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
[1]  
AUKEL H, 1994, VIROLOGY, V205, P34
[2]   Measles virus infection in rhesus macaques: Altered immune responses and comparison of the virulence of six different virus strains [J].
Auwaerter, PG ;
Rota, PA ;
Elkins, WR ;
Adams, RJ ;
DeLozier, T ;
Shi, YQ ;
Bellini, WJ ;
Murphy, BR ;
Griffin, DE .
JOURNAL OF INFECTIOUS DISEASES, 1999, 180 (04) :950-958
[3]   The Tat protein of human immunodeficiency virus type 1 is a substrate and inhibitor of the interferon-induced, virally activated protein kinase, PKR [J].
Brand, SR ;
Kobayashi, R ;
Mathews, MB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (13) :8388-8395
[4]   IDENTIFICATION OF INTERFERON-RESISTANT SUBPOPULATIONS IN SEVERAL STRAINS OF MEASLES-VIRUS - POSITIVE SELECTION BY GROWTH OF THE VIRUS IN BRAIN-TISSUE [J].
CARRIGAN, DR ;
KNOX, KK .
JOURNAL OF VIROLOGY, 1990, 64 (04) :1606-1615
[5]   Two roads diverged:: Interferon α/β- and interleukin 12-mediated pathways in promoting T cell interferon γ responses during viral infection [J].
Cousens, LP ;
Peterson, R ;
Hsu, S ;
Dorner, A ;
Altman, JD ;
Ahmed, R ;
Biron, CA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (08) :1315-1327
[6]  
CRESPI M, 1988, S AFR MED J, V73, P711
[7]   The V protein of simian virus 5 inhibits interferon signalling by targeting STAT1 for proteasome-mediated degradation [J].
Didcock, L ;
Young, DF ;
Goodbourn, S ;
Randall, RE .
JOURNAL OF VIROLOGY, 1999, 73 (12) :9928-9933
[8]   ROLE OF IMMUNIZATIONS IN THE RECENT DECLINE IN CHILDHOOD MORTALITY AND THE CHANGES IN THE FEMALE/MALE MORTALITY RATIO IN RURAL SENEGAL [J].
DULOU, AD ;
PISON, G ;
AABY, P .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1995, 142 (06) :643-652
[9]   DEGREE AND LENGTH OF VIREMIA IN ADULTS WITH MEASLES [J].
FORTHAL, DN ;
AARNAES, S ;
BLANDING, J ;
DELAMAZA, L ;
TILLES, JG .
JOURNAL OF INFECTIOUS DISEASES, 1992, 166 (02) :421-424
[10]   Measles virus suppresses cell-mediated immunity by interfering with the survival and functions of dendritic and T cells [J].
FugierVivier, I ;
ServetDelprat, C ;
Rivailler, P ;
Rissoan, MC ;
Liu, YJ ;
RabourdinCombe, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (06) :813-823