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

Enterovirus-like particles have been reported in the acute phase of both epidemic and sporadic non-A, non-B (NANB) hepatitis. To examine whether these particles were the causative agent in the two types of disease, 29 patients with acute viral hepatitis in a north Indian epidemic outbreak and 9 with sporadic acute disease were investigated. 25 (86%) of 29 patients with epidemic hepatitis and 5 (56%) of 9 with sporadic disease were diagnosed as having enterically-transmitted-NANB hepatitis by exclusion. Virus-like particles (VLP) of 30-34 nm were detected in stool of 1 patient with epidemic and 1 with sporadic hepatitis. The VLPs crossreacted serologically and a specific IgM response was seen in acute epidemic and sporadic serum samples. After inoculation with infected stool rhesus monkeys had a mild rise in liver enzymes, and bile samples contained VLPs. These results suggest that the aetiological agent in epidemic and sporadic disease is the same.
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PMID:Common aetiological agent for epidemic and sporadic non-A, non-B hepatitis. 135 Nov 89

To investigate the antiviral CD4+ T cell response in coronavirus MHV-JHM-induced encephalomyelitis, spleen and thymic lymphocytes from diseased rats were stimulated in culture with virus Ag, expanded and tested for their specificity to viral proteins and nucleocapsid (N) and spike (S) proteins that had been expressed in bacteria. A strong T cell response specific for N was measurable during acute disease, whereas S-specific T cells were only detectable in rats with a later onset of disease. CD4+ T cell lines with specificity for virus and either N or S protein were established and their influence on the course of a mouse hepatitis virus-JHM infection was investigated. All lines were of the CD4+ phenotype. Both N and S protein-specific CD4+ T cells conferred protection to infected Lewis rats and reduced the amount of infectious virus in the central nervous system. After transfer of CD4+ T cells and challenge with virus, an increase in the antiviral IgM response occurred, but neutralizing antibodies were not detectable during the period of virus clearance. Previous CD8+ cell depletion did not abrogate protection mediated by CD4+ T cell line transfer.
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PMID:Nucleocapsid or spike protein-specific CD4+ T lymphocytes protect against coronavirus-induced encephalomyelitis in the absence of CD8+ T cells. 165 90

We investigated 17 patients (12 males and 5 females, ages 2 to 57 years old) with posttransfusion non-A, non-B hepatitis to determine relationships between clinical courses and hepatitis C virus (HCV) markers. The patients were grouped according to time course of abnormal serum alanine aminotransferase (ALT) levels into three categories (chronic biochemical disease, biochemically resolved chronic disease, and acute disease). Latest serum samples (1.3 to 10.8 years after blood transfusion) were used to detect antibodies against C100-3 antigen (anti-HCV) by enzyme-linked immunosorbent assay and HCV sequences by polymerase chain reaction (PCR) assay. Of the 17 patients, 13 patients (76.5%) were anti-HCV positive and 8 patients (47.1%), including one anti-HCV negative case, were positive for HCV RNA. In total, 14 patients (82.4%) were positive for either HCV markers. With respect to clinical course, HCV RNA was detected in six of eight patients (75%) with chronic biochemical disease, and in two of five patients (40%) with biochemically resolved chronic disease. HCV RNA was not detectable in convalescent sera from four patients with acute disease. These results show that there is a relationship between clinical status and HCV viremia, but that normal liver function tests do not always represent the clearance of the virus. Viremia in two patients with normal ALT level suggests that hepatitis is not only caused by viral cytopathic effects, but also by immunologic reactions against virus-infected cells. Thus, PCR is useful in determining the persistence of HCV infection as well as to diagnose anti-HCV negative HCV infection.
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PMID:Serum hepatitis C virus sequences in posttransfusion non-A, non-B hepatitis. 170 30

Antibody-containing plasma from patients recovered from Argentine hemorrhagic fever (AHF) is of proven value in treatment of the acute disease, but the possibility of transmitting blood-borne organisms such as HIV and hepatitis virus detracts from this approach. Purified human immune plasma fractions IgG1,2,4, IgG1,2,3,4 and F(ab')2 neutralized Junin virus in vitro. IgG1,2,3,4 and IgG1,2,4 lysed (in the presence of complement) cells infected with Junin virus, and protected infected guinea pigs from AHF. However, large quantities of the immune F(ab')2 fraction from the same plasma pool failed to protect guinea pigs from death, to increase the mean time to death, and to diminish virus load in target organs of infected guinea pigs. This suggests that elimination of infected cells rather than virus neutralization may play a critical role in protection against Junin virus.
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PMID:Protection of guinea pigs against experimental Argentine hemorrhagic fever by purified human IgG: importance of elimination of infected cells. 196 45

