Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Oct 12;7(10):165.
doi: 10.3390/cells7100165.

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

Affiliations
Review

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

Muttiah Barathan et al. Cells. .

Abstract

Hepatitis C virus (HCV) represents a challenging global health threat to ~200 million infected individuals. Clinical data suggest 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 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.

Keywords: apoptosis; chronic infection; hepatitis C virus; immunity; viral persistence.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Similar articles

Cited by

References

    1. Pfaender S., Brown R.J., Pietschmann T., Steinmann E. Natural reservoirs for homologs of hepatitis C virus. Emerg. Microbes Infect. 2014;3:e21. doi: 10.1038/emi.2014.19. - DOI - PMC - PubMed
    1. Li H.C., Lo S.Y. Hepatitis C virus: Virology, diagnosis and treatment. World J. Hepatol. 2015;7:1377–1389. doi: 10.4254/wjh.v7.i10.1377. - DOI - PMC - PubMed
    1. Pinter M., Trauner M., Peck-Radosavljevic M., Sieghart W. Cancer and liver cirrhosis: Implications on prognosis and management. ESMO Open. 2016;1:e000042. doi: 10.1136/esmoopen-2016-000042. - DOI - PMC - PubMed
    1. Khan A.A., Ahmad H., Saif N., Idrees M., Bajwa M.A. Frequency distribution of hepatitis in three districts of Hazara division. Asian J. Med. Sci. 2010;2:37–39.
    1. Palumbo E. Pegylated interferon and ribavirin treatment for hepatitis C virus infection. Ther. Adv. Chronic Dis. 2011;2:39–45. doi: 10.1177/2040622310384308. - DOI - PMC - PubMed