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Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection

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Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection. / Kim, Arthur Y; Schulze zur Wiesch, Julian; Kuntzen, Thomas; Timm, Joerg; Kaufmann, Daniel E; Duncan, Jared E; Jones, Andrea M; Wurcel, Alysse G; Davis, Benjamin T; Gandhi, Rajesh T; Robbins, Gregory K; Allen, Todd M; Chung, Raymond T; Lauer, Georg M; Walker, Bruce D.

in: PLOS MED, Jahrgang 3, Nr. 12, 12.2006, S. e492.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kim, AY, Schulze zur Wiesch, J, Kuntzen, T, Timm, J, Kaufmann, DE, Duncan, JE, Jones, AM, Wurcel, AG, Davis, BT, Gandhi, RT, Robbins, GK, Allen, TM, Chung, RT, Lauer, GM & Walker, BD 2006, 'Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection', PLOS MED, Jg. 3, Nr. 12, S. e492. https://doi.org/10.1371/journal.pmed.0030492

APA

Kim, A. Y., Schulze zur Wiesch, J., Kuntzen, T., Timm, J., Kaufmann, D. E., Duncan, J. E., Jones, A. M., Wurcel, A. G., Davis, B. T., Gandhi, R. T., Robbins, G. K., Allen, T. M., Chung, R. T., Lauer, G. M., & Walker, B. D. (2006). Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection. PLOS MED, 3(12), e492. https://doi.org/10.1371/journal.pmed.0030492

Vancouver

Kim AY, Schulze zur Wiesch J, Kuntzen T, Timm J, Kaufmann DE, Duncan JE et al. Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection. PLOS MED. 2006 Dez;3(12):e492. https://doi.org/10.1371/journal.pmed.0030492

Bibtex

@article{1678527b1402445683ab0d5d877893ce,
title = "Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection",
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.",
keywords = "CD4-Positive T-Lymphocytes/immunology, Comorbidity, Cross-Sectional Studies, HIV Core Protein p24/immunology, HIV-1/physiology, Hepacivirus/genetics, Hepatitis C/epidemiology, Humans, Immunoassay, Interferon-gamma/immunology, Lymphocyte Count, RNA, Viral/analysis, Recurrence, Viremia/epidemiology",
author = "Kim, {Arthur Y} and {Schulze zur Wiesch}, Julian and Thomas Kuntzen and Joerg Timm and Kaufmann, {Daniel E} and Duncan, {Jared E} and Jones, {Andrea M} and Wurcel, {Alysse G} and Davis, {Benjamin T} and Gandhi, {Rajesh T} and Robbins, {Gregory K} and Allen, {Todd M} and Chung, {Raymond T} and Lauer, {Georg M} and Walker, {Bruce D}",
year = "2006",
month = dec,
doi = "10.1371/journal.pmed.0030492",
language = "English",
volume = "3",
pages = "e492",
journal = "PLOS MED",
issn = "1549-1277",
publisher = "Public Library of Science",
number = "12",

}

RIS

TY - JOUR

T1 - Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection

AU - Kim, Arthur Y

AU - Schulze zur Wiesch, Julian

AU - Kuntzen, Thomas

AU - Timm, Joerg

AU - Kaufmann, Daniel E

AU - Duncan, Jared E

AU - Jones, Andrea M

AU - Wurcel, Alysse G

AU - Davis, Benjamin T

AU - Gandhi, Rajesh T

AU - Robbins, Gregory K

AU - Allen, Todd M

AU - Chung, Raymond T

AU - Lauer, Georg M

AU - Walker, Bruce D

PY - 2006/12

Y1 - 2006/12

N2 - 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.

AB - 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.

KW - CD4-Positive T-Lymphocytes/immunology

KW - Comorbidity

KW - Cross-Sectional Studies

KW - HIV Core Protein p24/immunology

KW - HIV-1/physiology

KW - Hepacivirus/genetics

KW - Hepatitis C/epidemiology

KW - Humans

KW - Immunoassay

KW - Interferon-gamma/immunology

KW - Lymphocyte Count

KW - RNA, Viral/analysis

KW - Recurrence

KW - Viremia/epidemiology

U2 - 10.1371/journal.pmed.0030492

DO - 10.1371/journal.pmed.0030492

M3 - SCORING: Journal article

C2 - 17194190

VL - 3

SP - e492

JO - PLOS MED

JF - PLOS MED

SN - 1549-1277

IS - 12

ER -