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Use of a rodent model to show that varicella‐zoster virus ORF61 is dispensable for establishment of latency
Author(s) -
Sato Hitoshi,
Pesnicak Lesley,
Cohen Jeffrey I.
Publication year - 2003
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10326
Subject(s) - virology , virus , biology , latent virus , infectivity , virus latency , latency (audio) , varicella zoster virus , mutant , gene , viral replication , genetics , electrical engineering , engineering
Varicella‐zoster virus (VZV) results in a latent infection in humans after primary infection. Latency has also been established in guinea pigs and rats after inoculation with the virus. It was found that infection of cotton rats with the Oka vaccine strain of VZV results in a latent infection. To begin to identify which genes are required for latency, we infected cotton rats with VZV strain Oka that is deleted for ORF61. ORF61 protein transactivates certain VZV promoters and enhances the infectivity of viral DNA in transient transfections. Deletion of ORF61 results in abnormal syncytia and impairs the growth of VZV in vitro. Inoculation of cotton rats with ORF61‐deleted Oka virus resulted in latent VZV infection in the nervous system similar to that seen for animals infected with parental virus. Thus, the cotton rat can be used to study the ability of mutants in the Oka vaccine strain of VZV to establish latent infection. J. Med. Virol. 70:S79–S81, 2003. © 2003 Wiley‐Liss, Inc.