Pseudorabies virus (PRV) is protected from complement attack by cellular factors and glycoprotein C (gC)

被引:16
作者
Maeda, K
Hayashi, S
Tanioka, Y
Matsumoto, Y
Otsuka, H
机构
[1] Univ Tokyo, Grad Sch Agr & Life Sci, Dept Global Anim Resource Sci, Bunkyo Ku, Tokyo 1138657, Japan
[2] Cent Inst Expt Anim, Primate Lab, Miyamae Ku, Kawasaki, Kanagawa 216, Japan
关键词
PRV; complement; gC; homologous restriction;
D O I
10.1016/S0168-1702(01)00417-8
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Swine kidney derived CPK cells were resistant to swine complement attack in vitro while rabbit kidney derived RK13 cells were destroyed by swine complement. To rabbit complement, RK13 cells were resistant but CPK cells were sensitive. This phenomenon was known as homologous restriction (Proc. Natl. Acad. Sci. USA 78 (1981) 5118). The gC deletion mutant of pseudorabies virus (PRVdlgC) grown in CPK cells was resistant to swine complement while the same virus grown in RK13 cells was neutralized by swine complement. PRVdlgC grown in RK13 cells was more resistant to rabbit complement than the virus grown in CPK cells. Hence, the sensitivity of PRVdlgC to swine or rabbit complement was similar to that of the cells in which the virus was grown. It would appear that cell derived factors were present on the virion and they were protective against homologous complement but not against heterologous complement. The expression of gC rendered PRV more resistant to swine or rabbit complement, but the protective effect of gC was much less than that of cell derived factors. The best protection against complement was obtained when gC and cell derived factors were coexistent on the virion. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:79 / 87
页数:9
相关论文
共 37 条
[1]   BREFELDIN-A ARRESTS THE MATURATION AND EGRESS OF HERPES-SIMPLEX VIRUS-PARTICLES DURING INFECTION [J].
CHEUNG, P ;
BANFIELD, BW ;
TUFARO, F .
JOURNAL OF VIROLOGY, 1991, 65 (04) :1893-1904
[2]   CD59, AN LY-6-LIKE PROTEIN EXPRESSED IN HUMAN LYMPHOID-CELLS, REGULATES THE ACTION OF THE COMPLEMENT MEMBRANE ATTACK COMPLEX ON HOMOLOGOUS CELLS [J].
DAVIES, A ;
SIMMONS, DL ;
HALE, G ;
HARRISON, RA ;
TIGHE, H ;
LACHMANN, PJ ;
WALDMANN, H .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (03) :637-654
[3]   COMPLEMENT COMPONENT C3B BINDS DIRECTLY TO PURIFIED GLYCOPROTEIN-C OF HERPES-SIMPLEX VIRUS TYPES-1 AND TYPES-2 [J].
EISENBERG, RJ ;
DELEON, MP ;
FRIEDMAN, HM ;
FRIES, LF ;
FRANK, MM ;
HASTINGS, JC ;
COHEN, GH .
MICROBIAL PATHOGENESIS, 1987, 3 (06) :423-435
[4]   Live-cell analysis of a green fluorescent protein-tagged herpes simplex virus infection [J].
Elliott, G ;
O'Hare, P .
JOURNAL OF VIROLOGY, 1999, 73 (05) :4110-4119
[5]   VIRAL ACTIVATION OF THE COAGULATION CASCADE - MOLECULAR-INTERACTIONS AT THE SURFACE OF INFECTED ENDOTHELIAL-CELLS [J].
ETINGIN, OR ;
SILVERSTEIN, RL ;
FRIEDMAN, HM ;
HAJJAR, DP .
CELL, 1990, 61 (04) :657-662
[6]   GLYCOPROTEIN-C OF HERPES-SIMPLEX VIRUS-1 ACTS AS A RECEPTOR FOR THE C3B COMPLEMENT COMPONENT ON INFECTED-CELLS [J].
FRIEDMAN, HM ;
COHEN, GH ;
EISENBERG, RJ ;
SEIDEL, CA ;
CINES, DB .
NATURE, 1984, 309 (5969) :633-635
[7]  
Friedmann R., 1986, PSYCHOL MARKET, V3, P1
[8]   Egress of alphaherpesviruses: Comparative ultrastructural study [J].
Granzow, H ;
Klupp, BG ;
Fuchs, W ;
Veits, J ;
Osterrieder, N ;
Mettenleiter, TC .
JOURNAL OF VIROLOGY, 2001, 75 (08) :3675-3684
[9]   HOMOLOGOUS SPECIES RESTRICTION IN LYSIS OF ERYTHROCYTES BY TERMINAL COMPLEMENT PROTEINS [J].
HANSCH, GM ;
HAMMER, CH ;
VANGURI, P ;
SHIN, ML .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1981, 78 (08) :5118-5121
[10]   Human and rodent decay-accelerating factors (CD55) are not species restricted in their complement-inhibiting activities [J].
Harris, CL ;
Spiller, OB ;
Morgan, BP .
IMMUNOLOGY, 2000, 100 (04) :462-470