Franklin Steve Azebaze Agueguia^1,, Paul Talla², Marie Claire Okomo Assoumou³, Cedric Happi Mbakam¹, Elise Guiedem¹, Martha Tongo Mesembe¹, Emilia Lyonga¹, George Mondinde Ikomey¹

In Chronic Viral Hepatitis B (VHB), the mechanisms of the CD95-CD178 signaling pathway, and the associated genetic polymorphism, together with the cirrhotic process remains unclear. We evaluate the involvement of CD95-CD178 and associated genetic polymorphisms in viral persistence and hepatic cytolysis in patients with chronic VHB. Whole blood from 343 Chronic VHB patients were collected and, CD95 and CD178 levels were performed by Flow cytometry and ELISA, respectively. Genotyping of CD95-670 A/G, CD95-1377 G/A and CD178-844 C/T polymorphisms was performed using PCR-RFLP. The searches and quantifications of the DNA of the HBV were carried out by qPCR. Data were analyzed using GraphPad PRISM 7.0, with the significance threshold set at p ≤ 0.05 and a 95% confidence interval. Out of 343 patients, 105 (30.61%) were healthy and 238 (69.39%) were HBV-infected. Plasma levels of CD95 and CD178 were significantly elevated in HBV-infected patients compared to healthy patients, and in cirrhotic patients compared to non-cirrhotic patients. There were statistically significant correlations between CD95 and fibrosis scores, between CD95 and HBV viral load, between CD178 and fibrosis scores, between CD178 and HBV viral load, and between HBV viral load and the fibrosis score. The genotypic frequencies of CD95-670 A/G and CD178-844 C/T were significantly different between infected and healthy patients. Increased expression of CD95-670 A/G AG genotypes, CD95-1377 G/A GG genotypes, and CD178-844 C/T CT genotypes are associated with the severity of hepatic fibrosis, overexpression of CD95 and CD178 in patients infected with HBV, and by implication, the increase and persistence of the viral load of the Hepatitis B virus (HBV).

VHB, CD95-CD178, genetic polymorphism, HVB viral load, fibrosis, cirrhosis