CONTEXT: Conflicting reports exist regarding the effect of hepatitis C virus (HCV) on the progression of human immunodeficiency virus (HIV) disease. OBJECTIVE: To assess the effect of HCV infection on clinical and immunologic progression of HIV disease and immunologic response to highly active antiretroviral therapy (HAART). DESIGN: Prospective cohort study. SETTING: University-based, urban HIV clinic in the United States. PATIENTS: There were 1955 patients enrolled between January 1995 and January 2001 who were eligible for analysis because of having at least 1 return visit to the clinic and being free of acquired immunodeficiency syndrome (AIDS) at enrollment. Median (interquartile range) length of follow-up was 2.19 (1.00-3.50) years for HCV-infected and 2.00 (1.00-3.00) years for HCV-uninfected patients. MAIN OUTCOME MEASURES: Progression to an AIDS-defining illness, survival, and progression to a CD4 cell count below 200/microL; CD4 cell count change following initiation of effective HAART (resulting in a viral load of <400 copies/mL recorded at > or = 75% of measurements). RESULTS: No difference was detected in the risk of acquiring an AIDS-defining illness (HCV-infected patients, 231 events [26.4%] and HCV-uninfected patients, 264 events [24.4%]; relative hazard [RH], 1.03; 95% confidence interval [CI], 0.86-1.23) or in the risk of death (HCV-infected patients, 153 deaths [17.5%] and HCV-uninfected patients, 168 deaths [15.5%]; RH, 1.05; 95% CI, 0.85 -1.30). Although an increased risk of death was detected in the subgroup of 429 HCV-infected patients with a baseline CD4 cell count of 50/microL through 200/microL (RH, 1.51; 95% CI, 1.01-2.27), after adjustment for exposure to HAART and its effectiveness in a multivariate Cox regression analysis, death was not independently associated with HCV infection in this subgroup (RH, 1.01; 95% CI, 0.65-1.56). Similarly, in those receiving effective HAART (n = 208), there was no difference in the increase in CD4 cell count or CD4 percentage during HAART in HCV-infected compared with HCV-uninfected patients. CONCLUSIONS: Among patients in this urban US cohort, we did not detect evidence that HCV infection substantially alters the risk of dying, developing AIDS, or responding immunologically to HAART, especially after accounting for differences in its administration and effectiveness.
CONTEXT: Conflicting reports exist regarding the effect of hepatitis C virus (HCV) on the progression of human immunodeficiency virus (HIV) disease. OBJECTIVE: To assess the effect of HCV infection on clinical and immunologic progression of HIV disease and immunologic response to highly active antiretroviral therapy (HAART). DESIGN: Prospective cohort study. SETTING: University-based, urban HIV clinic in the United States. PATIENTS: There were 1955 patients enrolled between January 1995 and January 2001 who were eligible for analysis because of having at least 1 return visit to the clinic and being free of acquired immunodeficiency syndrome (AIDS) at enrollment. Median (interquartile range) length of follow-up was 2.19 (1.00-3.50) years for HCV-infected and 2.00 (1.00-3.00) years for HCV-uninfectedpatients. MAIN OUTCOME MEASURES: Progression to an AIDS-defining illness, survival, and progression to a CD4 cell count below 200/microL; CD4 cell count change following initiation of effective HAART (resulting in a viral load of <400 copies/mL recorded at > or = 75% of measurements). RESULTS: No difference was detected in the risk of acquiring an AIDS-defining illness (HCV-infectedpatients, 231 events [26.4%] and HCV-uninfectedpatients, 264 events [24.4%]; relative hazard [RH], 1.03; 95% confidence interval [CI], 0.86-1.23) or in the risk of death (HCV-infectedpatients, 153 deaths [17.5%] and HCV-uninfectedpatients, 168 deaths [15.5%]; RH, 1.05; 95% CI, 0.85 -1.30). Although an increased risk of death was detected in the subgroup of 429 HCV-infectedpatients with a baseline CD4 cell count of 50/microL through 200/microL (RH, 1.51; 95% CI, 1.01-2.27), after adjustment for exposure to HAART and its effectiveness in a multivariate Cox regression analysis, death was not independently associated with HCV infection in this subgroup (RH, 1.01; 95% CI, 0.65-1.56). Similarly, in those receiving effective HAART (n = 208), there was no difference in the increase in CD4 cell count or CD4 percentage during HAART in HCV-infected compared with HCV-uninfectedpatients. CONCLUSIONS: Among patients in this urban US cohort, we did not detect evidence that HCV infection substantially alters the risk of dying, developing AIDS, or responding immunologically to HAART, especially after accounting for differences in its administration and effectiveness.
Authors: Lynn E Taylor; Marisa Holubar; Kunling Wu; Ronald J Bosch; David L Wyles; John A Davis; Kenneth H Mayer; Kenneth E Sherman; Karen T Tashima Journal: Clin Infect Dis Date: 2011-01-31 Impact factor: 9.079
Authors: Lena Al-Harthi; John Voris; Wenbo Du; David Wright; Marek Nowicki; Toni Frederick; Alan Landay; Andrea Kovacs Journal: J Infect Dis Date: 2006-03-17 Impact factor: 5.226
Authors: Morris Sherman; Vincent Bain; Jean-Pierre Villeneuve; Robert P Myers; Curtis Cooper; Steven Martin; Catherine Lowe Journal: Can J Infect Dis Med Microbiol Date: 2004-11 Impact factor: 2.471