Truncated oncoproteins of retroviruses and hepatitis B virus: A lesson in contrasts.
Journal
Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
ISSN: 1567-7257
Titre abrégé: Infect Genet Evol
Pays: Netherlands
ID NLM: 101084138
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
received:
18
03
2019
revised:
14
05
2019
accepted:
27
05
2019
pubmed:
4
6
2019
medline:
2
4
2020
entrez:
2
6
2019
Statut:
ppublish
Résumé
Members of the virus families Retroviridae and Hepadnaviridae use reverse transcriptase (RT) to synthesize a DNA copy of their genomic and pregenomic RNA, respectively, during the viral life cycle. A group of viruses belonging to Retroviridae ("acute transforming" retroviruses) as well as human hepatitis B virus (HBV), the prototype member of Hepadnaviridae (hepadnaviruses) are able to cause malignant neoplasms in infected hosts, due to the expression of pleiotropic "transforming proteins" encoded by the genomes of these reverse-transcribing tumor viruses. In this review we wish to compare the common and unique features of replication strategies characteristic of acute transforming retroviruses and HBV and summarize data related to the origin and evolution of their viral oncogenes either via transduction of cellular genes, or by accumulation of mutations in viral sequences that create a new open reading frame (overprinting). The exons of cellular genes (proto-onc genes or c-onc genes) incorporated into the genome of acute transforming retroviruses are regularly affected by deletions resulting in the expression of truncated viral oncoproteins which are frequently dysregulated compared to their cellular counterparts. These retroviral transforming proteins alter the behavior of their target cells (malignant transformation). HBx, a pleiotropic protein of HBV, regulates virus replication and contributes to hepatocarcinogenesis. In contrast to the v-onc genes of acute transforming retroviruses, the viral gene encoding the full-length, wild-type HBx (wtHBx) protein does not have a cellular counterpart. Mutations and deletions frequently affect, however, the HBV genome as well, resulting in the expression of truncated HBx proteins (trHBx) in liver cells. Truncated, especially C-terminal truncated variants of HBx (Ct-HBX proteins), may facilitate initiation and progression of liver carcinoma.
Identifiants
pubmed: 31152910
pii: S1567-1348(19)30097-8
doi: 10.1016/j.meegid.2019.05.020
pii:
doi:
Substances chimiques
Oncogene Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
342-357Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.