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

Interaction of a single dose (36 mg/kg body wt) of the organochlorine pesticide dieldrin with mouse peritoneal macrophages was examined in C57Bl/6, (C57Bl/6 X A/J)F1, and A/J strains of different genetic resistance to mouse hepatitis virus 3 (MHV3) infection. In vivo studies showed increased susceptibility to MHV3 acute disease of C57Bl/6 and (C57Bl/6 X A/J)F1 animals challenged with the pesticide. Significant decrease of mean time of death in dieldrin-exposed, MHV3-infected susceptible C57Bl/6 mice was observed similarly upon po or ip administration of a single, sublethal dose of dieldrin. In addition, decrease of humoral response to the virus was quantified by determination of anti-MHV3 IgG antibodies in spleen cell supernatant fractions and in blood sera of dieldrin-exposed C57Bl/6 mice. A single dose of dieldrin did not alter the in vivo resistance of A/J animals to acute MHV3 disease. The resistant A/J mice, however, showed increased mortality upon two subsequent exposures to dieldrin followed by infection with high lethal doses of MHV3. Phagocytic activity, cell adherence capacity, and attachment and uptake of 3H-radiolabeled MHV3 by C57Bl/6 peritoneal macrophages were determined by in vitro studies. These affector activities of peritoneal macrophages were slightly decreased or unchanged in cells originating from animals exposed to the pesticide. However, the intrinsic activity of MHV3 restriction appeared to be affected in macrophages derived from dieldrin-treated animals: (i) peritoneal C57Bl/6 macrophages collected from the early phase of acute MHV3 disease contained increased MHV3 antigen and (ii) increased cytolysis was observed after in vitro MHV3 infection of macrophages originating from dieldrin-exposed C57Bl/6 mice.
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PMID:Increased susceptibility to mouse hepatitis virus 3 of peritoneal macrophages exposed to dieldrin. 299 59

Hepatitis D virus is a defective human pathogen that requires hepatitis B virus for its replication. A hybridization-based assay for the 1.75 kb RNA genome of hepatitis D virus was developed using as probe a radiolabeled transcript of a cloned cDNA fragment (pKD3 hepatitis D virus DNA). Sera from 120 chronic carriers of HBsAg with confirmed hepatitis D virus infection were analyzed for the presence of hepatitis D virus RNA. Serum hepatitis D virus RNA was detected in 43 of 74 (58%) patients with chronic liver disease; some patients were positive for hepatitis D virus RNA in multiple samples over a period of several years. Serum hepatitis D virus RNA was present in 17 of 28 (61%) patients during the acute phase of clinical hepatitis and was not detected after recovery from acute disease or in 18 asymptomatic chronic HBsAg carriers with antibody to hepatitis D virus. The presence of hepatitis D virus RNA correlated with other known markers of active hepatitis D virus replication; all chronic active liver disease patients with serum hepatitis D virus RNA were positive for antihepatitis D antigen IgM, and 34 of 37 (92%) had hepatitis D antigen in their liver biopsy specimens. The assay for hepatitis D virus RNA provides a direct and noninvasive method for the detection of hepatitis D virus in serum and will be useful in the study of the natural history of type D hepatitis, the identification of chronic hepatitis D virus carriers likely to transmit hepatitis D virus and the selection and monitoring of patients for potential antiviral therapy.
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PMID:Type D hepatitis: the clinical significance of hepatitis D virus RNA in serum as detected by a hybridization-based assay. 379 7

Hepatitis delta virus is a defective virus that can replicate only in the presence of hepatitis B virus. To determine the prevalence, circumstances of transmission, and clinical importance of infection with hepatitis delta virus, we obtained data on 262 patients with post-transfusion hepatitis who were positive for the hepatitis B surface antigen (HBsAg) even though they had received blood screened for it. We also studied 94 HBsAg carriers who were receiving repeated blood transfusions for other diseases, and 103 HBsAg carriers with hemophilia who were receiving various forms of coagulation factors. Antibody to hepatitis delta virus was found in 9 of 262 patients (3.5 per cent) with post-transfusion hepatitis, 5 of 234 (2 per cent) with self-limited disease, and 4 of 28 (14.5 per cent) with fulminant disease (P less than 0.05). The absence of IgM antibodies to the hepatitis B core antigen indicated that three of the nine patients with both HBsAg and antibodies to hepatitis delta virus had been carriers of HBsAg at the time of transfusion, and the acute disease represented the combined effects of the two viruses. Antibody to hepatitis delta virus was found in 3 of 94 Italian carriers of HBsAg who were receiving repeated blood transfusions, in none of 24 Brazilian, East German, or Australian hemophiliac carriers infused with clotting factors prepared from single or mini-pool volunteer plasma, and in 27 to 100 per cent of 79 hemophiliac carriers from European and U.S. series who received coagulation factors manufactured from large pools of plasma. We conclude that infection with hepatitis delta virus is likely to be more severe than infection with hepatitis B virus alone and that screening for HBsAg provides a high degree of safety in preventing infection with hepatitis delta virus, but that the risk is considerably greater in patients who are already carriers of HBsAg. We recommend that HBsAg carriers be given only blood derivatives prepared from a single donor or mini-pool donors.
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PMID:Risk of post-transfusion infection with the hepatitis delta virus. A multicenter study. 399 Jul 49

