HIV AND COMPLEMENT - ROLE OF THE COMPLEMENT-SYSTEM IN HIV-INFECTION

被引:22
作者
MARSCHANG, P [1 ]
EBENBICHLER, CF [1 ]
DIERICH, MP [1 ]
机构
[1] LUDWIG BOLTZMANN INST AIDS FORSCH,INNSBRUCK,AUSTRIA
关键词
HIV; COMPLEMENT; COMPLEMENT RECEPTORS; ENHANCEMENT OF INFECTION; HIV PATHOGENESIS;
D O I
10.1159/000236616
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
HIV, in contrast to animal retroviruses, is not lysed by human serum but nevertheless the virus as well as virus-infected cells activate the complement system efficiently. HIV activates the classical pathway by binding Clq to the transmembrane protein gp41. On the surface of HIV-infected cells, both the alternative and the classical pathway are activated. Complement-treated HIV has an enhanced ability to infect cells carrying receptors for C3 fragments. By this mechanism complement can target the virus to certain cells, e.g. follicular dendritic cells. HIV-infected complement-coated cells can interact with complement receptor carrying cells and thereby spread the infection or cause the destruction of the infected cells. Due to direct or indirect effects of HIV the complement system is in an activated state and the cellular expression of complement receptors as well as regulatory molecules is modified in the blood of HIV-infected patients.
引用
收藏
页码:113 / 117
页数:5
相关论文
共 54 条
[1]   CELLULAR PROTEINS BOUND TO IMMUNODEFICIENCY VIRUSES - IMPLICATIONS FOR PATHOGENESIS AND VACCINES [J].
ARTHUR, LO ;
BESS, JW ;
SOWDER, RC ;
BENVENISTE, RE ;
MANN, DL ;
CHERMANN, JC ;
HENDERSON, LE .
SCIENCE, 1992, 258 (5090) :1935-1938
[2]   ANTIBODIES AND COMPLEMENT ENHANCE BINDING AND UPTAKE OF HIV-1 BY HUMAN MONOCYTES [J].
BAKKER, LJ ;
NOTTET, HSLM ;
DEVOS, NM ;
DEGRAAF, L ;
VANSTRIJP, JAG ;
VISSER, MR ;
VERHOEF, J .
AIDS, 1992, 6 (01) :35-41
[3]   THE AIDS-ASSOCIATED RETROVIRUS IS NOT SENSITIVE TO LYSIS OR INACTIVATION BY HUMAN-SERUM [J].
BANAPOUR, B ;
SERNATINGER, J ;
LEVY, JA .
VIROLOGY, 1986, 152 (01) :268-271
[4]   MECHANISM OF ANTIBODY-INDEPENDENT ACTIVATION OF THE 1ST COMPONENT OF COMPLEMENT (CL) ON RETROVIRUS MEMBRANES [J].
BARTHOLOMEW, RM ;
ESSER, AF .
BIOCHEMISTRY, 1980, 19 (13) :2847-2853
[5]   COMPLEMENT RECEPTOR TYPE-2 MEDIATES INFECTION OF THE HUMAN CD4-NEGATIVE RAJI B-CELL LINE WITH OPSONIZED HIV [J].
BOYER, V ;
DELIBRIAS, C ;
NORAZ, N ;
FISCHER, E ;
KAZATCHKINE, MD ;
DESGRANGES, C .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1992, 36 (06) :879-883
[6]   COMPLEMENT MEDIATES HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION OF A HUMAN T-CELL LINE IN A CD4-INDEPENDENT AND ANTIBODY-INDEPENDENT FASHION [J].
BOYER, V ;
DESGRANGES, C ;
TRABAUD, MA ;
FISCHER, E ;
KAZATCHKINE, MD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (05) :1151-1158
[7]   MEMBRANE EXPRESSION AND FUNCTION OF COMPLEMENT RECEPTORS CR-1 AND CR3 ON NEUTROPHILS FROM HIV-INFECTED SUBJECTS - MODULATION BY RTNF-ALPHA AND RGM-CSF [J].
CAPSONI, F ;
MINONZIO, F ;
COLOMBO, G ;
ONGARI, AM ;
BONARA, P ;
RIZZARDI, GP ;
LAZZARIN, A ;
ZANUSSI, C .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1992, 36 (04) :541-546
[8]   COMPLEMENT ACTIVATION IS ASSOCIATED WITH THE PRESENCE OF SPECIFIC HUMAN IMMUNODEFICIENCY VIRUS (HIV) ANTI-HIV IMMUNE-COMPLEXES IN PATIENTS WITH ACQUIRED IMMUNODEFICIENCY SYNDROME-RELATED COMPLEX OR LYMPHOADENOPATHY SYNDROME [J].
CARINI, C ;
PERRICONE, R ;
FRATAZZI, C ;
FONTANA, L ;
DECAROLIS, C ;
DAMELIO, R ;
SIRIANNI, MC ;
AIUTI, F .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1989, 30 (03) :347-353
[9]   GENETIC-ANALYSIS OF CR-1 (THE C3B COMPLEMENT RECEPTOR, CD35) EXPRESSION ON ERYTHROCYTES OF HIV-INFECTED INDIVIDUALS [J].
COHEN, JHM ;
GEFFRIAUD, C ;
CAUDWELL, V ;
KAZATCHKINE, MD .
AIDS, 1989, 3 (06) :397-399
[10]  
Cooper N.R., 1986, IMMUNOBIOLOGY COMPLE, P139