Murid herpesvirus-4 lacking thymidine kinase reveals route-dependent requirements for host colonization

Gill, Michael B., Wright, Debbie E., Smith, Christopher M., May, Janet S. and Stevenson, Philip G. (2009) Murid herpesvirus-4 lacking thymidine kinase reveals route-dependent requirements for host colonization. Journal of General Virology, 90 6: 1461-1470. doi:10.1099/vir.0.010603-0


Author Gill, Michael B.
Wright, Debbie E.
Smith, Christopher M.
May, Janet S.
Stevenson, Philip G.
Title Murid herpesvirus-4 lacking thymidine kinase reveals route-dependent requirements for host colonization
Journal name Journal of General Virology   Check publisher's open access policy
ISSN 0022-1317
1465-2099
Publication date 2009-01-01
Year available 2009
Sub-type Article (original research)
DOI 10.1099/vir.0.010603-0
Volume 90
Issue 6
Start page 1461
End page 1470
Total pages 10
Place of publication Reading, Berks, United Kingdom
Publisher Society for General Microbiology
Language eng
Subject 2406 Virology
Abstract Gammaherpesviruses infect at least 90% of the world's population. Infection control is difficult, in part because some fundamental features of host colonization remain unknown, for example whether normal latency establishment requires viral lytic functions. Since human gammaherpesviruses have narrow species tropisms, answering such questions requires animal models. Murid herpesvirus-4 (MuHV-4) provides one of the most tractable. MuHV-4 genomes delivered to the lung or peritoneum persist without lytic replication. However, they fail to disseminate systemically, suggesting that the outcome is inoculation route-dependent. After upper respiratory tract inoculation, MuHV-4 infects mice without involving the lungs or peritoneum. We examined whether host entry by this less invasive route requires the viral thymidine kinase (TK), a gene classically essential for lytic replication in terminally differentiated cells. MuHV-4 TK knockouts delivered to the lung or peritoneum were attenuated but still reached lymphoid tissue. In contrast, TK knockouts delivered to the upper respiratory tract largely failed to establish a detectable infection. Therefore TK, and by implication lytic replication, is required for MuHV-4 to establish a significant infection by a non-invasive route.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Clinical Medical Virology Centre Publications
 
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