We have observed the development of long-term sequelae in four cases of experimentally induced non-A, non-B (NANB) hepatitis in chimpanzees. These sequelae were characterized by the following manifestations: nonprotection against challenge with autologous infectious plasma following acute disease and subtle histopathological alterations typical of long-lasting viral hepatitis. These manifestations were observed in animals infected with either of two human inocula. Whether or not these inocula represent sources of single or multiple etiologic agents is not known. However, our studies suggest that these inocula share at least one common etiologic agent. Further, these results may represent an atypical chronology of convalescence from viral hepatitis infection. For example, the convalescent stage of a type B hepatitis infection may be expected to occur within 6 to 8 months following exposure, whereas true convalescence in NANB hepatitis may be protracted over several months to several years. Thus, future efforts to identify the causative agent(s) of NANB hepatitis, and efforts to define the immune response in NANB, must take into consideration these studies.
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PMID:Long-term sequelae of non-A, non-B hepatitis in experimentally infected chimpanzees. 614 98

The authors present the results of studying encephalomyelitis caused by the neurotropic (IHM) strain of the murine hepatitis virus in 60 mice of the C3H line infected intracerebrally at the age of 4 weeks. Morphological examinations of the brain carried out on the 5th-13th day (the acute period) and the 14th-30th day (the subacute stage) have shown that it is myelin-producing cells that are affected first in this form of encephalomyelitis, while the periaxonal process observed is a consequence of this affection. Proofs of this conclusion are presented. It is shown that in subacute encephalomyelitis, similar processes develop. Degeneration and infection of oligodendrocytes are not so pronounced in that case, as in the acute disease. However, destruction of even individual oligodendrocytes may lead (due to the peculiarities of their structure and function) to an avalanche-like process of demyelinization. It is supposed that the vesicular degeneration of myelin may arise in the sites of close contact between the myelin membranes and the cells of inflammation infiltrates (release of lysosomal enzymes and toxic products formed in edema). In the latter case the viruses serve as an antigen depot that causes and maintains the inflammatory process.
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PMID:[Demyelinization process in acute and subacute experimental encephalomyelitis]. 629 31

The sensitivity of mice to mouse hepatitis virus 3 (MHV3) varies according to strain, age, and immune status of the animals. In semisusceptible strains, mice surviving the acute phase of infection develop a chronic disease characterized by the occurrence of paralysis, virus persistence, and immunodeficiency. Persistent MHV3 infections established in vitro in YAC and RDM -4 mouse lymphoid cell lines were characterized by virus production, presence of cytoplasmic viral antigens, and cell lysis. The occurrence of cell "crisis" in YAC cells was manifested by a sharp increase in cell lysis and in the number of fluorescent cells and, concomitantly, by a marked decrease in virus titers. A relationship was observed among the percentage of fluorescent cells, cell lysis, and virus yield and was modulated by renewal of culture media, change in temperature, or inhibition of cellular RNA synthesis. Cell cloning and antibody treatment experiments indicated that viral transmission was performed by viral infection of newly permissive cells produced by the division of uninfected cells in the culture and not by transmission of viral information by infected dividing cells. The biological and biochemical properties of MHV3 variants derived from persistently infected YAC lymphoid cells were characterized. Thermosensitivity and thermolability of cloned viruses originating from persistently infected YAC cells, as well as parent virus suspensions, were studied. A similar heterogeneity was observed when YAC-derived cloned substrains (YAC-MHV3) were compared with parent-derived cloned viruses, indicating that no selection of temperature-sensitive mutants was induced in persistently infected YAC cells. However, the capacity of MHV3 to induce a lethal acute disease when injected into susceptible mice was lost very rapidly. The absence of pathogenicity was related to the induction of a subclinical infection which elicited defense mechanisms. These data suggest, therefore, that MHV3 replication in lymphoid cell lines leads to induction or selection of variants which maintain pathogenicity in vitro but display reduced pathogenic effects in vivo.
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PMID:Persistent infection with mouse hepatitis virus 3 in mouse lymphoid cell lines. 632 31

