Evasion of host defenses by measles virus: Wild-type measles virus infection interferes with induction of alpha/beta interferon production

被引:134
作者
Naniche, D
Yeh, A
Eto, D
Manchester, M
Friedman, RM
Oldstone, MBA
机构
[1] Scripps Res Inst, Dept Neuropharmacol, Div Virol, La Jolla, CA 92037 USA
[2] Uniformed Serv Univ Hlth Sci, Dept Pathol, Bethesda, MD 20814 USA
关键词
D O I
10.1128/JVI.74.16.7478-7484.2000
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Measles is a highly contagious disease currently responsible for over one million childhood deaths, particularly in the developing world. Since alpha/beta interferons (IFNs) are pivotal players both in nonspecific antiviral immunity and in specific cellular responses, their induction or suppression by measles virus (MV) could influence the outcome of a viral infection. In this study we compare the IFN induction and sensitivity of laboratory-passaged attenuated MV strains Edmonston and Moraten with those of recent wild-type viruses isolated and passaged solely on human peripheral blood mononuclear cells (PBMC) or on the B958 marmoset B-cell line. We report that two PBMC-grown wild-type measles isolates and two B958-grown strains of MV induce 10- to 10-fold-lower production of IFN by phytohemagglutinin-stimulated peripheral blood lymphocytes (PBL) compared to Edmonston and Moraten strains of measles. Preinfection of PBL with these non-IFN-inducing MV isolates prevents Edmonston-induced but not double-stranded-RNA-induced IFN production. This suggests that the wild-type viruses can actively inhibit Edmonston-induced IFN synthesis and that this is not occurring by double-stranded RNA. Furthermore, the wild-type MV is more sensitive than Edmonston MV to the effect of IFN, MV is thus able to suppress the synthesis of the earliest mediator of antiviral immunity, IFN-alpha/beta. This could have important implications in the virulence and spread of MV.
引用
收藏
页码:7478 / 7484
页数:7
相关论文
共 51 条
[21]  
Lehtonen A, 1997, J IMMUNOL, V159, P794
[22]  
Luft T, 1998, J IMMUNOL, V161, P1947
[23]   Clinical isolates of measles virus use CD46 as a cellular receptor? [J].
Manchester, M ;
Eto, DS ;
Valsamakis, A ;
Liton, PB ;
Fernandez-Muñoz, R ;
Rota, PA ;
Bellini, WJ ;
Forthal, DN ;
Oldstone, MBA .
JOURNAL OF VIROLOGY, 2000, 74 (09) :3967-3974
[24]   INTERFERON INDUCTION BY VIRUSES .19. VESICULAR STOMATITIS VIRUS-NEW-JERSEY - HIGH MULTIPLICITY PASSAGES GENERATE INTERFERON-INDUCING, DEFECTIVE-INTERFERING PARTICLES [J].
MARCUS, PI ;
GACCIONE, C .
VIROLOGY, 1989, 171 (02) :630-633
[25]   Interferon induction by viruses .23. Interferon induction as a quasispecies marker of vesicular stomatitis virus populations [J].
Marcus, PI ;
Rodriguez, LL ;
Sekellick, MJ .
JOURNAL OF VIROLOGY, 1998, 72 (01) :542-549
[26]   Type I interferons keep activated T cells alive [J].
Marrack, P ;
Kappler, J ;
Mitchell, T .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (03) :521-529
[27]   The interleukin-12-mediated pathway of immune events is dysfunctional in human immunodeficiency virus-infected individuals [J].
Marshall, JD ;
Chehimi, J ;
Gri, G ;
Kostman, JR ;
Montaner, LJ ;
Trinchieri, G .
BLOOD, 1999, 94 (03) :1003-1011
[28]   Variations in the interferon-inducing capacity of Sendai virus subpopulations [J].
Mattana, P ;
Viscomi, GC .
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, 1998, 18 (06) :399-405
[29]   Experimental measles .1. Pathogenesis in the normal and the immunized host [J].
McChesney, MB ;
Miller, CJ ;
Rota, PA ;
Zhu, YD ;
Antipa, L ;
Lerche, NW ;
Ahmed, R ;
Bellini, WJ .
VIROLOGY, 1997, 233 (01) :74-84
[30]   Targeted disruption of the STAT1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway [J].
Meraz, MA ;
White, JM ;
Sheehan, KCF ;
Bach, EA ;
Rodig, SJ ;
Dighe, AS ;
Kaplan, DH ;
Riley, JK ;
Greenlund, AC ;
Campbell, D ;
CarverMoore, K ;
DuBois, RN ;
Clark, R ;
Aguet, M ;
Schreiber, RD .
CELL, 1996, 84 (03) :431-442