The Effect of Mouse Hepatitis Virus Infection on the Microcirculation of the Liver

Abstract

Mouse hepatitis virus type 3 infection results in strain-dependent liver disease. The effects of mouse hepatitis virus type 3 on the microcirculation of the liver in both fully susceptible (Balb/cJ) and fully resistant (A/& mice were studied. In Balb/cJ mice, 6 to 12 h r following infection, abnormalities in liver blood flow were observed which consisted of granular blood flow in both terminal hepatic and terminal portal venules. In addition, sinusoidal microthrombi were present predominantly in periportal areas. By 24 to 48 hr, liver cell edema and small focal lesions were prominent. At 48 hr, thrombi and hepatocellular necrosis were widespread, and blood was shunted from damaged areas into patent sinusoids. In sharp contrast to these abnormal findings, normal streamlined blood flow was present in the resistant A/J animals at all time points following infection. Since large amounts of virus were demonstrated by immunofluorescene in and by recovery and growth from livers of both resistant and susceptible strains, the presence of the virus per se cannot explain the abnormalities observed.

Hepatitis B Virus-induced hFGL2 Transcription Is Dependent on c-Ets-2 and MAPK Signal Pathway

“…We and others have demonstrated viral proteins are potent inducers of host gene expression (3)(4)(5)(6)(7)(8)(9)20). Taken together with our previous studies, the data suggest that viral proteins and cytokines may play a synergic role in the activation of hFGL2 prothrombinase gene resulting in fibrin deposition, disturbances of microcirculation, and finally hepatocyte necrosis in patients with fulminant hepatitis or severe CHB (16,17,22,23,39,40).…”

Clinical significance of hepatic derangement in severe acute respiratory syndrome

“…The underlying cause for ALT elevation was uncertain but several mechanisms were worth considering. Direct pathogenic effect of SARS-CoV on the liver is unlikely due to the failure of identification of SARS-CoV or specific hepatitis features in the liver at autopsy in previous reports [20][21][22][23] . Elevated ALT might be related to the prescribed medications including antibiotics and high dose ribavirin.…”

Biology of portal hypertension

“…An early study utilized mice on a susceptible genetic background infected with the murine hepatitis virus, an RNA coronavirus that can cause a spectrum of liver disease including fulminant hepatic failure. These mice exhibited thrombi in the hepatic microvasculature concordant with viral liver injury [77], suggesting a link between sinusoidal thrombosis/microvascular blockage and liver damage that was supported in further studies [78]. Other animal studies using a model of carbon tetrachloride (CCl 4 )-induced liver damage demonstrated sinusoidal deposition of fibrin/fibrinogen and fibronectin in the damaged liver in the shortterm, and deposition in fibrous septa in long-term liver damage, leading to the hypothesis that clotting was an important step in the fibrotic response of the liver [79].…”