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.
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.
Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA.
Takahiro
T
Niizuma
Leigh
L
Zerboni
Marvin H
MH
Sommer
Hideki
H
Ito
Stewart
S
Hinchliffe
Ann M
AM
Arvin
D000818:Animals; D002644:Chickenpox / Q000503:physiopathology / Q000821:virology; D002522:Chlorocebus aethiops; D003360:Cosmids; D004195:Disease Models, Animal; D017353:Gene Deletion; D006562:Herpes Zoster / Q000503:physiopathology / Q000821:virology; D014645:Herpesvirus 3, Human / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D016513:Mice, SCID; D016366:Open Reading Frames; D011995:Recombination, Genetic; D012867:Skin / Q000821:virology*; D013601:T-Lymphocytes / Q000821:virology*; D014183:Transplantation, Heterologous; D014407:Tumor Cells, Cultured; D014709:Vero Cells; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism*; D014779:Virus Replication
D014764:Viral Proteins