{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:44:14Z","timestamp":1792025054695,"version":"4.4.0"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2007,4,15]],"date-time":"2007-04-15T00:00:00Z","timestamp":1176595200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2007,4,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Superinfection exclusion is the ability of an established virus infection to interfere with infection by a second virus. In this study, we found that Huh-7.5 cells acutely infected with hepatitis C virus (HCV) genotype 2a (chimeric strain J6\/JFH) and cells harboring HCV genotype 1a, 1b, or 2a full-length or subgenomic replicons were resistant to infection with cell culture-produced HCV (HCVcc). Replicon-containing cells became permissive for HCVcc infection after treatment with an HCV-specific protease inhibitor. With the exception of cells harboring a J6\/JFH-FLneo replicon, infected or replicon-containing cells were permissive for HCV pseudoparticle (HCVpp) entry, demonstrating a postentry superinfection block downstream of primary translation. The surprising resistance of J6\/JFH-FLneo replicon-containing cells to HCVpp infection suggested a defect in virus entry. This block was due to reduced expression of the HCV coreceptor CD81. Further analyses indicated that J6\/JFH may be toxic for cells expressing high levels of CD81, thus selecting for a CD81\n                    <jats:sup>low<\/jats:sup>\n                    population. CD81 down regulation was not observed in acutely infected cells, suggesting that this may not be a general mechanism of HCV superinfection exclusion. Thus, HCV establishes superinfection exclusion at a postentry step, and this effect is reversible by treatment of infected cells with antiviral compounds.\n                  <\/jats:p>","DOI":"10.1128\/jvi.01748-06","type":"journal-article","created":{"date-parts":[[2007,2,7]],"date-time":"2007-02-07T20:19:35Z","timestamp":1170879575000},"page":"3693-3703","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":142,"title":["Superinfection Exclusion in Cells Infected with Hepatitis C Virus"],"prefix":"10.1128","volume":"81","author":[{"given":"Donna M.","family":"Tscherne","sequence":"first","affiliation":[{"name":"Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew J.","family":"Evans","sequence":"additional","affiliation":[{"name":"Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"von Hahn","sequence":"additional","affiliation":[{"name":"Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher T.","family":"Jones","sequence":"additional","affiliation":[{"name":"Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zania","family":"Stamataki","sequence":"additional","affiliation":[{"name":"Division of Immunity and Infection, Institute of Biomedical Research, University of Birmingham Medical School, Birmingham 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