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

Viral pathogenicity results when there is an imbalance between viral replication and the host's immune defenses. The immune system plays and important role in the outcome of an acute disease induced by the mouse hepatitis virus type 3 (MHV3). Of use in the study of the role of viral properties involved in its pathogenicity is the attenuated escape mutants. We reported that two MHV3 escape mutants were attenuated in their ability to deplete T cell subpopulations in the spleen in BALB/c mice according to inoculation route and time postinfection. The highly attenuated CL12 mutant cannot induce depletion in T cells following intraperitoneal (i.p.) or intranasal (i.n.) inoculations, at three days postinfection (p.i.). The less attenuated 51.6 mutant, however, maintained the ability to deplete T cells following i.p. inoculation, as described for the pathogenic MHV3. In contrast, no depletion of T cells following i.n. inoculation was induced with this mutant. The use of such mutants enables us to dissect the role of each compartment of the immune system.
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PMID:T cell immunodeficiency involved in pathogenicity of attenuated MHV3 mutants. 883 Apr 79

Between 1980 and 1994, 540 patients with acute viral hepatitis were admitted to hospital at the Department of Infectious Diseases of Catania (eastern Sicily). Twenty-five patients out of 540 were assessed as having non-A, non-B, non-C hepatitis. These subjects were studied for anti-HEV IgM and IgG seroprevalence by testing serial serum samples collected 1, 4, 12 and 24 weeks after the onset of acute disease. Fourteen of 25 samples (56%) seroconverted to anti-HEV IgG antibodies. No sample was positive for anti-HEV IgG at week 1, ten samples were positive at week 4 and the remainder at week 12. Anti-HEV reactivity was maintained until week 24 in all cases. In 11 of the 14 patients seroconverting to anti-HEV, the presence of IgM anti-HEV was found, which appeared in the sample from week 1 and gradually disappeared thereafter. Identified risk factors for HEV transmission included travel in the tropics and shellfish ingestion (anti-HEV positive versus anti-HEV negative: p < 0.05). HEV-related hepatitis is not yet a major public health problem in Sicily but, from our data, the trend of its incidence is clearly upwards. The high incidence of faecally-orally transmitted diseases in Sicily, the crucial position of Sicily in the middle of the Mediterranean Sea (where HEV largely circulates) and the increase of migration from developing countries are all factors which should increase awareness for a more active surveillance of the spread of HEV in our area.
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PMID:Acute hepatitis E in Catania (eastern Sicily) 1980-1994. The role of hepatitis E virus. 933 69

Hepatitis virus infection poses an important health problem to adolescents because of the morbidity of acute disease, the risk of chronic hepatitis, and the risk of vertical transmission during pregnancy. This paper reviews the epidemiology, clinical course, and prevention of hepatitis viral infections in adolescents.
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PMID:Hepatitis in Adolescents. 1035 Jul 73

The neurotropic JHM strain of mouse hepatitis virus (JHMV) produces an acute CNS infection characterized by encephalomyelitis and demyelination. The immune response cannot completely eliminate virus, resulting in persistence associated with chronic ongoing CNS demyelination. The contribution of humoral immunity to viral clearance and persistent infection was investigated in mice homozygous for disruption of the Ig mu gene (IgM-/-). Acute disease developed with equal kinetics and severity in IgM-/- and syngeneic C57BL/6 (wt) mice. However, clinical disease progressed in IgM-/- mice, while wt mice recovered. Viral clearance during acute infection was similar in both groups, supporting a primary role of cell-mediated immunity in viral clearance. In contrast to wt mice, in which infectious virus was reduced to below detection following acute infection, increasing infectious virus was recovered from the CNS of the IgM-/- mice following initial clearance. No evidence was obtained for selection of variant viruses nor was there an apparent loss of cell-mediated immunity in the absence of Ab. Passive transfer of anti-JHMV Ab following initial clearance prevented reactivation of infectious virus within the CNS of IgM-/- mice. These data demonstrate the clearance of infectious virus during acute disease by cell-mediated immunity. However, immunologic control is not maintained in the absence of anti-viral Ab, resulting in recrudescence of infectious virus. These data suggest that humoral immunity plays no role in controlling virus during acute infection, but plays an important role in establishing and maintaining CNS viral persistence.
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PMID:Antibody prevents virus reactivation within the central nervous system. 1035 87

Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.
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PMID:Q fever. 1051 1

Acute and chronic demyelination are hallmarks of CNS infection by the neurotropic JHM strain of mouse hepatitis virus. Although infectious virus is cleared by CD8+ T cells, both viral RNA and activated CD8+ T cells remain in the CNS during persistence potentially contributing to pathology. To dissociate immune from virus-mediated determinants initiating and maintaining demyelinating disease, mice were infected with two attenuated viral variants differing in a hypervariable region of the spike protein. Despite similar viral replication and tropism, one infection was marked by extensive demyelination and paralysis, whereas the other resulted in no clinical symptoms and minimal neuropathology. Mononuclear cells from either infected brain exhibited virus specific ex vivo cytolytic activity, which was rapidly lost during viral clearance. As revealed by class I tetramer technology the paralytic variant was superior in inducing specific CD8+ T cells during the acute disease. However, after infectious virus was cleared, twice as many virus-specific IFN-gamma-secreting CD8+ T cells were recovered from the brains of asymptomatic mice compared with mice undergoing demyelination, suggesting that IFN-gamma ameliorates rather than perpetuates JHM strain of mouse hepatitis virus-induced demyelination. The present data thus indicate that in immunocompetent mice, effector CD8+ T cells control infection without mediating either clinical disease or demyelination. In contrast, demyelination correlated with early and sustained infection of the spinal cord. Rapid viral spread, attributed to determinants within the spike protein and possibly perpetuated by suboptimal CD8+ T cell effector function, thus ultimately leads to the process of immune-mediated demyelination.
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PMID:Contributions of CD8+ T cells and viral spread to demyelinating disease. 1075 1

