Chinese hamster ovary cells are non-permissive towards infection with coxsackievirus B3 despite functional virus-receptor interactions

被引:10
作者
Kramer, B [1 ]
Huber, M [1 ]
Kern, C [1 ]
Klingel, K [1 ]
Kandolf, R [1 ]
Selinka, HC [1 ]
机构
[1] UNIV TUBINGEN,INST PATHOL,DEPT MOL PATHOL,D-72076 TUBINGEN,GERMANY
关键词
coxsackie B virus receptor; A-particles; block in viral entry;
D O I
10.1016/S0168-1702(96)01438-4
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Viral infection is a complex process which includes binding and interaction of the virus with specific cell surface receptors, uptake and uncoating of the virus, and finally replication. Chinese hamster ovary (CHO) cells are non-permissive towards infection with coxsackieviruses of group B (CVB), although they do express a putative CVB-specific receptor protein. In order to localize the block of infection in CHO cells, these cells were tested for binding of radiolabelled CVB3, receptor-mediated transformation of virions into A-particles, and replication of the viral genome. Binding of CVB3 to CHO cells was found to be comparable to the binding of this virus to permissive cell lines. Detergent-solubilized membrane proteins of CHO cells were tested in virus overlay protein-binding assays (VOPBAs) and shown to express a 100 kDa CVB-binding membrane protein similar to the CVB receptor protein which we recently described for permissive HeLa cells. Incubation of CVB3 with intact CHO cells resulted in transformation of cell-bound virions into non-infectious A-particles (deprived of capsid protein VP4), demonstrating the functional activity of the CVB receptor protein on CHO hamster cells. Transfection of recombinant CVB3 cDNA or viral RNA into CHO cells resulted in the production of infectious CVB3 virions, implying that the failure of CVB to infect CHO cells is not caused by a defect in virus replication but results from a block in the uptake of virus particles into the cell after the initial steps of virus-receptor interactions. (C) 1997 Elsevier Science B.V.
引用
收藏
页码:149 / 156
页数:8
相关论文
共 34 条
[1]   VIRAL MYOCARDITIS AND ITS SEQUELAE [J].
ABELMANN, WH .
ANNUAL REVIEW OF MEDICINE, 1973, 24 :145-152
[2]   INFECTION BY ECHOVIRUSES-1 AND ECHOVIRUSES-8 DEPENDS ON THE ALPHA-2 SUBUNIT OF HUMAN VLA-2 [J].
BERGELSON, JM ;
STJOHN, N ;
KAWAGUCHI, S ;
CHAN, M ;
STUBDAL, H ;
MODLIN, J ;
FINBERG, RW .
JOURNAL OF VIROLOGY, 1993, 67 (11) :6847-6852
[3]   COXSACKIEVIRUS B3 ADAPTED TO GROWTH IN RD CELLS BINDS TO DECAY-ACCELERATING FACTOR (CD55) [J].
BERGELSON, JM ;
MOHANTY, JG ;
CROWELL, RL ;
JOHN, NFS ;
LUBLIN, DM ;
FINBERG, RW .
JOURNAL OF VIROLOGY, 1995, 69 (03) :1903-1906
[4]   DECAY-ACCELERATING FACTOR (CD55), A GLYCOSYLPHOSPHATIDYLINOSITOL-ANCHORED COMPLEMENT REGULATORY PROTEIN, IS A RECEPTOR FOR SEVERAL ECHOVIRUSES [J].
BERGELSON, JM ;
CHAN, M ;
SOLOMON, KR ;
STJOHN, NF ;
LIN, HM ;
FINBERG, RW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (13) :6245-6248
[5]   SPECIFIC ALTERATIONS OF COXSACKIEVIRUS B3 ELUTED FROM HELA CELLS [J].
CROWELL, RL ;
PHILIPSON, L .
JOURNAL OF VIROLOGY, 1971, 8 (04) :509-+
[6]  
CROWELL RL, 1976, CELL MEMBRANE RECEPT, P179
[7]   CHARACTERIZATION OF A 100-KILODALTON BINDING-PROTEIN FOR THE 6 SEROTYPES OF COXSACKIE-B VIRUSES [J].
DEVERDUGO, UR ;
SELINKA, HC ;
HUBER, M ;
KRAMER, B ;
KELLERMANN, J ;
HOFSCHNEIDER, PH ;
KANDOLF, R .
JOURNAL OF VIROLOGY, 1995, 69 (11) :6751-6757
[8]   A SEARCH FOR THE PRESENCE OF THE ENTEROVIRAL CAPSID PROTEIN VP-1 IN PANCREASES OF PATIENTS WITH TYPE-1 (INSULIN-DEPENDENT) DIABETES AND PANCREASES AND HEARTS OF INFANTS WHO DIED OF COXSACKIEVIRAL MYOCARDITIS [J].
FOULIS, AK ;
FARQUHARSON, MA ;
CAMERON, SO ;
MCGILL, M ;
SCHONKE, H ;
KANDOLF, R .
DIABETOLOGIA, 1990, 33 (05) :290-298
[9]   MODELING OF THE HUMAN INTERCELLULAR-ADHESION MOLECULE-1, THE HUMAN RHINOVIRUS MAJOR GROUP RECEPTOR [J].
GIRANDA, VL ;
CHAPMAN, MS ;
ROSSMANN, MG .
PROTEINS-STRUCTURE FUNCTION AND GENETICS, 1990, 7 (03) :227-233
[10]   THE MAJOR HUMAN RHINOVIRUS RECEPTOR IS ICAM-1 [J].
GREVE, JM ;
DAVIS, G ;
MEYER, AM ;
FORTE, CP ;
YOST, SC ;
MARIOR, CW ;
KAMARCK, ME ;
MCCLELLAND, A .
CELL, 1989, 56 (05) :839-847