info:eu-repo/semantics/article
Role of viral load in Hepatitis B virus evolution in persistently normal ALT chronically infected patients
Fecha
2019-01Registro en:
Gauder, Catalina; Mojsiejczuk, Laura Noelia; Tadey, Luciana; Mammana, Lilia; Bouzas, Maria Belen; et al.; Role of viral load in Hepatitis B virus evolution in persistently normal ALT chronically infected patients; Elsevier Science; Infection, Genetics and Evolution; 67; 1-2019; 17-22
1567-1348
CONICET Digital
CONICET
Autor
Gauder, Catalina
Mojsiejczuk, Laura Noelia
Tadey, Luciana
Mammana, Lilia
Bouzas, Maria Belen
Campos, Rodolfo Hector
Flichman, Diego Martin
Resumen
Chronic HBV infection has been associated with severe liver disease although most of them do not progress to this stage. Even though low replicative carriers form the largest group of HBV chronically infected patients, there is a paucity of longitudinal studies to evaluate the molecular evolution of the whole genome in this subset of patients. In this study, longitudinal samples from 10 patients with persistently normal ALT levels were collected. HBV full-length genome sequences were obtained from 3 samples per patient (baseline, 5 and 10-years of follow-up). Patients were grouped according to HBV-DNA level into <103 IU/ml (group A) or > 103 IU/ml (group B). The substitution rate was inversely related with HBV-DNA levels. Moreover, the rate in the 10-year follow-up was significantly higher in group A (6.9 × 10−4 ± 1.3 × 10−4) than group B (2.7 × 10−4 ± 7.4 × 10−5 substitution/site/year, p < .001). Most of the substitutions were in the Core region and the majority were non-synonymous changes. The rate of nucleotide substitution was inversely related to HBV-DNA levels, highlighting the role of viral load in the HBV intra-host dynamics, even in low replicative state patients. Moreover, the difference in the substitution rate between the analysed groups was mainly consequence of substitutions restricted to the Core region, particularly in the simple coding region and antigenic epitopes, which suggest that the immune pressure drives the different evolutionary behaviour of groups.