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

Maria Borsanyiova^1*Katarina Berakova²Brigita Benkoova³Michaela Pospisilova¹A. Michael Lindberg⁴Shubhada Bopegamage¹

• ¹Enterovirus Laboratory, Institute of Microbiology, Faculty of Medicine, Slovak Medical University, Bratislava, Slovakia
• ²Department of Pathology, Martin Bioptic Center, s.r.o, Zilina, Zilina, Slovakia
• ³Viral Hepatitis Laboratory, Institute of Microbiology, Faculty of Medicine, Slovak Medical University, Bratislava, Slovakia
• ⁴Department of Chemistry and Biomedical Sciences, Faculty of Health and Life Sciences, Linnaeus University, Kalmar, Sweden

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 in the serum were detected. 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 mice strains 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.