Naslov
In vivo potential of m152 gene of murine cytomegalovirus to evade control by MHC class I restricted T cells

Autori
Crnković, Irena ; Milotić, Irena ; Krmpotić, Astrid ; Polić, Bojan ; Trgovcich, Joanne ; Lučin, Pero ; Jonjić, Stipan ; Koszinowski, Ulrich

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

Izvornik
Annual meeting of the Croatian Immunological Society, Periodicum Biologorum 99 (1997), suppl. 2 / Vitale, Branko - Zagreb : Hrvatsko prirodoslovno društvo, 1997, 14-14

Skup
Annual meeting of the Croatian Immunological Society

Mjesto i datum
Zagreb, Hrvatska, 06.11.1997. - 07.11.1997

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Nije recenziran

Ključne riječi
citomegalovirus; izmicanje imunološkom nadzoru
(cytomegalovirus; immunoevasion)

Sažetak
Recognition and destruction of virus-infected cells by class I major histocompatibility complex (MHC) restricted cytotoxic T lymphocytes (CTL) is a central part of the immune systems attempts to control virus infection. Cytomegaloviruses (CMV) have diverse mechanisms to evade this type of immune response. Murine CMV (MCMV) encodes more than one gene product that interact with MHC class I maturation. The m152 gene encodes a 40 kD type I transmembrane glycoprotein that arrests the export of peptide loaded MHC class I complexes from the ERGIC/cis-Golgi compartment, and inhibits lysis by CTL (Ziegler et al., Immunity 8:57, 1997). There is no evidence, however, for the biological significance of this gene during viral infection in vivo. If the m152 gene effect on antigen presentation in the MHC class I pathway is relevant in vivo, the deletion of the gene should result in an attenuated virus mutant due to the increased susceptibility to CTL control. The attenuation effect should be absent or reduced in a mouse where this presentation pathway plays no role. The results indicate that recombinant MCMV with the deletion of the m152 gene has restricted replication capacity during the acute infection, compared with wild-type MCMV. Reintroduction of the m152 gene restores the wild-type pattern of virus replication and virulence. The attenuating effect of m152 deletion mutant is not observed in mice devoid of MHC class I molecules, and can be abolished in normal mice by depletion of T cells. Adoptive transfer studies revealed that m152 deletion mutant virus is more susceptible to control by both primed and nonprimed T cells. Although m152 is susceptible to CD8+ T cell control, the results of adoptive transfer studies indicate that this virus is also more susceptible to CD8-independent control mechanisms.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

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