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The simian varicella virus genome contains an invertible 665 base pair terminal element that is absent in the varicella zoster virus genome.

ABSTRACT: Simian varicella virus (SVV) causes chickenpox in monkeys, establishes latency and reactivates to produce zoster thus providing a model to study human varicella zoster virus (VZV) infection. Sequence analysis of a recombinant cosmid clone containing the left end of the SVV genome revealed a 665 base pair (bp) segment that is absent in VZV DNA. This segment inverts and contains 507 bp of unique sequences flanked on either side by 79 bp inverted repeats, making the SVV genome to be 124,785 bp in size. Part of the inverted repeat sequence (64 bp) is also present at the junction of the long and short segments of the SVV genome. The terminal DNA sequences are conserved among different SVV isolates and present in tissues from infected monkeys. The terminal region is transcriptionally active and is also present in the genomes of other animal varicelloviruses but absent in the VZV genome.

SUBMITTER: Mahalingam R

PROVIDER: S-EPMC2023966 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature

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The simian varicella virus genome contains an invertible 665 base pair terminal element that is absent in the varicella zoster virus genome.

Mahalingam Ravi R Gray Wayne L WL

Virology 20070606 2

Simian varicella virus (SVV) causes chickenpox in monkeys, establishes latency and reactivates to produce zoster thus providing a model to study human varicella zoster virus (VZV) infection. Sequence analysis of a recombinant cosmid clone containing the left end of the SVV genome revealed a 665 base pair (bp) segment that is absent in VZV DNA. This segment inverts and contains 507 bp of unique sequences flanked on either side by 79 bp inverted repeats, making the SVV genome to be 124,785 bp in s ...[more]

PMID: 17555785

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Project description:Varicella-zoster virus (VZV) is a human herpesvirus, which during primary infection typically causes varicella (chicken pox) and establishes lifelong latency in sensory and autonomic ganglia. Later in life, the virus may reactivate to cause herpes zoster (HZ; also known as shingles). To prevent these diseases, a live-attenuated heterogeneous vaccine preparation, vOka, is used routinely in many countries worldwide. Recent studies of another alphaherpes virus, infectious laryngotracheitis virus, demonstrate that live-attenuated vaccine strains can recombine in vivo, creating virulent progeny. These findings raised concerns about using attenuated herpesvirus vaccines under conditions that favor recombination. To investigate whether VZV may undergo recombination, which is a prerequisite for VZV vaccination to create such conditions, we here analyzed 115 complete VZV genomes. Our results demonstrate that recombination occurs frequently for VZV. It thus seems that VZV is fully capable of recombination if given the opportunity, which may have important implications for continued VZV vaccination. Although no interclade vaccine wild-type recombinant strains were found, intraclade recombinants were frequently detected in clade 2, which harbors the vaccine strains, suggesting that the vaccine strains have already been involved in recombination events, either in vivo or in vitro during passages in cell culture. Finally, previous partial and complete genomic studies have described strains that do not cluster phylogenetically to any of the five established clades. The additional VZV strains sequenced here, in combination with those previously published, have enabled us to formally define a novel sixth VZV clade.Although genetic recombination has been demonstrated to frequently occur for other human alphaherpesviruses, herpes simplex viruses 1 and 2, only a few ancient and isolated recent recombination events have hitherto been demonstrated for VZV. In the present study, we demonstrate that VZV also frequently undergoes genetic recombination, including strains belonging to the clade containing the vOKA strain.

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The simian varicella virus genome contains an invertible 665 base pair terminal element that is absent in the varicella zoster virus genome.

Publications

The simian varicella virus genome contains an invertible 665 base pair terminal element that is absent in the varicella zoster virus genome.

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