Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants

Coxsackieviruses (CVs) belong to the genus Enterovirus and family Picornaviridae. Mutants can arise within the replication cycle of RNA viruses. The prototype CVB2 Ohio-1 (CVB2/O) strain adapted to rhabdomyosarcoma (RD) cells induced cytolytic infection and showed three-point mutations in the genome...

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Main Authors: Maria Borsanyiova, Katarina Berakova, Brigita Benkoova, Michaela Pellerova, A. Michael Lindberg, Shubhada Bopegamage
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-07-01
Series:Acta Virologica
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Online Access:https://www.frontierspartnerships.org/articles/10.3389/av.2025.12740/full
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author Maria Borsanyiova
Katarina Berakova
Brigita Benkoova
Michaela Pellerova
A. Michael Lindberg
Shubhada Bopegamage
author_facet Maria Borsanyiova
Katarina Berakova
Brigita Benkoova
Michaela Pellerova
A. Michael Lindberg
Shubhada Bopegamage
author_sort Maria Borsanyiova
collection DOAJ
description Coxsackieviruses (CVs) belong to the genus Enterovirus and family Picornaviridae. Mutants can arise within the replication cycle of RNA viruses. The prototype CVB2 Ohio-1 (CVB2/O) strain adapted to rhabdomyosarcoma (RD) cells induced cytolytic infection and showed three-point mutations in the genome (CVB2/O/RD). The aim of this experimental study was to compare the effect of one or multiple viral mutations in viral protein 1 (VP1) or region 2C of CVB2/O on pathogenesis in two different mouse models. Male A/J and CD1 (10–12 g) mice were infected intraperitoneally with CVB2/O and its mutants or mock infected (control mice). Mice were sacrificed on days 0, 5, 7, 10, and 55 post infection. Blood, heart, and pancreas were collected for virological and histopathological analysis. The presence of viral RNA in the heart and pancreas of infected mice was studied. Different cytokines were detected in the serum. Pathological changes were absent in the hearts of infected mice. Maximum pathological changes were identified in the pancreas of infected A/J mice. Infiltration of pancreatic cells was observed depending on the mouse strain and mutants. CD1 mice were less susceptible to CVB2 infection. CVB2/O/VP1-Q164K mutant induced maximum changes in the pancreas of A/J-infected mice. We suggest that the single altered amino acid in the VP1 protein was related to the virulence factor and was associated with the pathology and presence of viral RNA in the pancreas of infected A/J mice.
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spelling doaj-art-38f5d6a12c5d4ad0b0c084f7ecda99602025-08-20T02:46:43ZengFrontiers Media S.A.Acta Virologica1336-23052025-07-016910.3389/av.2025.1274012740Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutantsMaria Borsanyiova0Katarina Berakova1Brigita Benkoova2Michaela Pellerova3A. Michael Lindberg4Shubhada Bopegamage5Enterovirus Laboratory, Institute of Microbiology, Faculty of Medicine, Slovak Medical University, Bratislava, SlovakiaDepartment of Pathology, Martinske Biopticke Centrum, s.r.o, Žilina, SlovakiaViral Hepatitis Laboratory, Institute of Microbiology, Faculty of Medicine, Slovak Medical University, Bratislava, SlovakiaEnterovirus Laboratory, Institute of Microbiology, Faculty of Medicine, Slovak Medical University, Bratislava, SlovakiaDepartment of Chemistry and Biomedical Sciences, Faculty of Health and Life Sciences, Linnaeus University, Kalmar, SwedenEnterovirus Laboratory, Institute of Microbiology, Faculty of Medicine, Slovak Medical University, Bratislava, SlovakiaCoxsackieviruses (CVs) belong to the genus Enterovirus and family Picornaviridae. Mutants can arise within the replication cycle of RNA viruses. The prototype CVB2 Ohio-1 (CVB2/O) strain adapted to rhabdomyosarcoma (RD) cells induced cytolytic infection and showed three-point mutations in the genome (CVB2/O/RD). The aim of this experimental study was to compare the effect of one or multiple viral mutations in viral protein 1 (VP1) or region 2C of CVB2/O on pathogenesis in two different mouse models. Male A/J and CD1 (10–12 g) mice were infected intraperitoneally with CVB2/O and its mutants or mock infected (control mice). Mice were sacrificed on days 0, 5, 7, 10, and 55 post infection. Blood, heart, and pancreas were collected for virological and histopathological analysis. The presence of viral RNA in the heart and pancreas of infected mice was studied. Different cytokines were detected in the serum. Pathological changes were absent in the hearts of infected mice. Maximum pathological changes were identified in the pancreas of infected A/J mice. Infiltration of pancreatic cells was observed depending on the mouse strain and mutants. CD1 mice were less susceptible to CVB2 infection. CVB2/O/VP1-Q164K mutant induced maximum changes in the pancreas of A/J-infected mice. We suggest that the single altered amino acid in the VP1 protein was related to the virulence factor and was associated with the pathology and presence of viral RNA in the pancreas of infected A/J mice.https://www.frontierspartnerships.org/articles/10.3389/av.2025.12740/fullcoxsackievirus B2mouse modelintraperitoneal infectionpathogenesismutant
spellingShingle Maria Borsanyiova
Katarina Berakova
Brigita Benkoova
Michaela Pellerova
A. Michael Lindberg
Shubhada Bopegamage
Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants
Acta Virologica
coxsackievirus B2
mouse model
intraperitoneal infection
pathogenesis
mutant
title Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants
title_full Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants
title_fullStr Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants
title_full_unstemmed Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants
title_short Intraperitoneal infection of A/J and CD1 mice with coxsackievirus B2 and its mutants
title_sort intraperitoneal infection of a j and cd1 mice with coxsackievirus b2 and its mutants
topic coxsackievirus B2
mouse model
intraperitoneal infection
pathogenesis
mutant
url https://www.frontierspartnerships.org/articles/10.3389/av.2025.12740/full
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