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Hepatitis C and Progression of HIV Disease
Mark S. Sulkowski, MD;
Richard D. Moore, MD;
Shruti H. Mehta, PhD, MPH;
Richard E. Chaisson, MD;
David L. Thomas, MD
JAMA. 2002;288:199-206.
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/µL; CD4 cell count change following initiation
of effective HAART (resulting in a viral load of <400 copies/mL recorded
at  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/µL through 200/µL
(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.
Author Affiliations: Division of Infectious
Diseases (Drs Sulkowski, Chaisson, and Thomas) and Division of General Internal
Medicine (Dr Moore), Department of Medicine, Johns Hopkins University School
of Medicine; and Department of Epidemiology, Johns Hopkins University Bloomberg
School of Public Health (Dr Mehta), Baltimore, Md.
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