Key result
Amino acid substitutions in the structural proteins (E, GP2, GP3, GP4, and GP5) of the equine arteritis virus enabled the establishment of persistent infection in low-passage HeLa cells.
Population
High-passage-number human cervix cells and low-passage-number human cervix cells
Design
Preclinical
Authors
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Establishes an in vitro EAV persistence model; leaves open in vivo relevance and broader arterivirus applications.
An in vitro model of EAV persistence in cell culture was established, demonstrating that specific substitutions in viral structural proteins are responsible for establishing persistent infection.
Zhang et al. (2008) studied Equine Arteritis Virus (EAV) infection. HeLa-H-EAVP80 virus and recombinant viruses vs. Virulent Bucyrus (VB) strain of EAV was evaluated on Establishment of persistent infection in HeLa-L cells. Amino acid substitutions in the structural proteins (E, GP2, GP3, GP4, and GP5) of the equine arteritis virus enabled the establishment of persistent infection in low-passage HeLa cells.
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