Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia

Shih Heng Chen, Yu Wen Lin, Anthony Griffiths, Wen Yen Huang, Shun Hua Chen

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Laboratory strains of herpes simplex virus lacking thymidine kinase (TK) cannot replicate acutely to detectable levels in mouse trigeminal ganglia and do not reactivate from latency. However, many pathogenic clinical isolates that are resistant to the antiviral drug acyclovir are heterogeneous populations of TK-negative (TK-) and TK-positive (TK+) viruses. To recapitulate this in vivo, mice were infected with mixtures of wild-type virus and a recombinant TK- mutant in various ratios. Following co-infection, the replication, number of latent viral genomes and reactivation efficiency of TK+ virus in trigeminal ganglia were reduced in a manner related to the amount of TK- virus in the inoculum. TK+ virus did not always complement the acute replication or increase the number of latent viral genomes of TK- mutant in mouse ganglia. Even so, TK+ virus could still confer the pathogenic phenotype to a TK- mutant, somehow providing sufficient TK activity in trans to permit a TK- mutant to reactivate from latently infected ganglia.

Original languageEnglish (US)
Pages (from-to)3495-3502
Number of pages8
JournalJournal of General Virology
Volume87
Issue number12
DOIs
StatePublished - Dec 2006
Externally publishedYes

Fingerprint

Trigeminal Ganglion
Thymidine Kinase
Simplexvirus
Coinfection
Viruses
Viral Genome
Ganglia
Acyclovir
Antiviral Agents

ASJC Scopus subject areas

  • Virology
  • Immunology

Cite this

Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia. / Chen, Shih Heng; Lin, Yu Wen; Griffiths, Anthony; Huang, Wen Yen; Chen, Shun Hua.

In: Journal of General Virology, Vol. 87, No. 12, 12.2006, p. 3495-3502.

Research output: Contribution to journalArticle

Chen, Shih Heng ; Lin, Yu Wen ; Griffiths, Anthony ; Huang, Wen Yen ; Chen, Shun Hua. / Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia. In: Journal of General Virology. 2006 ; Vol. 87, No. 12. pp. 3495-3502.
@article{32112366ce1b47e0a49ed8d5df4b6199,
title = "Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia",
abstract = "Laboratory strains of herpes simplex virus lacking thymidine kinase (TK) cannot replicate acutely to detectable levels in mouse trigeminal ganglia and do not reactivate from latency. However, many pathogenic clinical isolates that are resistant to the antiviral drug acyclovir are heterogeneous populations of TK-negative (TK-) and TK-positive (TK+) viruses. To recapitulate this in vivo, mice were infected with mixtures of wild-type virus and a recombinant TK- mutant in various ratios. Following co-infection, the replication, number of latent viral genomes and reactivation efficiency of TK+ virus in trigeminal ganglia were reduced in a manner related to the amount of TK- virus in the inoculum. TK+ virus did not always complement the acute replication or increase the number of latent viral genomes of TK- mutant in mouse ganglia. Even so, TK+ virus could still confer the pathogenic phenotype to a TK- mutant, somehow providing sufficient TK activity in trans to permit a TK- mutant to reactivate from latently infected ganglia.",
author = "Chen, {Shih Heng} and Lin, {Yu Wen} and Anthony Griffiths and Huang, {Wen Yen} and Chen, {Shun Hua}",
year = "2006",
month = "12",
doi = "10.1099/vir.0.82223-0",
language = "English (US)",
volume = "87",
pages = "3495--3502",
journal = "Journal of General Virology",
issn = "0022-1317",
publisher = "Society for General Microbiology",
number = "12",

}

TY - JOUR

T1 - Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia

AU - Chen, Shih Heng

AU - Lin, Yu Wen

AU - Griffiths, Anthony

AU - Huang, Wen Yen

AU - Chen, Shun Hua

PY - 2006/12

Y1 - 2006/12

N2 - Laboratory strains of herpes simplex virus lacking thymidine kinase (TK) cannot replicate acutely to detectable levels in mouse trigeminal ganglia and do not reactivate from latency. However, many pathogenic clinical isolates that are resistant to the antiviral drug acyclovir are heterogeneous populations of TK-negative (TK-) and TK-positive (TK+) viruses. To recapitulate this in vivo, mice were infected with mixtures of wild-type virus and a recombinant TK- mutant in various ratios. Following co-infection, the replication, number of latent viral genomes and reactivation efficiency of TK+ virus in trigeminal ganglia were reduced in a manner related to the amount of TK- virus in the inoculum. TK+ virus did not always complement the acute replication or increase the number of latent viral genomes of TK- mutant in mouse ganglia. Even so, TK+ virus could still confer the pathogenic phenotype to a TK- mutant, somehow providing sufficient TK activity in trans to permit a TK- mutant to reactivate from latently infected ganglia.

AB - Laboratory strains of herpes simplex virus lacking thymidine kinase (TK) cannot replicate acutely to detectable levels in mouse trigeminal ganglia and do not reactivate from latency. However, many pathogenic clinical isolates that are resistant to the antiviral drug acyclovir are heterogeneous populations of TK-negative (TK-) and TK-positive (TK+) viruses. To recapitulate this in vivo, mice were infected with mixtures of wild-type virus and a recombinant TK- mutant in various ratios. Following co-infection, the replication, number of latent viral genomes and reactivation efficiency of TK+ virus in trigeminal ganglia were reduced in a manner related to the amount of TK- virus in the inoculum. TK+ virus did not always complement the acute replication or increase the number of latent viral genomes of TK- mutant in mouse ganglia. Even so, TK+ virus could still confer the pathogenic phenotype to a TK- mutant, somehow providing sufficient TK activity in trans to permit a TK- mutant to reactivate from latently infected ganglia.

UR - http://www.scopus.com/inward/record.url?scp=33751431828&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33751431828&partnerID=8YFLogxK

U2 - 10.1099/vir.0.82223-0

DO - 10.1099/vir.0.82223-0

M3 - Article

C2 - 17098963

AN - SCOPUS:33751431828

VL - 87

SP - 3495

EP - 3502

JO - Journal of General Virology

JF - Journal of General Virology

SN - 0022-1317

IS - 12

ER -