%0 Journal Article
%T Expression of the UL16 glycoprotein of Human Cytomegalovirus protects the virus-infected cell from attack by natural killer cells
%A Mar Val¨¦s-G¨®mez
%A Helena Browne
%A Hugh T Reyburn
%J BMC Immunology
%D 2003
%I BioMed Central
%R 10.1186/1471-2172-4-4
%X Cells infected with the UL16 knockout virus were killed at substantially higher levels than cells infected with the wild-type virus. This increased killing could be correlated with a UL16-dependent reduction in surface expression of ligands for the NK cell activating receptor NKG2D.Expression of the UL16 glycoprotein was associated with protection of HCMV-infected cells from NK cell attack. This observation could be correlated with the downregulation of cell surface expression of NKG2D ligands. These data represent a first step towards understanding the mechanism(s) of action of the UL16 protein.Cytomegaloviruses (CMVs) are members of the ¦Â subgroup of the Herpesvirus family. Cytomegalovirus infection can be associated with severe, even fatal disease, but in the immunocompetent host, primary infection with CMV is normally controlled by the immune system. This immune control does not result in complete elimination of the virus. Instead, the virus persists for the lifetime of the host with occasional episodes of virus reactivation and shedding. One aspect of CMV biology that almost certainly contributes to this state of permanent cohabitation is that CMVs have acquired during their evolution an extensive repertoire of gene products that can function to modulate immune recognition of the virus and virus-infected cell. Human cytomegalovirus (HCMV), for example, encodes genes whose protein products are able to modulate or inhibit the action of virtually all the arms of the antiviral immune response, ie. interference with the presentation of viral antigens to CTLs, manipulation of cytokine responses, intervention on NK cell cytotoxicity and complement response (reviewed in [1,2]).The MHC class I restricted antigen presentation pathway is a particular target for HCMV immune subversion strategies, presumably because MHC class I restricted CD8+ cytotoxic T lymphocytes are critical effectors in the host defence against CMV infection [3-5]. However, other things being equal, a
%U http://www.biomedcentral.com/1471-2172/4/4