Hepatovirus 3ABC proteases and evolution of mitochondrial antiviral signaling protein (MAVS).
Chymotrypsin-like protease
Cross-species transmission
Innate immunity
Virus evolution
hepatitis A virus
Journal
Journal of hepatology
ISSN: 1600-0641
Titre abrégé: J Hepatol
Pays: Netherlands
ID NLM: 8503886
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
received:
24
11
2018
revised:
31
01
2019
accepted:
19
02
2019
pubmed:
17
3
2019
medline:
15
12
2020
entrez:
17
3
2019
Statut:
ppublish
Résumé
Unlike other hepatitis viruses that have infected primates for millions of years, hepatitis A virus (HAV) likely entered human populations only 10-12 thousand years ago after jumping from a rodent host. The phylogeny of modern hepatoviruses that infect rodents and bats suggest that multiple similar host shifts have occurred in the past. The factors determining such shifts are unknown, but the capacity to overcome innate antiviral responses in a foreign species is likely key. We assessed the capacity of diverse hepatovirus 3ABC proteases to cleave mitochondrial antiviral signaling protein (MAVS) and disrupt antiviral signaling in HEK293 and human hepatocyte-derived cell lines. We also applied maximum-likelihood and Bayesian algorithms to identify sites of diversifying selection in MAVS orthologs from 75 chiropteran, rodent and primate species. 3ABC proteases from bat, but not rodent hepatoviruses efficiently cleaved human MAVS at Glu 3ABC protease cleavage of MAVS is a conserved attribute of hepatoviruses, acting broadly across different mammalian species and associated with evidence of diversifying selection at cleavage sites in rodent and bat MAVS orthologs. The capacity of hepatoviruses to disrupt MAVS-mediated innate immune responses has shaped evolution of both hepatoviruses and their hosts, and facilitates cross-species transmission of hepatitis A. Hepatitis A virus, a common cause of acute hepatitis globally, is likely to have evolved from a virus that jumped from a rodent species to humans within the last 10-12 thousand years. Here we show that distantly related hepatoviruses, that infect bats and rodents today, express proteases that disrupt innate antiviral responses in human cells. This conserved attribute of hepatoviruses may have contributed to that ancient host species shift.
Sections du résumé
BACKGROUND & AIMS
Unlike other hepatitis viruses that have infected primates for millions of years, hepatitis A virus (HAV) likely entered human populations only 10-12 thousand years ago after jumping from a rodent host. The phylogeny of modern hepatoviruses that infect rodents and bats suggest that multiple similar host shifts have occurred in the past. The factors determining such shifts are unknown, but the capacity to overcome innate antiviral responses in a foreign species is likely key.
METHODS
We assessed the capacity of diverse hepatovirus 3ABC proteases to cleave mitochondrial antiviral signaling protein (MAVS) and disrupt antiviral signaling in HEK293 and human hepatocyte-derived cell lines. We also applied maximum-likelihood and Bayesian algorithms to identify sites of diversifying selection in MAVS orthologs from 75 chiropteran, rodent and primate species.
RESULTS
3ABC proteases from bat, but not rodent hepatoviruses efficiently cleaved human MAVS at Glu
CONCLUSIONS
3ABC protease cleavage of MAVS is a conserved attribute of hepatoviruses, acting broadly across different mammalian species and associated with evidence of diversifying selection at cleavage sites in rodent and bat MAVS orthologs. The capacity of hepatoviruses to disrupt MAVS-mediated innate immune responses has shaped evolution of both hepatoviruses and their hosts, and facilitates cross-species transmission of hepatitis A.
LAY SUMMARY
Hepatitis A virus, a common cause of acute hepatitis globally, is likely to have evolved from a virus that jumped from a rodent species to humans within the last 10-12 thousand years. Here we show that distantly related hepatoviruses, that infect bats and rodents today, express proteases that disrupt innate antiviral responses in human cells. This conserved attribute of hepatoviruses may have contributed to that ancient host species shift.
Identifiants
pubmed: 30876947
pii: S0168-8278(19)30141-2
doi: 10.1016/j.jhep.2019.02.020
pmc: PMC6581616
mid: NIHMS1526823
pii:
doi:
Substances chimiques
3ABC protein, virus
0
Adaptor Proteins, Signal Transducing
0
MAVS protein, human
0
Viral Nonstructural Proteins
0
Viral Proteases
EC 3.4.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
25-34Subventions
Organisme : NIAID NIH HHS
ID : R01 AI103083
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI131685
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI109965
Pays : United States
Informations de copyright
Copyright © 2019 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
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