Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
MECHANISMS FOR VIRUS-INDUCED LIVER-DISEASE - TUMOR NECROSIS FACTOR-MEDIATED PATHOLOGY INDEPENDENT OF NATURAL-KILLER AND T-CELLS DURING MURINE CYTOMEGALOVIRUS-INFECTION
Autore:
ORANGE JS; SALAZARMATHER TP; OPAL SM; BIRON CA;
Indirizzi:
BROWN UNIV,DIV BIOL & MED,DEPT MOL MICROBIOL & IMMUNOL,BOX G-B629 PROVIDENCE RI 02912 BROWN UNIV,DIV BIOL & MED,DEPT MOL MICROBIOL & IMMUNOL PROVIDENCE RI 02912 BROWN UNIV,DIV BIOL & MED,DEPT MED PROVIDENCE RI 02912
Titolo Testata:
Journal of virology
fascicolo: 12, volume: 71, anno: 1997,
pagine: 9248 - 9258
SICI:
0022-538X(1997)71:12<9248:MFVL-T>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
MONOCYTE PROCOAGULANT ACTIVITY; MOUSE HEPATITIS-VIRUS; FACTOR-ALPHA; INTERFERON-GAMMA; NK CELLS; HEPATOCYTE APOPTOSIS; ECTROMELIA VIRUS; MICE; REPLICATION; PATHOGENESIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
61
Recensione:
Indirizzi per estratti:
Citazione:
J.S. Orange et al., "MECHANISMS FOR VIRUS-INDUCED LIVER-DISEASE - TUMOR NECROSIS FACTOR-MEDIATED PATHOLOGY INDEPENDENT OF NATURAL-KILLER AND T-CELLS DURING MURINE CYTOMEGALOVIRUS-INFECTION", Journal of virology, 71(12), 1997, pp. 9248-9258

Abstract

The contribution of endogenous NK cells and cytokines to virus-induced liver pathology was evaluated during murine cytomegalovirus infections of mice. In immunocompetent C57BL/6 mice, the virus induced a self-limited liver disease characterized by hepatitis, with focal inflammation, and large grossly visible subcapsular necrotic foci. The inflammatory foci were most numerous and contained the greatest number of cells 3 days after infection; they colocalized with areas of viral antigenexpression. The largest number of necrotic foci was found 2 days after infection. Overall hepatic damage, assessed as increased expression of liver enzymes in serum, accompanied the development of inflammatoryand necrotic foci. Experiments with neutralizing antibodies demonstrated that although virus-induced tumor necrosis factor (TNF) can have antiviral effects, it also mediated significant liver pathology. TNF was required for development of hepatic necrotic foci and increased levels of liver enzymes in serum but not for increased numbers of inflammatory foci. The necrotic foci and liver enzyme indications of pathologyoccurred independently of NK and T cells, because mice rendered NK-cell deficient by treatment with antibodies, T-and B-cell-deficient Rag(-/-) mice, and NK-and T-cell-deficient E26 mice all manifested both parameters of disease. Development of necrotic foci and maximally increased levels of liver enzymes in serum also were TNF dependent in NK-cell-deficient mice. Moreover, in the immunodeficient E26 mice, virus-induced liver disease was progressive, with eventual death of the host, and neutralization of TNF significantly increased longevity. These results establish conditions separating hepatitis from significant liver damage and demonstrate a cytokine mediated component to viral pathogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 10:20:09