Liver Update: Significance of gut microbiota in management of hepatitis-B-virus-induced chronic liver disease |
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Liver Update: Significance of gut microbiota in management of hepatitis-B-virus-induced chronic liver disease

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Hepatitis B is one of the most frequently encountered infectious diseases globally. Epidemiological surveys suggest that there are 350 million chronic hepatitis B virus (HBV) carriers worldwide. The liver is connected to the small intestine by the bile duct that carries bile formed in the liver to the intestine and majority of the blood exiting stomach and intestines must pass through the liver. 

Human intestines exhibit a wide diversity of microbes, also known as the gut microbiota, which play an important role in host metabolic processes and host immune modulation, and effect host development and physiology (organ development). This gut microbiota gets altered, which is a common complication in liver disease and known to play a crucial role in induction and promotion of HBV-induced chronic liver disease progression. In addition, specific species among the intestinal commensal bacteria also induce their effects either by acting as a pathogen or a protective agent in the development of HBV-induced chronic liver disease. 

Therefore, it is evident that the gut microbiome acts as a fertile targets for prevention or management of HBV-induced chronic liver disease. By using this approach, researchers have developed a new strategy, known as faecal microbiota transplantation (FMT) which is a beneficial therapy for HBV-related disease. Nevertheless, the data available in this field is scarce and more studies are required to obtain relevant scientific data. Thus, new technologies have supported systematic studies of gut microbiota, and extracted realistic information about its composition and pathological variance. 

Source: Kang Y, Cai Y. Gut microbiota and hepatitis-B-virus-induced chronic liver disease: implications for faecal microbiota transplantation therapy. J Hosp Infect. 2017 Aug;96(4):342-348. 

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