Inhibition of natural killer cells by a cytomegalovirus MHC class I homologue in vivo

H. E. Farrell, H. Vally, D. M. Lynch, P. Fleming, G. R. Shellam, A. A. Scalzo and N. J. Davis-Poynter
Additional contact information
H. E. Farrell: University of Western Australia, Queen Elizabeth II Medical Centre
H. Vally: University of Western Australia, Queen Elizabeth II Medical Centre
D. M. Lynch: University of Western Australia, Queen Elizabeth II Medical Centre
P. Fleming: University of Western Australia, Queen Elizabeth II Medical Centre
G. R. Shellam: University of Western Australia, Queen Elizabeth II Medical Centre
A. A. Scalzo: University of Western Australia, Queen Elizabeth II Medical Centre
N. J. Davis-Poynter: University of Western Australia, Queen Elizabeth II Medical Centre

Nature, 1997, vol. 386, issue 6624, 510-514

Abstract: Abstract Herpesviruses, such as murine and human cytomegalovirus (MCMV and HCMV), can establish a persistent infection within the host and have diverse mechanisms as protection from host immune defences1. Several herpesvirus genes that are homologous to host immune modulators have been identified, and are implicated in viral evasion of the host immune response2,3. The discovery of a viral major histocompatibility complex (MHC) class I homologue, encoded by HCMV4, led to speculation that it might function as an immune modulator and disrupt presentation of peptides by MHC class I to cytotoxic T cells5. However, there is no evidence concerning the biological significance of this gene during viral infection. Recent analysis of the MCMV genome has also demonstrated the presence of a MHC class I homologue6. Here we show that a recombinant MCMV, in which the gene encoding the class I homologue has been disrupted, has severely restricted replication during the acute stage of infection compared with wild-type MCMV We demonstrate by in vivo depletion studies that natural killer (NK) cells are responsible for the attenuated phenotype of the mutant. Thus the viral MHC class I homologue contributes to immune evasion through interference with NK cell-mediated clearance.

Date: 1997
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/386510a0 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:386:y:1997:i:6624:d:10.1038_386510a0

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/386510a0

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().