The humoral immune response to acute infection by hepatitis C virus (HCV) is not yet perfectly clear in terms of immunoglobulin (Ig) response, diversity of HCV antigen, and the relation with hepatitis severity and antibody response. Serum IgM and IgG anti-HCV levels in patients with HCV and either acute hepatitis (AH) or fulminant hepatitis (FH) were investigated; the diversity of HCV antigen was investigated by RIBA test III. Of 22 AH patients, 12 (54.5%) were positive for IgM anti-HCV, mainly reacting to HCV core protein. The mean interval until the appearance of IgM anti-HCV after onset was 24.1+/-26.2 days. IgG anti-HCV mainly reacted to both core and NS-3 antigen, appearing 42.6+/-42.1 days after onset. From a serial study of 15 AH patients, it was considered that in seven AH patients (46. 7%), the IgM response would precede the IgG response. In another two AH patients, IgM anti-HCV was not detected during the acute disease phase. Of 48 chronic hepatitis patients with HCV-RNA, 40 patients were positive for IgM anti-HCV. Therefore, IgM anti-HCV was useful for diagnosis in some of the AH patients, but it was difficult to use for distinguishing between acute and chronic infection. All four FH patients with HCV-RNA were positive for both IgM and IgG antibody to HCV at onset. Their antibody titres were higher than those of AH patients. These results suggested that, as in FH due to HBV, FH due to HCV could induce strong and rapid humoral immunity.
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PMID:Humoral immune response in Japanese acute hepatitis patients with hepatitis C virus infection. 1097 46

Three new hepatitis viruses are reviewed; Hepatitis E Virus (HEV), Hepatitis G Virus (HGV), and Transfusion Transmitted Virus (TTV). Only HEV has been clearly associated with liver damage. It is transmitted by the fecal-oral route and tends to occur in poor socio-economic conditions. Acute disease is diagnosed by the presence of anti-HEV IgM antibodies in the serum. Hepatitis G virus and TTV are transmitted parenterally. HGV is the same agent as GBV-C. Although it is hepatotropic, and high levels of viremia may occur, pathogenicity to the liver has not been proven. TTV may also be transmitted by the fecal-oral route. It is abundant in liver tissue but, like HGV, pathogenicity has not been proven.
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PMID:New hepatitis viruses. 1106 53

Hepatitis E is the principal enterically-transmitted non-A, non-B, non-C hepatitis, responsible for large epidemics of acute hepatitis associated with fecal contamination of drinking water in under-developed and developing countries. In contrast, in the industrialized world, the infection occurs rarely and sporadically, usually in individuals who originated from or traveled to regions of known endemism. However, serological and virological studies have provided evidence that hepatitis E virus may be circulating in geographical areas not previously considered to be endemic. Hepatitis E is a self-limiting, acute disease with an overall mortality rate of 0.4-4%, although a more severe course has been observed in pregnant women, in whom mortality can rise to 20%. Enzyme immunoassays and polymerase chain reaction are available for definitive diagnosis. The immune serum globulins have not evidenced certain beneficial effects during hepatitis E epidemics, and candidate vaccines have not yet reached the clinical trial stage.
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PMID:[Viral hepatitis E. Current knowledge and future problems]. 1168 45

Q fever is a zoonotic disease caused by the bacterium Coxiella burnetii. The most common reservoirs are domesticated ruminants, primarily cattle, sheep, and goats. Humans acquire Q fever typically by inhaling aerosols or contaminated dusts derived from infected animals or animal products. Its highly infectious nature and aerosol route of transmission make C. burnetii a possible agent of bioterrorism. Although up to 60% of initial infections are asymptomatic, acute disease can manifest as a relatively mild, self-limited febrile illness, or more moderately severe disease characterized by hepatitis or pneumonia. It manifests less commonly as myocarditis, pericarditis, and meningoencephalitis. Chronic Q fever occurs in <1% of infected patients, months or years after initial infection. Chronic disease manifests most commonly as a culture-negative endocarditis in patients with valvular heart disease. During 2000-2001, a total of 48 patients who met the case definition of Q fever were reported to CDC. This report describes the case investigations for six of these patients, which indicate that these persons acquired Q fever probably through direct or indirect contact with livestock. To enhance surveillance efforts, health-care providers should report cases of Q fever to state health departments.
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PMID:Q fever--California, Georgia, Pennsylvania, and Tennessee, 2000-2001. 1240 8


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