dc.contributor.author | Kim, Arthur Yu-Shin | |
dc.contributor.author | Schulze zur Wiesch, Julian | |
dc.contributor.author | Kuntzen, Thomas | |
dc.contributor.author | Timm, Joerg | |
dc.contributor.author | Kaufmann, Daniel | |
dc.contributor.author | Duncan, Jared E. | |
dc.contributor.author | Jones, Andrea M. | |
dc.contributor.author | Wurcel, Alysse G. | |
dc.contributor.author | Davis, Benjamin Thomas | |
dc.contributor.author | Gandhi, Rajesh Tim | |
dc.contributor.author | Robbins, Gregory Kimball | |
dc.contributor.author | Allen, Todd | |
dc.contributor.author | Chung, Raymond Taeyong | |
dc.contributor.author | Lauer, Georg | |
dc.contributor.author | Walker, Bruce David | |
dc.date.accessioned | 2011-08-28T17:12:22Z | |
dc.date.issued | 2006 | |
dc.identifier.citation | Kim, Arthur Y., Julian Schulze zur Wiesch, Thomas Kuntzen, Joerg Timm, Daniel E Kaufmann, Jared E Duncan, Andrea M Jones, Alysse G. Wurcel, Benjamin T. Davis, Rajesh T. Gandhi, Gregory K. Robbins, Todd M. Allen, Raymond T. Chung, Georg M. Lauer, and Bruce D. Walker. 2006. Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection. PLoS Medicine 3(12): e492. | en_US |
dc.identifier.issn | 1549-1277 | en_US |
dc.identifier.uri | http://nrs.harvard.edu/urn-3:HUL.InstRepos:5118252 | |
dc.description.abstract | Background: Hepatitis C virus (HCV)-specific T cell responses are critical for spontaneous resolution of HCV viremia. Here we examined the effect of a lymphotropic virus, HIV-1, on the ability of coinfected patients to maintain spontaneous control of HCV infection. Methods and Findings: We measured T cell responsiveness by lymphoproliferation and interferon-\(\gamma\) ELISPOT in a large cohort of HCV-infected individuals with and without HIV infection. Among 47 HCV/HIV-1-coinfected individuals, spontaneous control of HCV was associated with more frequent HCV-specific lymphoproliferative (LP) responses (35%) compared to coinfected persons who exhibited chronic HCV viremia (7%, p = 0.016), but less frequent compared to HCV controllers who were not HIV infected (86%, p = 0.003). Preservation of HCV-specific LP responses in coinfected individuals was associated with a higher nadir CD4 count (r\(^2\) = 0.45, p < 0.001) and the presence and magnitude of the HCV-specific CD8\(^+\) T cell interferon-\(\gamma\) response (p = 0.0014). During long-term follow-up, recurrence of HCV viremia occurred in six of 25 coinfected individuals with prior control of HCV, but in 0 of 16 HIV-1-negative HCV controllers (p = 0.03, log rank test). In these six individuals with recurrent HCV viremia, the magnitude of HCV viremia following recurrence inversely correlated with the CD4 count at time of breakthrough (r = −0.94, p = 0.017). Conclusions: These results indicate that HIV infection impairs the immune response to HCV—including in persons who have cleared HCV infection—and that HIV-1-infected individuals with spontaneous control of HCV remain at significant risk for a second episode of HCV viremia. These findings highlight the need for repeat viral RNA testing of apparent controllers of HCV infection in the setting of HIV-1 coinfection and provide a possible explanation for the higher rate of HCV persistence observed in this population. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | Public Library of Science | en_US |
dc.relation.isversionof | doi://10.1371/journal.pmed.0030492 | en_US |
dc.relation.hasversion | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1705826/pdf/ | en_US |
dash.license | LAA | |
dc.subject | immunology | en_US |
dc.subject | infectious diseases | en_US |
dc.subject | microbiology | en_US |
dc.subject | virology | en_US |
dc.subject | infectious diseases | en_US |
dc.subject | sexually transmitted infections - other than HIV/AIDS | en_US |
dc.subject | microbiology | en_US |
dc.subject | sexually transmitted diseases | en_US |
dc.subject | HIV infection | en_US |
dc.subject | AIDS | en_US |
dc.title | Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection | en_US |
dc.type | Journal Article | en_US |
dc.description.version | Version of Record | en_US |
dc.relation.journal | PLoS Medicine | en_US |
dash.depositing.author | Walker, Bruce David | |
dc.date.available | 2011-08-28T17:12:22Z | |
dash.affiliation.other | HMS^Medicine-Massachusetts General Hospital | en_US |
dash.affiliation.other | HMS^Medicine-Massachusetts General Hospital | en_US |
dash.affiliation.other | HMS^Medicine-Massachusetts General Hospital | en_US |
dash.affiliation.other | HMS^Medicine-Massachusetts General Hospital | en_US |
dash.affiliation.other | SPH^Immunology and Infectious Diseases | en_US |
dc.identifier.doi | 10.1371/journal.pmed.0030492 | * |
dash.contributor.affiliated | Davis, Benjamin | |
dash.contributor.affiliated | Robbins, Gregory | |
dash.contributor.affiliated | Kaufmann, Daniel E. | |
dash.contributor.affiliated | Chung, Raymond | |
dash.contributor.affiliated | Kim, Arthur | |
dash.contributor.affiliated | Lauer, Georg | |
dash.contributor.affiliated | Gandhi, Rajesh | |
dash.contributor.affiliated | Allen, Todd | |
dash.contributor.affiliated | Walker, Bruce | |
dc.identifier.orcid | 0000-0001-6122-9245 | |