alexa HBV/HCV Infection and Inflammation
ISSN: 2157-7412

Journal of Genetic Syndromes & Gene Therapy
Open Access

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Review Article

HBV/HCV Infection and Inflammation

Mohammad Khalid Zakaria1, Anurag Sankhyan1, Ashraf Ali2, Kaneez Fatima3, Esam Azhar4,5 and Ishtiaq Qadri2*

1Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, 110029, India

2Department of Medical Biotechnology, King Fahad Medical Research Center, King Abdul Aziz University, Jeddah, Saudi Arabia

3IQ Institute of Infection and Immunity, Lahore, Pakistan

4Special Infectious Agents Unit-Biosafety Level 3, King Fahd Medical Research Center, King Abdul Aziz University, Jeddah, Kingdom of Saudi Arabia

5Medical Laboratory Technology Department, Faculty of Applied Medical Sciences King Abdul Aziz University, Jeddah, Kingdom of Saudi Arabia

Equal Contributors

*Corresponding Author:
Ishtiaq Qadri
Department of Medical Biotechnology, King Fahad Medical Research center
King Abdul Aziz University, Jeddah, Saudi Arabia
Tel: +966 53 516 8434
E-mail: [email protected]

Received date: July 23, 2014; Accepted date:September 17, 2014; Published date: September 23, 2014

Citation: Zakaria MK, Sankhyan A, Ali A, Fatima K, Azhar E, et al. (2014) HBV/HCV Infection and Inflammation. J Genet Syndr Gene Ther 5:241. doi:10.4172/2157-7412.1000241

Copyright: © 2014 Zakaria MK, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Liver is a key organ involved in the regulation of both systemic as well as local inflammatory responses. Hepatic inflammation is the hallmark of viral hepatitis caused by non-cytopathic Hepatitis B and C viruses (HBV and HCV). Both HBV and HCV induce several inflammatory responses, causing persistent liver injury, which manifests into progressive diseased state. This ultimately leads to fibrosis, cirrhosis and eventually hepatocellular carcinoma. The disease progression is mediated by a complex interplay of molecular pathways involving both viral and hepatic factors. The complex cellular crosstalk, involving pro-inflammatory cytokines, during the liver injury also causes extra hepatic disorders such as artherosclerosis, glomerulonephritis, arthritis, cardio vascular and brain disease. In addition, these viral infections have been reported to contribute to non-Hodgkin lymphoma, cholangio carcinoma and pancreatic cancer. Host genetics also play an important role in the HBV/HCV mediated viral hepatitis and the accumulation of mutations in the host genes responsible for mounting antiviral effects (cytokines and interferon receptors) has been shown to produce differential immune responses among individuals and increase susceptibility to chronic infections. Viral proteins are known to modulate the host immune response by a variety of mechanisms such as by exerting direct or indirect effects on the cytokine pathways, oxidative stress, miRNAs and other cellular processes. However, the complete network of cytokines involved in the disease pathogenesis is yet not fully understood. This review analyzes the interplay of inflammatory molecules and viral proteins, the impact of local and systemic inflammation during HBV and HCV infection and the contribution of host genetics to such responses.

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