence techniques. Current data suggest that hepatitis A is caused by a single viral agent lacking the morphologic heterogeneity of hepatitis B viral components and that there may be relative antigenic homogeneity between strains of virus recovered from various parts of the world. Serologic studies to date also indicate that hepatitis A virus is not a major contributing cause in post-transfusion hepatitis.
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PMID:Hepatitis A. 18 90

We evaluated the causes of 30 episodes of acute viral hepatitis in 13 patients who had multiple attacks. Two (seven per cent) of 30 bouts were caused by hepatitis A virus, and 12 (40%) by hepatitis B virus. No patient, however, had more than one attack with the serologic characteristics of Type A or Type B disease. Thus, there were 16 bouts (53 per cent) not attributable to either of the two recognized hepatitis viruses. None of these "non-A, non-B" episodes, evaluated for infectious mononucleosis and cytomegalovirus infection, could be ascribed to either. From this evidence, therefore, it appears that the clinical syndrome of viral hepatitis is produced not only by the two viruses (hepatitis A virus and hepatitis B virus) recognized since the 1940's but also, in all probability, by two non-A, non-B agents.
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PMID:Mutliple hepatitis viruses in multiple attacks of acute viral hepatitis. 18 10

Defective T-lymphocyte E rosette (ER) function associated with viral hepatitis A and B may be due to mechanisms extrinsic or intrinsic to the target lymphocyte. The extrinsic defect is induced by an immunoregulatory plasma lipoprotein (RIF) and has the capacity to regenerate ER function in vitro. The intrinsic defect is refractory to regeneration and is not associated with RIF. Although both mechanisms occur with high frequency during the acute phase of viral hepatitis they tend to segregate in accordance with progression of hepatocellular injury at later stages of the disease. The extrinsic defect was observed in 7 out of 8 patients with longstanding chronic active hepatitis and in 10 out of 10 patients with unresolved hepatitis 12 wk after the onset of jaundice. In contrast, none of nine patients with resolved hepatitis had extrinsically defective ER function 12 wk after the onset of jaundice whereas eight of them displayed an intrinsic defect of ER function at that time. Among the various viral and liver diseases studied RIF appeared to be specific for hepatitis A and B viral infections. None of 64 sera from a variety of viral infections including Epstein-Barr virus cytomegalovirus mononucleosis with associated hepatitis nor 15 sera from patients with several chronic nonviral liver diseases were positive for RIF. RIF and its associated extrinsic defect in ER function therefore appear to correlate with a particular type of hepatocellular injury initiated by the hepatitis A and B viruses that may have a propensity for persistence and(or) progression to an aggressive form of chronic hepatitis.
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PMID:Extrinsic modulation of human T-lymphocyte E rosette function associated with prolonged hepatocellular injury after viral hepatitis. 18 20


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