A cluster of acute non-A, non-B hepatitis comprising 12 blood donors was diagnosed in a plasmapheresis unit. Nine cases were followed-up for 2-5.5 years and seven out of them progressed to chronicity, as judged by biochemical abnormalities. In six, liver biopsy was performed 1 year after the acute disease revealing chronic active hepatitis in two, chronic persistent hepatitis in two, chronic lobular hepatitis in one and normal liver in one. Repeated biopsies showed progression to cirrhosis in one case of chronic active hepatitis, and resolution of the disease in another one, while in the remaining patients liver morphology remained unchanged. Circumstantial epidemiologic evidence suggests a single agent being the cause of the outbreak, which resulted in a broad spectrum of liver disease.
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PMID:A follow-up study of an outbreak of non-A, non-B hepatitis in a plasmapheresis unit. 210 4

During the last eighteen years (1970-1987) at the Infectious Diseases Clinic of the University of Pavia, Ospedale Policlinico S. Matteo, IRCCS, Pavia (referral Center for hepatitis in our district: 502534 inhabitants) we observed 4238 patients (2706 M = 63.8%; 1532 F = 36.2%) admitted with presumptive diagnosis of hepatitis. The male to female sex ratio was 1.78 and average age was 38 (1-90) years. Acute viral hepatitis was diagnosed in 3238 patients (76.4%), 1960 of which were males (60.5%) and 1278 (39.5%) females, with an average age of 35 (1-88) years. The possible route of transmission was: drug addition in 487 patients (15%), blood transfusion in 464 (14.3%), other (sexual, professional, familiar) in 332 (10.3%), unknown in 1955 (60.4%). Chronic hepatitis (CH) was diagnosed according to the European Association for the Study of the Liver (EASL) and to the International Association for the Study of the Liver (IASL) in 848 patients (20%), 704 M(83%) and 144 F (17%) with an average age of 48 (2-90) years. 463 patients (54.5%) were biopsied during admission, 385 (45.5%) received definitive diagnosis by clinical and previous histologic records. CAH was found in 268 (57.9%), CPH in 161 (34.8%) and CLH in 20 (4.3%) patients. Other liver diseases (steatosis, cirrhosis, HCC) were identified in 152 subjects (3%). The prevalence of A, B, NANB and Delta hepatitis virus and HI virus in the acute disease was respectively of 5.4%, 54.8%, 33.9%, 0.28% and 0.77%. In CH the HBV aetiology accounted for 49.1%, NANB virus for 44.5%, co/super infection with HDV for 15%. Among factors involved in pathogenesis of chronic hepatitis we focused attention on drug addition which was found in 129 (28.7%) patients, blood transfusion in 70 (15.6%), HIV infection in 35 of 166 (21.1%). The data still demonstrate the high prevalence of HBV aetiology of CH and existence of co-factors in the pathogenesis of chronicity. The lack of markers for NANB infection persists as the main problem in the diagnosis of liver disease. This work was supported by grant 40% from M.P.I.: "Epatiti virali acute e croniche"....
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PMID:The spectrum of chronic hepatitis in the last two decades in a university hospital for infectious diseases. 249 35

An extensive and detailed differential presentation of light and electron microscopic aspects of the various types of hepatitis B, non-A, non-B, and autoimmune hepatitis which is of equal practical and diagnostic importance for both clinicians and pathologists, remains to be written. Nowadays, hepatitis A, occurring only as an acute disease, can be diagnosed reliably by means of serological test making liver biopsy in these patients obsolete. The group of patients with hepatitis B, non-A, non-B, and autoimmune type are investigated by light and electron microscopy under the following aspects: - Are there special morphologies of the different groups? - Are the morphologic changes of a nature to provide conclusions concerning the mechanisms of cell and tissue injury? The following, more detailed questions may be added: - Can the assumption that the non-A, non-B agents induce direct cytopathic cell injury (brought forward in the literature) be confirmed by further investigations? - Does the pattern of injury in hepatitis B indicate an immune mediated pathway of cell lesion, as inferred by clinical observations and in vitro investigations? - Is there a correlation between the partially elucidated effector mechanisms in autoimmune hepatitis and histopathologic patterns? One of our comparison groups was made up of normal subjects. As paradigm of a virus induced cytopathic hepatitis, on the other hand, HSV infected mice were investigated by light microscopy and electron microscopy. With the help of immunohistologic and immunoelectron microscopic techniques an in situ characterization of the inflammatory infiltrate was attempted. Hepatitis B. The histopathologic pattern of hepatitis B in our biopsies is characterized by a more ore less dense lymphocytic infiltrate of portal tracts and lobules with a simultaneous polymorphism of hepatocytes. A centrilobular localization of the lymphocytic infiltrates and liver cell damage in many cases is obvious. The lymphocytes are frequently found in close contact with liver cells exhibiting emperipolesis. Ground glass hepatocytes, pathognomonic for hepatitis B, were present in about half of the cases with chronic hepatitis. Non-A, non-B hepatitis. Light microscopic analysis of the cases with non-A, non-B hepatitis exhibits a heterogeneous picture; on account of the known epidemiologic and experimental studies as well as of the clinical data, this was not unexpected.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Viral and autoimmune hepatitis. Morphologic and pathogenetic aspects of cell damage in hepatitis with potential chronicity. 252 40

