HERPES-SIMPLEX VIRUS TYPE-1 AND PSEUDORABIES VIRUS BIND TO A COMMON SATURABLE RECEPTOR ON VERO CELLS THAT IS NOT HEPARAN-SULFATE

被引:54
作者
LEE, WC [1 ]
FULLER, AO [1 ]
机构
[1] UNIV MICHIGAN, SCH MED, DEPT MICROBIOL & IMMUNOL, 6736 MED SCI 2, ANN ARBOR, MI 48109 USA
关键词
D O I
10.1128/JVI.67.9.5088-5097.1993
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Herpes simplex virus type 1 (HSV-1) and pseudorabies virus (PRV) infect different natural hosts but are very similar in structure, replicative cycle, and entry into cultured cells. We determined whether HSV-1 and PRV use the same cellular components during entry into Vero cells, which are highly susceptible to each virus but are not from native hosts for either. UV-inactivated virions of either HSV-1 or PRV could saturate cell surfaces to block infection of challenge HSV-1 or PRV. In the presence of saturating levels for infection of either virus, radiolabeled virus bound well and in a heparin-sensitive manner. This result shows that heparan sulfate proteoglycans on Vero cells are not the limiting cellular component. To identify the virus component required for blocking, we used an HSV-1 null mutant virus lacking gB, gD, or gH as blocking virus. Virions lacking gB were able to block infection of challenge virus to the same level as did virus containing gB. In contrast, virions lacking gD lost all and most of the ability to block infection of HSV-1 and PRV, respectively. HSV-1 lacking gH and PRV lacking gp50 also were less competent in blocking infection of challenge virus. We conclude that HSV-1 and PRV bind to a common receptor for infection of Vero cells. Although both viruses bind a heparin-like cell component on many cells, including Vero cells, they also attach to a different and limited cell surface component that is bound at least by HSV-1 gD and possibly gH and to some degree by PRV gp50 but not gB. These results clearly demonstrate binding of both HSV-1 and PRV to a common cell receptor that is not heparan sulfate and demonstrate that several types of attachment occur for both viruses during infectious entry.
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收藏
页码:5088 / 5097
页数:10
相关论文
共 54 条
[1]   CHARACTERIZATION OF DEFECTIVE INTERFERING VIRAL PARTICLES PRESENT IN A POPULATION OF PSEUDORABIES VIRIONS [J].
BENPORAT, T ;
DEMARCHI, JM ;
KAPLAN, AS .
VIROLOGY, 1974, 61 (01) :29-37
[2]  
BENPORAT T, 1985, HERPESVIRUSES, V3, P105
[3]   NUCLEOTIDE-SEQUENCE OF A REGION OF THE HERPES-SIMPLEX VIRUS TYPE-1 GB GLYCOPROTEIN GENE - MUTATIONS AFFECTING RATE OF VIRUS ENTRY AND CELL-FUSION [J].
BZIK, DJ ;
FOX, BA ;
DELUCA, NA ;
PERSON, S .
VIROLOGY, 1984, 137 (01) :185-190
[4]   ROLE OF GLYCOPROTEIN-B OF HERPES-SIMPLEX VIRUS TYPE-1 IN VIRAL ENTRY AND CELL-FUSION [J].
CAL, WH ;
GU, BH ;
PERSON, S .
JOURNAL OF VIROLOGY, 1988, 62 (08) :2596-2604
[5]   GLYCOPROTEIN-D OF HERPES-SIMPLEX VIRUS ENCODES A DOMAIN WHICH PRECLUDES PENETRATION OF CELLS EXPRESSING THE GLYCOPROTEIN BY SUPERINFECTING HERPES-SIMPLEX VIRUS [J].
CAMPADELLIFIUME, G ;
QI, S ;
AVITABILE, E ;
FOATOMASI, L ;
BRANDIMARTI, R ;
ROIZMAN, B .
JOURNAL OF VIROLOGY, 1990, 64 (12) :6070-6079
[6]   ENTRY OF HERPES-SIMPLEX VIRUS-1 IN BJ CELLS THAT CONSTITUTIVELY EXPRESS VIRAL GLYCOPROTEIN D IS BY ENDOCYTOSIS AND RESULTS IN DEGRADATION OF THE VIRUS [J].
CAMPADELLIFIUME, G ;
ARSENAKIS, M ;
FARABEGOLI, F ;
ROIZMAN, B .
JOURNAL OF VIROLOGY, 1988, 62 (01) :159-167
[7]  
DEAN HJ, 1991, 16TH INT HERP WORKSH
[8]   NUCLEOTIDE-SEQUENCES OF HERPES-SIMPLEX VIRUS TYPE-1 (HSV-1) AFFECTING VIRUS ENTRY, CELL-FUSION, AND PRODUCTION OF GLYCOPROTEIN-GB (VP7) [J].
DELUCA, N ;
BZIK, DJ ;
BOND, VC ;
PERSON, S ;
SNIPES, W .
VIROLOGY, 1982, 122 (02) :411-423
[9]   EXCRETION OF NON-INFECTIOUS VIRUS-PARTICLES LACKING GLYCOPROTEIN-H BY A TEMPERATURE-SENSITIVE MUTANT OF HERPES-SIMPLEX VIRUS TYPE-1 - EVIDENCE THAT GH IS ESSENTIAL FOR VIRION INFECTIVITY [J].
DESAI, PJ ;
SCHAFFER, PA ;
MINSON, AC .
JOURNAL OF GENERAL VIROLOGY, 1988, 69 :1147-1156
[10]   CONSTRUCTION AND PROPERTIES OF A MUTANT OF HERPES-SIMPLEX VIRUS TYPE-1 WITH GLYCOPROTEIN-H CODING SEQUENCES DELETED [J].
FORRESTER, A ;
FARRELL, H ;
WILKINSON, G ;
KAYE, J ;
DAVISPOYNTER, N ;
MINSON, T .
JOURNAL OF VIROLOGY, 1992, 66 (01) :341-348