The genetic variability of genotype F1b Hepatitis B virus core gene is associated with the outcome of acute hepatitis. Results from the acute hepatitis B global study

MARCIANO S; MENDIZABAL M; CALZETTA P; FLICHMAN D; MARCIANO S; MENDIZABAL M; CALZETTA P; FLICHMAN D; TRINKS J ; FRANCO A; ESPOSITO I; ARRIGO D; LIVELLARA B; GIUNTA D; VUJACICH C; TRINKS J ; GADANO A; FRANCO A; ESPOSITO I; ARRIGO D; GIUNTA D; LIVELLARA B; VUJACICH C; GADANO A

Punta Cana

Congreso; XXV Congreso de la Asociación Latinoamericana para el Estudio del Hígado; 2018

Asociación Latinoamericana para el Estudio de las Enfermedades del Hígado (ALEH)

Background. Acute hepatitis B virus (HBV) infection in adults spontaneously resolves in most cases, but can induce acute liver failure (ALF) or evolve to chronic hepatitis (CH) in some patients. Viral and host genetic variability have been associated with the development of CH and/or ALF in some HBV genotypes. Aim. To analyze the association of viral and host genetic variability with the outcome of acute HBV infection in patients infected with genotype F1b. Material and methods. In the Global Study 200 patients with acute HBV were prospectively included. Patients were followed for 6 months and divided into two groups according to the evolution of the acute infection: group 1 including patients who resolved the infection (HBsAg clearance during the follow up) and showed preserved liver function during the evolution; and group 2 including patients who evolved to CH (HBsAg persistence > 6 months of follow up) or developed acute severe hepatitis (prothrombin time < 50% without encephalopathy) or ALF (prothrombin time < 50% and any grade of hepatic encephalopathy). In the present sub-study only patients infected with HBV genotype F1b were included. The association of viral and host variables (detailed in table 1) with the evolution of the acute hepatitis was explored with bivariate statistics. Results. 26 patients were included: 10 in group 1 (resolved infection) and 16 in the group 2 (10 with evolution to CH; 6 with acute severe hepatitis or ALF). Comparison among groups is shown in the table 1. The rs3077-C and rs2856718-C alleles were recessively associated with evolution to CH and HBsAg clearance, respectively. The number of pre-core/core mutations, pre-core/core mutation rate and Shannon entropy were significantly higher in group 2 patients. Conclusions. These results suggest that apart from the previously described host genetic diversity, the genetic variability of the HBV core gene is associated with an unfavorable evolution of acute hepatitis B in patients infected with genotype F1b.