Hepatitis C virus has a genetically determined lymphotropism through co-receptor B7.2

Chia-Lin Chen, Jeffrey Y. Huang, Chun-Hsiang Wang, Stanley M Tahara, Lin Zhou, Yasuteru Kondo, Joel Schechter, Lishan Su, Michael M C. Lai, Takaji Wakita, François-Loïc Cosset, Jae U Jung and Keigo Machida ()
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Chia-Lin Chen: Keck School of Medicine, University of Southern California
Jeffrey Y. Huang: Keck School of Medicine, University of Southern California
Chun-Hsiang Wang: Keck School of Medicine, University of Southern California
Stanley M Tahara: Keck School of Medicine, University of Southern California
Lin Zhou: Keck School of Medicine, University of Southern California
Yasuteru Kondo: Keck School of Medicine, University of Southern California
Joel Schechter: Keck School of Medicine, University of Southern California
Lishan Su: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Michael M C. Lai: Keck School of Medicine, University of Southern California
Takaji Wakita: National Institute of Infectious Diseases
François-Loïc Cosset: International Center for Infectiology Research, Team EVIR
Jae U Jung: Keck School of Medicine, University of Southern California
Keigo Machida: Keck School of Medicine, University of Southern California

Nature Communications, 2017, vol. 8, issue 1, 1-17

Abstract: Abstract B-cell infection by hepatitis C virus (HCV) has been a controversial topic. To examine whether HCV has a genetically determined lymphotropism through a co-receptor specific for the infection by lymphotropic HCV, we established an infectious clone and chimeric virus of hepatotropic and lymphotropic HCV strains derived from an HCV-positive B-cell lymphoma. The viral envelope and 5′-UTR sequences of the lymphotropic HCV strain were responsible for the lymphotropism. Silencing of the virus sensor, RIGI, or overexpression of microRNA-122 promoted persistent viral replication in B cells. By cDNA library screening, we identified an immune cell-specific, co-stimulatory receptor B7.2 (CD86) as a co-receptor of lymphotropic HCV. Infection of B cells by HCV inhibited the recall reaction to antigen stimulation. Together, a co-receptor B7.2 enabled lymphotropic HCV to infect memory B cells, leading to inhibition of memory B-cell function and persistent HCV infection in HCV-infected hosts.

Date: 2017
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DOI: 10.1038/ncomms13882

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