May 20-23, 2001
Preliminary study Results Show HCV in Blood Reflects HCV in Liver Cells
In HCV you frequently here that HCV can be cured as opposed to HIV. HIV requires continuous therapy to control HIV viral load. In HCV, therapy is for a limited defined period of time, usually one year.
Several studies show that in HCV, if a patient has negative HCV viral load 6 months after stopping therapy (called a sustained virologic response) about 95% of the patients sustain PCR negativity 3-11 years of follow-up. This suggests that HCV is different than HIV and may be curable for some patients.
A frequently asked question, since we talk about a cure in HCV, is does reduction or "elimination" of HCV viral load in blood correlate with what is seen in the liver cells.
The preliminary results of this study suggest yes, what you see in the blood correlates with what you see in the liver, suggesting that if you attain PCR negativity 6 months after stopping treatment and sustain that you should see the same in the liver cells.
Further investigation is needed and as time goes by we will be accumulating more data as more patients are treated and we have longer follow-up.
PLASMA HEPATITIS C VIRUS (HCV) RNA IS COMPARABLE TO HEPATIC HCV RNA WHEN
OBTAINED WHILE ON THERAPY AT THE END OF TREATMENT AS A PREDICTOR OF SUSTAINED
RESPONSE IN PATIENTS WITH CHRONIC HEPATITIS C INFECTION
Lino J. Deguzman, Jose M. Nieto, Arrowhead Regional Medical Ctr, Colton, CA; Shelley A. Deguzman, Inland Empire Digest Disease & Liver Ctr, Redlands, CA; Andrew Conrad, National Genetics Institute, Culver City, CA; Bradley Collins, Arrowhead Regional Medical Ctr, Colton, CA
Introduction: Plasma HCV RNA PCR (HCVPCR) is the standard used to determine sustained response (SR) to interferon (IFN) +/- ribavirin. We need to determine if other reservoirs of HCV are more reliable in predicting SR.
The aim of this prospective study was to see if plasma or peripheral blood mononuclear cell (PBMC) HCVPCR could serve as a non-invasive comparison to hepatic HCV PCR in predicting SR at the end of treatment (TX) just prior to cessation of TX.
Methods: 38 pts (19 males)with chronic HCV were TX. 20 pts received std dose Rebetron or induction dose IFN + Ribavirin and 18 pts received IFN monotherapy (3-5MU QD-QOD). The median age was 47 and 47% (18/38) were genotype 1. 26 pts were naive and 12 were previously TX. All pts had a baseline and a 12 month end-of-TX liver biopsy. Using the Superquant Method (NGI), quantitative HCVPCR was simultaneously measured on the plasma, PBMC and hepatic tissue.
Results: The PPV and specificity was 100% in all 3 reservoirs.
Conclusion: As expected,the highest negative predictive value (NPV) or the highest likelihood for a SR was consistently seen in the naive and genotype non-1 pts in all three reservoirs. It is unclear however, why pts treated with IFN monotherapy had a higher NPV than pts TX with Rebetron. >From this data, it appears that quantitative plasma HCVPCR routinely used today closely mimics hepatic HCVPCR in determining response to antiviral therapy. Measurement of hepatic HCVPCR does not seem to add additional information that plasma HCVPCR already provides.