Abstract:
:Cardioviruses cause diseases in many animals including, in rare cases, humans. Although they share common features with all picornaviruses, cardioviruses have unique properties that distinguish them from other family members, including enteroviruses. One feature shared by all picornaviruses is the covalent attachment of VPg to the 5' end of genomic RNA via a phosphotyrosyl linkage. For enteroviruses, this linkage is cleaved by a host cell protein, TDP2. Since TDP2 is divergently required during enterovirus infections, we determined if TDP2 is necessary during infection by the prototype cardiovirus, EMCV. We found that EMCV yields are reduced in the absence of TDP2. We observed a decrease in viral protein accumulation and viral RNA replication in the absence of TDP2. In contrast to enterovirus infections, we found that TDP2 is modified at peak times of EMCV infection. This finding suggests a unique mechanism for cardioviruses to regulate TDP2 activity during infection.
journal_name
Virologyjournal_title
Virologyauthors
Maciejewski S,Ullmer W,Semler BLdoi
10.1016/j.virol.2018.01.010subject
Has Abstractpub_date
2018-03-01 00:00:00pages
139-146eissn
0042-6822issn
1096-0341pii
S0042-6822(18)30010-2journal_volume
516pub_type
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