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Pregled bibliografske jedinice broj: 567105

Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus


Bubić, Ivan; Wagner, Markus; Krmpotić, Astrid; Saulig, Tanja; Kim, Sungjin; Yokoyama, Wayne; Jonjić, Stipan; Koszinowski, Ulrich
Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus // Journal of virology, 78 (2004), 14; 7536-7544 doi:10.1128/JVI.78.14.7536-7544.2004 (međunarodna recenzija, članak, znanstveni)


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Naslov
Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus

Autori
Bubić, Ivan ; Wagner, Markus ; Krmpotić, Astrid ; Saulig, Tanja ; Kim, Sungjin ; Yokoyama, Wayne ; Jonjić, Stipan ; Koszinowski, Ulrich

Izvornik
Journal of virology (0022-538X) 78 (2004), 14; 7536-7544

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
cytomegalovirus; innate immunity; NK cells

Sažetak
Mouse strains are either resistant or susceptible to murine cytomegalovirus (MCMV). Resistance is determined by the Cmv1(r) (Ly49h) gene, which encodes the Ly49H NK cell activation receptor. The protein encoded by the m157 gene of MCMV has been defined as a ligand for Ly49H. To find out whether the m157 protein is the only Ly49H ligand encoded by MCMV, we constructed the m157 deletion mutant and a revertant virus. Viruses were tested for susceptibility to NK cell control in Ly49H+ and Ly49H- mouse strains. Deletion of the m157 gene abolished the viral activation of Ly49H+ NK cells, resulting in higher virus virulence in vivo. Thus, in the absence of m157, Ly49H+ mice react like susceptible strains. 129/SvJ mice lack the Ly49H activation NK cell receptor but express the inhibitory Ly49I NK cell receptor that binds to the m157 protein. The Deltam157 inhibitory phenotype was weak because MCMV encodes a number of proteins that mediate NK inhibition, whose contribution could be shown by another mutant.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti



POVEZANOST RADA


Ustanove:
Medicinski fakultet, Rijeka

Profili:

Avatar Url Astrid Krmpotić (autor)

Avatar Url Stipan Jonjić (autor)

Avatar Url Ivan Bubić (autor)

Avatar Url Tanja Saulig (autor)

Poveznice na cjeloviti tekst rada:

doi jvi.asm.org

Citiraj ovu publikaciju:

Bubić, Ivan; Wagner, Markus; Krmpotić, Astrid; Saulig, Tanja; Kim, Sungjin; Yokoyama, Wayne; Jonjić, Stipan; Koszinowski, Ulrich
Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus // Journal of virology, 78 (2004), 14; 7536-7544 doi:10.1128/JVI.78.14.7536-7544.2004 (međunarodna recenzija, članak, znanstveni)
Bubić, I., Wagner, M., Krmpotić, A., Saulig, T., Kim, S., Yokoyama, W., Jonjić, S. & Koszinowski, U. (2004) Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus. Journal of virology, 78 (14), 7536-7544 doi:10.1128/JVI.78.14.7536-7544.2004.
@article{article, author = {Bubi\'{c}, Ivan and Wagner, Markus and Krmpoti\'{c}, Astrid and Saulig, Tanja and Kim, Sungjin and Yokoyama, Wayne and Jonji\'{c}, Stipan and Koszinowski, Ulrich}, year = {2004}, pages = {7536-7544}, DOI = {10.1128/JVI.78.14.7536-7544.2004}, keywords = {cytomegalovirus, innate immunity, NK cells}, journal = {Journal of virology}, doi = {10.1128/JVI.78.14.7536-7544.2004}, volume = {78}, number = {14}, issn = {0022-538X}, title = {Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus}, keyword = {cytomegalovirus, innate immunity, NK cells} }
@article{article, author = {Bubi\'{c}, Ivan and Wagner, Markus and Krmpoti\'{c}, Astrid and Saulig, Tanja and Kim, Sungjin and Yokoyama, Wayne and Jonji\'{c}, Stipan and Koszinowski, Ulrich}, year = {2004}, pages = {7536-7544}, DOI = {10.1128/JVI.78.14.7536-7544.2004}, keywords = {cytomegalovirus, innate immunity, NK cells}, journal = {Journal of virology}, doi = {10.1128/JVI.78.14.7536-7544.2004}, volume = {78}, number = {14}, issn = {0022-538X}, title = {Gain of Virulence Caused by Loss of a Gene in Murine Cytomegalovirus}, keyword = {cytomegalovirus, innate immunity, NK cells} }

Časopis indeksira:


  • Current Contents Connect (CCC)
  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
    • SCI-EXP, SSCI i/ili A&HCI
  • Scopus
  • MEDLINE


Citati:





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