1994
DOI: 10.1016/s0923-2516(07)80034-3
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The virulence of mouse hepatitis virus 3, as evidenced by permissivity of cultured hepatic cells toward escape mutants

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Cited by 15 publications
(37 citation statements)
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“…Infections with attenuated variants of MHV3, however, induced higher levels of immunosuppressive cytokines or delayed production of the latter. It has been demonstrated previously that the attenuation levels of virus variants reflect their inability to infect LSEC (51·6-MHV3) or LSEC and KC (CL12-MHV3) [25], suggesting that their mild virulent phenotype may depend upon the integrity of LSEC and KC cells and their role in the control of liver inflammation through the production of immunosuppressive cytokines. In addition, the lower disturbance in immunosuppressive cytokines induced by the higher attenuated CL12-MHV3 variant when compared with the low attenuated 51·6-MHV3 variant indicates that the integrity of KC cells is more important than that of LSEC in the control of inflammatory responses during acute viral hepatitis.…”
Section: Cell Populations Viral Infection † Times Post-infection (H)mentioning
confidence: 96%
See 1 more Smart Citation
“…Infections with attenuated variants of MHV3, however, induced higher levels of immunosuppressive cytokines or delayed production of the latter. It has been demonstrated previously that the attenuation levels of virus variants reflect their inability to infect LSEC (51·6-MHV3) or LSEC and KC (CL12-MHV3) [25], suggesting that their mild virulent phenotype may depend upon the integrity of LSEC and KC cells and their role in the control of liver inflammation through the production of immunosuppressive cytokines. In addition, the lower disturbance in immunosuppressive cytokines induced by the higher attenuated CL12-MHV3 variant when compared with the low attenuated 51·6-MHV3 variant indicates that the integrity of KC cells is more important than that of LSEC in the control of inflammatory responses during acute viral hepatitis.…”
Section: Cell Populations Viral Infection † Times Post-infection (H)mentioning
confidence: 96%
“…The 51·6-MHV3 variant is less virulent than L2-MHV3, killing mice within 5-9 days, inducing moderate liver necrosis and infecting KC cells, but not LSEC [25]. The highly attenuated CL12-MHV3 variant induces the death of mice within 8-10 days, minor hepatitis with perivascular inflammatory foci, no immunodeficiency and undetectable infectious virions in LSEC or KC [25]. However, viral replication in liver was similar for pathogenic parental virus and attenuated variants [26], suggesting that the gravity of hepatitis depends on the intensity of the inflammatory response.…”
Section: Introductionmentioning
confidence: 99%
“…[10][11][12] Histopathological studies revealed an extensive necrosis with inflammatory perivascular foci and impairment of immunosuppressive cytokines such as IL-4, IL-10, prostaglandin E 2 (PGE 2 ) and transforming growth factor (TGF)-b. 13,14 Carcinoembryonic antigen cell adhesion molecules 1 (CEACAM1), previously known as biliary glycoproteins, are members of the immunoglobulin superfamily. 15 Murine CEACAM1 proteins are mostly present in the liver and intestine and have been reported to act as receptors for different bacterial and viral pathogens, including MHV.…”
Section: Introductionmentioning
confidence: 99%
“…It has been proposed that an autocrine loop initiated by an interaction beween lymphocytes and Kupffer cells can cause CD4 ϩ activation and IFN-␥ production, which in turn may induce NO release by Kupffer cells to suppress T cell proliferation (23,24). Kupffer cells are an important target for pathogenic L2-MHV3 replication in the liver (25,26), suggesting that this proposed mechanism would be altered during viral infection. YAC-MHV3 replication was lower in macrophages than that produced by pathogenic L2-MHV3 infection (27), suggesting that the tolerance, which is under control by Kupffer cells, would not be disturbed in YAC-MHV3-infected mice.…”
mentioning
confidence: 99%
“…In addition, the number of leucocytes adhering to intrahepatic EC is controlled by a leucocyte-EC interactions and remains constant even if the total number or circulating leukocytes varies over time (30). However, EC are an important target for pathogenic L2-MHV3 replication but not for attenuated viral strains (25,26). Other cytokines, such as IL-10 and prostanoids released by Kupffer cells, downregulate leukocyte adhesion to intrahepatic EC by decreasing surface expression of CD54 and CD116 (29) and then avoiding the recruitment of lymphoid cells and the immune-mediated liver damage by antigens from portal venous blood (31,32).…”
mentioning
confidence: 99%