Causative agent and treatment of Hepatitis E

Hepatitis is a galling of the liver. Viruses are adjudged as the causative agent of hepatitis diseases. There are 6 types of hepatitis virus, available types, hepatitis A, hepatitis B hepatitis C, hepatitis D, hepatitis E and hepatitis G. Here we study about hepatitis E virus. Hepatitis E   is a RNA icosahedral virus. It is a positive –sense, single –stranded and non-enveloped organism.

Shape of Hepatitis E Virus 
This virus usually transmitted by fecal or can passed by oral route. It is also considered as water borne disease. In recent years, the emergence of hepatitis E virus (HEV) is a common phenomenon and its detrimental outcome is chronic diseases in the worldwide. The causative agent of hepatitis E is HEV virus and it causes high mortality during pregnancy, sometimes this symptoms lead to chronic hepatitis in immunocompromised patients. It damages the humoral immune response, solid –organ, stem-cell -transplant-patients and it also damages nerve system and kidney. Genotypes 1 and 2 are mainly existed in developing countries, while genotype 3 and 4 are prevalented in developing and high-incoming countries. However, genotype 3 and 4 are mainly responsible for hepatitis E.
Recent study showed that due to the replication of HEV in the ovary a huge structural and molecular changes may happen of infecting area are which is induced by Hepatitis E Virus and can be observed after intraperitoneal injection of HEV in rabbits. It was observed that after 28 and 49 days post inactions Positive-negative -strand HEV RNA was detectable.

Positive HEV open reading rams 2 and 3 signals were observed in the ovaries by immuno-histochemistry staining .Observed the ovarian in cell necrosis and lymphocyte infiltration and found the result. The result is the ratio of normal follicles decreased, whereas the ratio of atresia follicles increased in the HEV RNA-positive ovaries compared to control group by counting of allices at all levels. In addition, TUNEL results showed that apoptosis in follicle cells and oocytes was promoted by hepatitis inaction’s the ovary is the one of the replication sites of HEV. The expression of HEV RNA and antigen in ovarian tissue caused structural and molecular changes that prompted germ cell apoptosis. HEV can replicate or effect in different stages. According to World Health Organization, approximately 20 million infections occur annually, resulting in 3.3 million cases of hepatitis E and >44,000 deaths. There is no specific therapy against the hepatitis E virus. Someone suggested chemotherapy to remove this disease specially because it response 80-85% patients. Someone said that to prevent the release of the progeny viruses from the infected cells is an attractive strategy to limit spread of the virus.

Interaction between the viral open perusing rami 3 and the host tumor weakness quality 101 proteins have been appeared to be fundamental or arrival of the genotype-3 HCV rom the infected cells. Hepatitis E is also called pig model. Because of scientists are successfully generated immunoglobulin heavy chain JH(-/-)knockout  gnotobiotic  pigs using CRISPR/Cas9 technology, established a novel JH(-/-)knockout and wild type  gnotobiotic pig model for HEV ,and  systemically determined the dynamic of acute HEV inaction in gnotobiotic piglets developed more produced HEV-specific lesions than other studies using conventional pigs, and the infected JH(-/-)knockout pigs had significantly enlarged livers. Thus there is not a specific treatment to remove this problem so we should find a specific treatment for it. This article or blog will facilitate future studies of HEV pathogenicity.


Prepared by:
Sumit Kumar Baral
B.Sc. Student in Microbiology
Jagannath University, Bangladesh

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