Preprint Review Version 1 This version is not peer-reviewed

Viral Persistence and Chronicity in Hepatitis C Virus Infection: Role of T-Cell Apoptosis, Senescence and Exhaustion

Version 1 : Received: 2 October 2018 / Approved: 2 October 2018 / Online: 2 October 2018 (16:34:19 CEST)

A peer-reviewed article of this Preprint also exists.

Barathan, M.; Mohamed, R.; Yong, Y.K.; Kannan, M.; Vadivelu, J.; Saeidi, A.; Larsson, M.; Shankar, E.M. Viral Persistence and Chronicity in Hepatitis C Virus Infection: Role of T-Cell Apoptosis, Senescence and Exhaustion. Cells 2018, 7, 165. Barathan, M.; Mohamed, R.; Yong, Y.K.; Kannan, M.; Vadivelu, J.; Saeidi, A.; Larsson, M.; Shankar, E.M. Viral Persistence and Chronicity in Hepatitis C Virus Infection: Role of T-Cell Apoptosis, Senescence and Exhaustion. Cells 2018, 7, 165.

Journal reference: Cells 2018, 7, 165
DOI: 10.3390/cells7100165

Abstract

Hepatitis C virus (HCV) represents a challenging global health threat in ~200 million infected individuals. Clinical data suggests that only ~10-15% of acutely HCV-infected individuals will achieve spontaneous viral clearance despite exuberant virus-specific immune responses, which is largely attributed to difficulties in recognizing the pathognomonic symptoms during the initial stages of exposure to the virus. Given the paucity of a suitable small animal model, it is also equally challenging to study the early phases of viral establishment. Further, the host factors contributing to HCV chronicity in a vast majority of acutely HCV-infected individuals largely remain unexplored. The last few years have witnessed a surge in studies showing that HCV adopts a myriad mechanisms to disconcert virus-specific immune responses in the host to establish persistence that includes, but not limited to viral escape mutations, viral growth at privileged sites, and antagonism. Here, we discussed a few hitherto poorly explained mechanisms employed by HCV that are believed to lead to chronicity in infected individuals. A better understanding of these mechanisms would aid the design of improved therapeutic targets against viral establishment in susceptible individuals.

Subject Areas

apoptosis; viral persistence, hepatitis C virus; immunity; chronic infection

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