Viral pathogenicity may be regulated by host defense mechanisms at the virus-immune cell interaction level. The immune system plays an important role in the outcome of acute disease induced by the mouse hepatitis virus type 3 (MHV3) virus. The lymphoid cells act as effectors in the virus elimination as well as targets for viral replication. In order to demonstrate a correlation between MHV3 pathogenicity and viral replication in lymphocytes, genetically-determined resistant A/J and susceptible C57BL/6 mice were infected with pathogenic (L2-MHV3) or nonpathogenic (YAC-MHV3) viral strains. Pathogenicity and histopathologic studies have revealed that lymphoid organs such as thymus and spleen, showed injuries or atrophy in susceptible mice infected with L2-MHV3. No histopathologic lesions in the lymphoid organs occurred in C57BL/6 mice infected with YAC-MHV3 or A/J mice infected with both viruses. The mechanisms involved in the lymphoid injuries were studied regarding viral replication in the lymphoid organs and cells in infected mice. Results indicate that cell depletion in lymphoid organs is caused by a complete viral replication in lymphoid cells. Thy1.2+ and surface IgM+ lymphoid cells from susceptible C57BL/6 mice infected with L2-MHV3 were permissive to viral replication and to subsequent cell lysis. No cell lysis, however, occurred in lymphoid cells from C57BL/6 mice infected with YAC-MHV3 and A/J mice infected with both virus strains. In vitro studies, with purified T and B cell populations were performed to determine the mechanism effecting susceptibility or resistance to viral-induced cell lysis occurring in such cells. A blockade, probably occurring at the viral RNA polymerase activity level, prevents viral replication in resistant cells between the stages of fixation of the virus at the cell-surface receptor and the viral protein translation. These experiments indicate that an intrinsic virus-specific resistant mechanism occurs in lymphoid cells that plays a major role in the viral pathogenicity.
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PMID:Mouse hepatitis virus 3 replication in T and B lymphocytes correlate with viral pathogenicity. 254 12

The route of entry into the central nervous system (CNS) of most neurtropic viruses has not been established. The coronavirus, mouse hepatitis virus strain JHM (MHV-JHM), causes acute encephalomyelitis and acute and chronic demyelinating diseases and is an important model system for virus-induced neurological disease. Suckling C57BL/6 mice infected intranasally with MHV-JHM develop either the acute encephalomyelitis or a late onset, symptomatic demyelinating encephalomyelitis, depending on whether they are nursed by unimmunized or immunized dams. Analysis by in situ hybridization was used to determine the route of entry of MHV-JHM into the CNS in these mice. At early times, viral RNA was detected only in the trigeminal and olfactory nerves and in their immediate connections in all mice. A few days later, MHV-JHM RNA was found throughout the brain in mice dying of the acute encephalomyelitis, but remained confined to the entry sites in mice which did not develop acute disease. These results suggest that MHV-JHM enters the CNS via an interneuronal route in all mice, but that the presence of maternal antibody prevents the dissemination of virus via extracellular fluid. In addition, MHV-JHM may establish low-level persistence in the trigeminal or olfactory nerve or in one of its connections in mice that do not develop acute encephalomyelitis.
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PMID:Spread of a neurotropic murine coronavirus into the CNS via the trigeminal and olfactory nerves. 254 29

Hepatitis serology was used to assess the nature and extent of hepatitis B virus (HBV) infection in the population of a residential centre for people with a mental handicap comprising 56 with Down's Syndrome (DS) and 193 with other mental handicaps (OMH). Markers of HBV were present in 170 cases (68%), of which 25 (10%) were HBsAg positive and potential carriers and 145 IgG anti-HBc positive (58%) indicating exposure to but not necessarily immunity from the virus. Of 25 who were HBsAg positive five were HBeAg positive, 17 were anti-HBe positive, two were HBsAg positive only and one was anti-HBe plus IgM anti-HBc positive. Age and length of residence were significantly associated with HBsAg, IgG anti-HBc and total markers of infection but the degree of mental handicap was not and the DS/OMH ratio only with HBsAg. The results indicated widespread HBV infection, no acute disease cases, relatively few infectious cases and a pre-disposition of DS residents to retain HBsAg in their sera. Vaccination of staff and at risk residents is recommended.
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PMID:Hepatitis B in a residential population with a mental handicap. 275 30


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