Key result
Reverse genetic analysis demonstrated that recombination of capsid proteins (VP1 and/or VP2) between Saffold virus and Theiler's murine encephalomyelitis virus did not produce viable virus.
Reverse genetic analysis demonstrates that natural recombination of capsid proteins between Saffold virus and Theiler's murine encephalomyelitis virus does not occur, suggesting host range shifts via this mechanism are unlikely.
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Constrains picornavirus recombination models; leaves open non-capsid mechanisms for host-range shifts in vivo.
Saffold virus (SAFV) which belongs to the species Theilovirus of the genus Cardiovirus of the family Picornaviridae is a novel human cardiovirus identified in 2007. However, the pathogenicity of SAFV to humans still remains unclear. Recent studies by the phylogenetic and recombination analyses of Theilovirus suggest that there are no recombination events between viruses of the different type (e.g. SAFV and Theiler’s murine encephalomyelitis virus (TMEV)). Information on the recombination events of these viruses will be helpful to better understand the host specificity and pathogenicity of SAFV. In the present study, we performed the reverse genetic analysis to investigate the possibility of the recombination between SAFV and TMEV. The recombination of the capsid protein (VP1 and/or VP2) by reverse genetics between SAFV and TMEV did not happen, although the recombination of the non-capsid protein, L, occurred. These results strongly suggest that the shift of host range from rodents to humans or from humans to rodents by natural recombination of capsid protein(s) within Theiloviruses does not happen. The present results will provide the valuable information for the studies on the pathogenicity of SAFV.
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Himeda et al. (2011) studied Theilovirus infection (in vitro). Reverse genetic recombination of capsid (VP1/VP2) and non-capsid (L) proteins vs. Original viruses (SAFV-3, TMEV-DA, TMEV-GDVII) was evaluated on Production of infectious viral particles (cytopathic effects and viral titers). Reverse genetic analysis demonstrated that recombination of capsid proteins (VP1 and/or VP2) between Saffold virus and Theiler's murine encephalomyelitis virus did not produce viable virus.
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