Construction of Varicella-Zoster Virus Recombinants from Parent Oka Cosmids and Demonstration that ORF65 Protein Is Dispensable for Infection of Human Skin and T Cells in the SCID-hu Mouse Model

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Abstract
We generated an ORF65 deletion mutant by using a cosmid system constructed from the genome of a low-passage clinical isolate (P-Oka). Using the SCID-hu mouse model, we demonstrated that the ORF65 protein is dispensable for viral replication in skin and T cells, which are critical host cell targets during primary varicella-zoster virus infection.