Affiliations: [a] Therapeutic Chemistry Department, Division of Pharmaceutical Industries and Drug Research, National Research Centre, Dokki, Cairo, Egypt | [b] Microbial Biotechnology Department, Division of Genetic Engineering and Biotechnology, National Research Centre, Dokki, Cairo, Egypt
Correspondence:
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Corresponding author: Reem El-Shenawy, Microbial Biotechnology Department, Division of Genetic Engineering and Biotechnology, National Research Centre, Dokki 12622, Cairo, Egypt. Tel.: +20 1001425396; E-mail: reem_elshanaweey@yahoo.com.
Abstract: This study aimed to evaluate the prognostic value of baseline macrophage inflammatory protein (MIP)-1β/IL12p40 ratio for antiviral treatment outcome in HCV genotype 4 patients. METHODS: Sera of 450 treatment-naïve chronic HCV patients and 50 healthy individuals were collected. Liver transaminases, total bilirubin and albumin were biochemically tested, viral RNA was quantified, and circulating MIP-1β and IL-12p40 were estimated using human anti-MIP-1β and IL-12p40 antibodies in Sandwich ELISA. RESULTS: No difference was observed in the baseline chemokines levels between responders and relapsers, but the later had a significantly higher MIP-1β/IL-12p40 ratio (P< 0.0001). Multivariate regression analysis of baseline characteristics showed that gender, age, viral load, albumin level and chemokine ratios can significantly predict treatment outcome (P= 0.0114, 0.0095, 0.042, 0.0004 and < 0.0001; respectively). Accordingly, a predictive threshold of baseline chemokine ratio was calculated and it showed an AUC of 0.6917 (P= 0.0108; 95% CI: 0.5566 to 0.8268). The calculated threshold for predicting virologic response was 8.245, with positive and negative predictive values of 92.98% and 100%; respectively. The chemokine ratios had significant correlations with liver transaminases in treated groups whether pre or post-treatment. CONCLUSION: Baseline MIP-1β/IL-12p40 ratio represents a non-invasive prognostic biomarker that would provide shorter treatment duration and minimizes the emergence of drug-resistant variants in HCV genotype 4-patients.
