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Hepatitis B infection caused by the hepatitis B virus is a life-threatening cause of liver fibrosis, cirrhosis, and hepatocellular carcinoma. Researchers have produced multiple in vivo models for hepatitis B virus (HBV) and, currently, there are no specific laboratory animal models available to study HBV pathogenesis or immune response; nonetheless, their limitations prevent them from being used to study HBV pathogenesis, immune response, or therapeutic methods because HBV can only infect humans and chimpanzees. The current study is the first of its kind to identify a suitable chemically induced liver cirrhosis/HCC model that parallels HBV pathophysiology. Initially, data from the peer-reviewed literature and the GeneCards database were compiled to identify the genes that HBV and seven drugs (acetaminophen, isoniazid, alcohol, D-galactosamine, lipopolysaccharide, thioacetamide, and rifampicin) regulate. Functional enrichment analysis was performed in the STRING server. The network HBV/Chemical, genes, and pathways were constructed by Cytoscape 3.6.1. About 1546 genes were modulated by HBV, of which 25.2% and 17.6% of the genes were common for alcohol and lipopolysaccharide-induced hepatitis. In accordance with the enrichment analysis, HBV activates the signaling pathways for apoptosis, cell cycle, PI3K-Akt, TNF, JAK-STAT, MAPK, chemokines, NF-kappa B, and TGF-beta. In addition, alcohol and lipopolysaccharide significantly activated these pathways more than other chemicals, with higher gene counts and lower FDR scores. In conclusion, alcohol-induced hepatitis could be a suitable model to study chronic HBV infection and lipopolysaccharide-induced hepatitis for an acute inflammatory response to HBV.

Background: Obesity has a negative effect on health, leading to reduced life expectancy and/or increased health problems. It is one of the underlying causes of non-communicable chronic diseases like type II diabetes, stroke etc. The study was aimed to compare blood glucose levels in obese and non-obese students in a medical college and to show that obese students are more prone to develop type II diabetes.Methods: A total 20 obese subjects with age and sex matched 20 non-obese subjects were chosen. Their venous blood samples were collected after 12 hours of fasting and analysed for fasting blood sugar (FBS) and haemoglobin A1c (HbA1c).Result: Results of the study showed that obese students have significant (p<0.001) high blood glucose and HbA1c levels as compared to non-obese students.Conclusion: The obese students are prone to develop type II diabetes due to changes in body metabolism as a result of change in fat distribution.