Naslov
Cytomegaloviral evasion of T cell and NK cell responses

Autori
Jonjić, Stipan

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Drugi hrvatski mikrobiološki kongres s međunarodnim sudjelovanjem-priopćenja / Prukner-Radovčić, Estella ; Hajsig, Danko ; Presečki, Vladimir - Zagreb : Hrvatsko mikrobiološko društvo, 2000

Skup
Drugi hrvatski mikrobiološki kongres s međunarodnim sudjelovanjem

Mjesto i datum
Brijuni, Hrvatska, 03.10.2000. - 06.10.2000

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Domaća recenzija

Ključne riječi
CMV; evasion; T cell; NK cell

Sažetak
Cytomegaloviruses (CMVs) represent prototype viruses of the â-subgroup of herpesviruses with highly restricted host range. Human CMV (HCMV) causes life-threatening disease in immunodeficient patients. CMVs establish lifelong latent infections and, after periodic reactivation from latency, use a panel of immune evasion proteins to survive and replicate in the face of fully primed host immunity. The CD8+ T cells are decisive for control of infections by CMVs. To achieve effective surveillance of virus-infected cells, CD8+ T cells need to recognize viral peptides in the context of MHC class I molecules at the surface of infected cells. Presentation of viral peptides via this pathway requires degradation of viral proteins by the proteasome and the translocation of the peptides into the endoplasmic reticulum (ER) by transporters associated with antigen presentation (TAP) for loading into the binding groove of nascent MHC class I molecules and subsequent egress of MHC complexes to the cell surface. The HCMV encodes at least four viral polypeptides, each of which can independently interfere with MHC class I antigen presentation to inhibit efficient recognition of infected cells by CTL. In mouse CMV (MCMV) at least three genes affect MHC class I molecules. The MCMV early glycoprotein gp40 encoded by the m152 gene blocks the export of MHC class I complexes form the ER/-Golgi compartment and thereby prevents the presentation of viral peptides to CTL. Two additional MCMV proteins, the product of the m04 and of the m06 genes form complexes with MHC class I molecules. Downregulation of MHC class I by CMVs should make the cells susceptible to attack by NK cells that recognise the "missing self". Both HCMV and MCMV express decoy molecules which prevent infected cells from destruction by NK lymphocytes by engaging their inhibitory receptors. The potential significance of immunoevasive viral genes for virus control in vivo will be discussed.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA