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HIV reduces body's ability to control hepatitis C replication
HIV infection significantly impairs the body’s ability to keep the replication of the hepatitis C virus (HCV) under control when coinfection occurs, says an international group of researchers in an article published in the June 1st edition of the Journal of Infectious Diseases (now online).
HCV infection has emerged as an increasingly serious problem in people with both infections – despite the ability of antiretrovirals to keep HIV under control.
And the way in which HCV acts in a coinfection is significantly different than in people who only have HCV infection.
The authors of this study have compared HCV-specific T-cell responses in two groups of patients: 55 HIV-positive men with acute HCV infection and eight people infected with just HCV. They also looked at HCV persistence: how long the virus stays active in the body.
They found that the majority of coinfected patients (95%) developed persistent HCV infection, a significantly higher proportion than in the HCV infected controls (65%) and more than quoted in previous studies of HCV persistence in monoinfected patients (75%).
They say this strongly suggests that concurrent HIV infection favours HCV persistence.
There was also a significantly higher HCV viral load among coinfected patients than in those with HCV only, implying poorer virological control of HCV in HIV coinfection during the acute phase of infection.
T-cell responses were weaker in coinfection, they add, suggesting HIV affects the cell-mediated responses to HCV during the acute phase, contributing to reduced clearance and control of HCV.
The authors say these results in acute HCV infection add to previous research which suggests that HIV significantly impairs cell-mediated responses to HCV antigens during chronic infection.
Reference
Danta M et al. Impact of HIV on host-virus interactions during early hepatitis C virus infection, Journal of Infectious Diseases 197 (online edition), 2008.
HCV infection has emerged as an increasingly serious problem in people with both infections – despite the ability of antiretrovirals to keep HIV under control.
And the way in which HCV acts in a coinfection is significantly different than in people who only have HCV infection.
The authors of this study have compared HCV-specific T-cell responses in two groups of patients: 55 HIV-positive men with acute HCV infection and eight people infected with just HCV. They also looked at HCV persistence: how long the virus stays active in the body.
They found that the majority of coinfected patients (95%) developed persistent HCV infection, a significantly higher proportion than in the HCV infected controls (65%) and more than quoted in previous studies of HCV persistence in monoinfected patients (75%).
They say this strongly suggests that concurrent HIV infection favours HCV persistence.
There was also a significantly higher HCV viral load among coinfected patients than in those with HCV only, implying poorer virological control of HCV in HIV coinfection during the acute phase of infection.
T-cell responses were weaker in coinfection, they add, suggesting HIV affects the cell-mediated responses to HCV during the acute phase, contributing to reduced clearance and control of HCV.
The authors say these results in acute HCV infection add to previous research which suggests that HIV significantly impairs cell-mediated responses to HCV antigens during chronic infection.
Reference
Danta M et al. Impact of HIV on host-virus interactions during early hepatitis C virus infection, Journal of Infectious Diseases 197 (online edition), 2008.
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