Abstract:
:While trying to generate a site-directed deletion in the ORF63 latency-associated gene of varicella-zoster virus (VZV) Oka, we constructed a virus with an unexpected rearrangement. The virus has a small deletion in both copies of ORF63 and two copies of a cassette inserted between ORFs 64/65 and 68/69 containing (a) truncated ORF62, (b) ORF63 with a small deletion, and (c) full-length ORF64. The virus was not impaired for growth in human cells, induced higher levels of neutralizing antibodies in guinea pigs, and was impaired for latency in cotton rats compared with parental virus (p=0.0022). Additional mutants containing the same truncation in ORF62, with or without the ORF63 deletion, were less impaired for latency. A VZV Oka mutant, replicating to similar titers and inducing a comparable immune response as parental virus, but impaired for latency, might serve as a safer vaccine and be less likely to reactivate to cause zoster.
journal_name
Virologyjournal_title
Virologyauthors
Ambagala AP,Krogmann T,Qin J,Pesnicak L,Cohen JIdoi
10.1016/j.virol.2010.01.007subject
Has Abstractpub_date
2010-04-10 00:00:00pages
194-200issue
2eissn
0042-6822issn
1096-0341pii
S0042-6822(10)00017-6journal_volume
399pub_type
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