Mechanisms of hepatic injury in murine hepatitis virus type 3 infection (original) (raw)
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The Effect of Mouse Hepatitis Virus Infection on the Microcirculation of the Liver
Hepatology, 2007
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.
International Journal of Pharmacy & Integrated Health Sciences
Viral HepatitisEvery one of us has heard the word “hepatitis” and considered it a fatal disease. “Viral hepatitis” is the inflammation of the liver that is caused by a nasty family of viruses. Due to hepatitis, it is estimated that globally 1.34 million people died per year and it is also reported that about 80% of cases of liver cancer are only caused by hepatitis B and Hepatitis C together. The number of patients having this infection is amplifying each year, which is quite an alarming situation (1). Viral Hepatitis Modes of TransmissionHAV (Hepatitis A Virus) transmitted by the contaminated water (fecal-oral route), and for HBV (Hepatitis B Virus) and HBC (Hepatitis C Virus)There are mainly four modes of transmission, these are;1. Via blood2. Through sexually contact3. Through needle sharing during drug administration and4. From an infected mother to baby.Further, health care professionals who are dealing with the patients and their sample are also at higher risk.
Activation of the Immune Coagulation System by Murine Hepatitis Virus Strain 3
Clinical Infectious Diseases, 1989
Viral infections result in alterations in hemostasis and coagulation. It has previously been shown that susceptibility to murine hepatitis virus strain 3 (MHV-3), a coronavirus, correlates directly with the spontaneous, T lymphocyte-instructed expression of a procoagulant monokine that exhibits prothrombin-cleaving activity (procoagulant activity [PCA]). A biologic role for PCA in the pathogenesis of MHV-3 infection is suggested by results of in vivo microscopic observations made during acute MHV-3 infection. Recently, it has been demonstrated that prostaglandin E2 abrogates the induction of PCA by MHV-3 both in vivo and in vitro and prevents hepatic necrosis and the associated microcirculatory changes. These data suggest that MHV-3 induces cellular injury through the activation of the coagulation cascade and provide further evidence for a role for PCA in the pathogenesis of MHV-3 infection.
Potential mechanisms of hepatitis B virus induced liver injury
World Journal of Gastroenterology, 2014
Chronic active hepatitis (CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma. The histological end points of CAH are chronic inflammation, fibrosis and cirrhosis which are coupled with increased DNA synthesis in cirrhotic vs healthy normal livers. The potential mechanism involved in CAH includes a combination of processes leading to liver cell necrosis, inflammation and cytokine production and liver scaring (fibrosis). The severity of liver damage is regulated by Hepatitis B virus genotypes and viral components. The viral and cellular factors that contribute to liver injury and discussed in this article. Liver injury caused by the viral infection affects many cellular processes such as cell signaling, apoptosis, transcription, DNA repair which in turn induce radical effects on cell survival, growth, transformation and maintenance. The consequence of such perturbations is resulted in the alteration of bile secretion, gluconeogenesis, glycolysis, detoxification and metabolism of carbohydrates, proteins, fat and balance of nutrients. The identification and elucidation of the molecular pathways perturbed by the viral proteins are important in order to design effective strategy to minimize and/or restore the hepatocytes injury.