Journal
CELLS
Volume 7, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/cells7100165
Keywords
apoptosis; viral persistence; hepatitis C virus; immunity; chronic infection
Categories
Funding
- High Impact Research (HIR), University of Malaya [625/1/HIR/139]
- University Malaya Fellowship Scheme [FG019-17AFR]
- Swedish Research Council [AI52731]
- Swedish Physicians Against AIDS Research Foundation
- Swedish International Development Cooperation Agency
- SIDA SARC
- VINNMER for Vinnova
- Linkoping University Hospital Research Fund
- CALF
- Swedish Society of Medicine (SvenskaLakaresallskapet)
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Hepatitis C virus (HCV) represents a challenging global health threat to similar to 200 million infected individuals. Clinical data suggest that only similar to 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 myriad mechanisms to disconcert virus-specific immune responses in the host to establish persistence, which includes, but is not limited to viral escape mutations, viral growth at privileged sites, and antagonism. Here we discuss 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.
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