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Sustained Response to Anti-HCV Therapy Higher During Acute Infection in HIV Positives
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18th Conference on Retroviruses and Opportunistic Infections, February 27-March 2, 2011, Boston
Mark Mascolini
About two thirds of HIV-positive men with acute HCV infection achieved a sustained virologic response (SVR) to pegylated interferon plus ribavirin (PegIFN/RBV) in four European countries [1]. That rate is much higher than SVRs seen in HCV/HIV-coinfected people treated during chronic HCV infection. As in chronic infection, response rates were better with HCV genotypes 2 and 3 than with genotypes 1 and 4.
Most people chronically coinfected with HCV and HIV carry HCV genotype 1 or 4, both of which respond to PegIFN/RBV worse than genotypes 2 and 3. NEAT Study Group investigators planned this analysis to determine whether response rates follow that pattern during acute HCV infection in people with HIV.
The study involved 238 HIV-positive men in the United Kingdom, France, Germany, and Austria who were diagnosed with acute HCV infection. While 207 men began PegIFN/RBV, 31 began PegIFN alone. Most men (85%) took a weight-based dose of ribavirin. Follow-up began in 2002, and the primary outcome was SVR--undetectable HCV RNA 24 weeks after treatment ends.
Median age of these men was 39 years (interquartile range [IQR] 34 to 43), 94% became infected through gay sex, 3% through drug injection, and 3% for undetermined reasons. Median CD4 count measured 474 (IQR 363 to 625) and median HIV load 50 copies (IQR 50 to 15,839). Two thirds of the men were taking antiretrovirals. Median HCV load measured 770,259 IU/mL (IQR 218,000 to 2,300,000). Only one quarter of the men had clinical symptoms of acute HCV infection.
Median time to anti-HCV treatment initiation was 9.6 weeks (IQR 4.6 to 16), and median time to first negative HCV RNA was 8 weeks (IQR 4 to 12). Most men (66.4%) had HCV genotype 1, 5.9% had genotype 2, 12.2% had genotype 3, and 15.5% had genotype 4. Anti-HCV therapy lasted 24 weeks in 70% and 48 weeks in 30%.
Rapid virologic response (RVR, HCV RNA negative 4 weeks after treatment began), early virologic response (EVR, negative 12 weeks after treatment began), end-of-treatment response (ETR, negative at end of treatment), and SVR were high overall but greater in men infected with genotype 2 or 3 than with genotype 1 or 4:
RVR: 51% genotype 1/4, 64.7% genotype 2/3 (not significant, P = 0.184)
EVR: 72.7% genotype 1/4, 90.3% genotype 2/3 (P = 0.04)
ETR: 76.4% genotype 1/4, 94.9% genotype 2/3 (P = 0.008)
SVR: 64.6% genotype 1/4, 81.4% genotype 2/3 (P = 0.046)
In multivariate analysis, attaining RVR independently raised chances of reaching SVR (P < 0.001), as did infection with genotype 2 or 3 versus 1 or 4 (P = 0.043). Factors not associated with SVR in this analysis included baseline CD4 count, baseline HIV load, baseline HCV load, median maximum alanine aminotransferase, clinical symptoms of acute HCV infection, PegIFN/RBV versus PegIFN alone, and combination antiretroviral therapy.
Neither severity nor total number of adverse events differed by HCV genotype (2 or 3 versus 1 or 4). Frequency of ribavirin or PegIFN dose reductions did not differ by HCV genotype. Forty-three people (18%) stopped treatment because of toxicity, but the stopping rate did not differ by HCV genotype.
The NEAT investigators concluded that "early antiviral treatment of acute HCV infection in HIV-coinfected individuals results in SVR rates which are far higher regardless of HCV genotype than SVR rates in treatment of chronic HCV coinfection."
Reference
1. Boesecke C, Stellbrink HJ, Mauss S, et al. Does baseline HCV genotype have an impact upon treatment outcome of acute HCV infection in HIV co-infected individuals. 18th Conference on Retroviruses and Opportunistic Infections. February 27-March 2, 2011. Boston. Abstract 113.
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