The murine cytomegalovirus chemokine homolog, m131/129, is a determinant of viral pathogenicity

Fleming, Peter, Davis-Poynter, Nicholas, Degli-Esposti, Mariapia, Densley, Eloise, Papadimitriou, John, Shellam, Geoffrey and Farrell, Helen (1999) The murine cytomegalovirus chemokine homolog, m131/129, is a determinant of viral pathogenicity. Journal of Virology, 73 8: 6800-6809.

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ35692_OA.pdf Full text (open access) application/pdf 1.99MB 0
Author Fleming, Peter
Davis-Poynter, Nicholas
Degli-Esposti, Mariapia
Densley, Eloise
Papadimitriou, John
Shellam, Geoffrey
Farrell, Helen
Title The murine cytomegalovirus chemokine homolog, m131/129, is a determinant of viral pathogenicity
Journal name Journal of Virology   Check publisher's open access policy
ISSN 0022-538X
1098-5514
Publication date 1999-08-01
Year available 1999
Sub-type Article (original research)
Open Access Status File (Publisher version)
Volume 73
Issue 8
Start page 6800
End page 6809
Total pages 10
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Subject 1103 Clinical Sciences
Abstract Chemokines are important mediators of the early inflammatory response to infection and modify a wide range of host immune responses. Functional homologs of cellular chemokines have been identified in a number of herpesviruses, suggesting that the subversion of the host chemokine response contributes to the pathogenesis of these viruses. Transcriptional and reverse transcription-PCR analyses demonstrated that the murine cytomegalovirus (MCMV) chemokine homolog, m131, was spliced at the 3' end to the adjacent downstream open reading frame, m129, resulting in a predicted product of 31 kDa, which is significantly larger than most known chemokines. The in vivo impact of m131/129 was investigated by comparing the replication of MCMV mutants having m131/129 deleted (Delta m131/129) with that of wild-type (wt) MCMV. Our studies demonstrate that both wt and Delta m131/129 viruses replicated to equivalent levels during the first 2 to 3 days following in vivo infection. However, histological studies demonstrated that the early inflammatory response elicited by Delta m131/129 was reduced compared with that of wt MCMV. Furthermore, the Delta m131/129 mutants failed to establish a high-titer infection in the salivary glands, These results suggest that m131/129 possesses proinflammatory properties in vivo and is important for the dissemination of MCMV to or infection of the salivary gland. Notably, the Delta m131/129 mutants were cleared more rapidly from the spleen and liver during acute infection compared with wt MCMV. The accelerated clearance of the mutants was dependent on NK cells and cells of the CD4(+) CD8(+) phenotype. These data suggest that m131/129 may also contribute to virus mechanisms of immune system evasion during early infection, possibly through the interference of NK cells and T cells.
Keyword Virology
Dna-sequence
Interferon-gamma
Virus Type-1
Receptor
Infection
Protein
Poxvirus
Inflammation
Herpesvirus
Encodes
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: Clinical Medical Virology Centre Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 93 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 0 times in Scopus Article
Google Scholar Search Google Scholar
Created: Mon, 13 Aug 2007, 11:14:43 EST