An effect of replication of certain viruses in murine monocytic macrophages was manifested by depletion of cells through degenerative and necrotizing changes in thymus-dependent areas of lymphoid structures. In mice infected with murine hepatitis virus (MHV-3) or lactate dehydrogenase virus, these changes were transient in mice killed on postinoculation day (PID) 2. To study these morphologic changes due to viral replication, adult Swiss specific-pathogen-free homozygous nude mice (nu/nu) and their heterozygous haired littermates (nu/+) were inoculated with 10(5) LD50 of MHV-3, euthanatized, and necropsied on PID 1, 2, 4, 6, 8, and 10 along with noninoculated controls. The nu/+ and nu/nu mice killed on PID 2 had lymphocytic karyorrhexis and depletion of cells in the thymus-dependent area. In the heterozygote, these characteristic lesions were transient; whereas in the homozygote, lesions persisted and were present in survivors euthanatized and necropsied on PID 16. Although the intensity of lesions due to MHV-3 varied between nu/+ and nu/nu mice, virus titers determined on liver homogenates were similar for the homozygote and heterozygote during acute disease. Nude and nonnude mice given lactate dehydrogenase virus and killed on PID 2 had a transient depletion of lymphocytes; whereas mice given lymphocytic choriomeningitis virus and killed on PID 4 had a similar lesion. Lesions neither occurred when mice were treated with silica before inoculation, indicating that functional monocytic macrophages were required, nor occurred when another virus, herpes simplex virus type 1, was given.
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PMID:Comparison of early splenic changes associated with replication of viruses in murine monocytic macrophages. 632 45

A case of babesiosis in an asplenic individual is reported. A course characterized by fever, haemolysis, hepatitis, depressed mental status and non-cardiac pulmonary oedema was observed. Studies performed on the patient's lymphocytes revealed profound depression in mitogenic responses during her acute disease which returned to normal with recovery. Serum factor(s) were implicated in causing these changes. Review of the literature on babesiosis in asplenic hosts revealed European patients with disease caused by bovine species of Babesia are at significantly higher risk of a fatal outcome than North Americans with disease caused by murine species.
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PMID:Babesiosis in asplenic hosts. 633 94

Aetiological studies were carried out on 407 cases of acute viral hepatitis during two consecutive years in two general hospitals in Palermo, Sicily. Two hundred ninety-seven showed serological evidence of hepatitis A virus (HAV) infection and 73 of hepatitis B virus (HBV) infection. Of the remaining 37, two had a serologically diagnosed cytomegalovirus hepatitis, while 35 were classified as non-A, non-B (NANB) hepatitis. The frequency of the different major agents of acute viral hepatitis was notably influenced by the age of the patients, HAV being prevalent in children and HBV and NANB in adults. About one-fourth of the adult cases of sporadic, acute viral hepatitis were attributed to NANB virus(es). The acute disease appeared less severe than B hepatitis, as indicated by the duration of jaundice, peak serum bilirubin, and aminotransferase levels. No history of drug addiction or of parenteral exposure to blood or blood products was obtained from the presumed NANB hepatitis patients.
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PMID:Non-A, non-B hepatitis in Palermo, western Sicily. 641 55

Developments in viral hepatitis have been traced from Saul Krugman's distinction of two types, MS1 and MS2 (A and B), and Baruch S. Blumberg's discovery of Australia antigen. Hepatitis A has been grown in tissue culture, the structure of the virus is known, and the acute disease can be diagnosed. Knowledge of the molecular biology of the more complex hepatitis B virion has allowed the development of an effective vaccine and distinction of replicative and nonreplicative stages of infection. Integration, in the hepatocyte, of hepatitis B viral DNA into host DNA is the precursor of liver cancer. The infection of hepatitis B carriers with another infectious agent, delta, has added a new dimension to the problem. Other unidentified causes of hepatitis have been lumped together as non-A, non-B, and these remain to be defined and accurately diagnosed.
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PMID:Landmark perspective: Landmarks in viral hepatitis. 642 56


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