Complement-opsonized HIV: the free rider on its way to infection

被引:47
作者
Stoiber, H
Pruenster, M
Ammann, CG
Dierich, MP
机构
[1] Innsbruck Med Univ, Insst Hyg & Social Med, A-6020 Innsbruck, Austria
[2] Ludwig Boltzmann Inst AIDS Res, Innsbruck, Austria
关键词
complement; HIV; infection; pathogenesis; infectious synapse;
D O I
10.1016/j.molimm.2004.06.024
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The complement system (C) is one of the main Immoral components of innate immunity. Three major tasks of C against invading pathogens are: (i) lysis of pathogens by the formation of the membrane attack complex (MAC); (ii) opsonization of pathogens with complement fragments to favor phagocytosis; and (iii) attraction of inflammatory cells by chemotaxis. Like other particles, HIV activates C and becomes opsonized. To escape complement-mediated lysis, HIV has adopted various properties, which include the acquisition of HIV-associated molecules (HAMs) belonging to the family of complement regulators, such as CD46, CD55, CD59, and the interaction with humoral regulatory factors like factor H (fH). Opsonized virus may bind to complement receptor positive cells to infect them more efficiently or to remain bound on the surface of such cells. In the latter case HIV can be transmitted to cells susceptible for infection. This review discusses several aspects of C-HIV interactions and provides a model for the dynamics of this process. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:153 / 160
页数:8
相关论文
共 76 条
[41]   DECAY-ACCELERATING FACTOR (CD55) PROTECTS HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 FROM INACTIVATION BY HUMAN-COMPLEMENT [J].
MARSCHANG, P ;
SODROSKI, J ;
WURZNER, R ;
DIERICH, MP .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1995, 25 (01) :285-290
[42]   Recruitment of HIV and its receptors to dendritic cell-T cell junctions [J].
McDonald, D ;
Wu, L ;
Bohks, SM ;
KewalRamani, VN ;
Unutmaz, D ;
Hope, TJ .
SCIENCE, 2003, 300 (5623) :1295-1297
[43]   INTERLEUKIN-1 AND TUMOR NECROSIS FACTOR-ALPHA CAN BE INDUCED FROM MONONUCLEAR PHAGOCYTES BY HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 BINDING TO THE CD4 RECEPTOR [J].
MERRILL, JE ;
KOYANAGI, Y ;
CHEN, ISY .
JOURNAL OF VIROLOGY, 1989, 63 (10) :4404-4408
[44]   B cells of HIV-1-infected patients bind virions through CD21-complement interactions and transmit infectious virus to activated T cells [J].
Moir, S ;
Malaspina, A ;
Li, YX ;
Chun, TW ;
Lowe, T ;
Adelsberger, J ;
Baseler, M ;
Ehler, LA ;
Liu, SY ;
Davey, RT ;
Mican, JAM ;
Fauci, AS .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (05) :637-645
[45]   Neutralizing and infection-enhancing antibody responses to human immunodeficiency virus type 1 in long-term nonprogressors [J].
Montefiori, DC ;
Pantaleo, G ;
Fink, LM ;
Zhou, JT ;
Zhou, JY ;
Bilska, M ;
Miralles, GD ;
Fauci, AS .
JOURNAL OF INFECTIOUS DISEASES, 1996, 173 (01) :60-67
[46]   Extrahepatic complement biosynthesis: Where, when and why? [J].
Morgan, BP ;
Gasque, P .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1997, 107 (01) :1-7
[47]  
NIELSEN HV, 1994, J IMMUNOL, V153, P2021
[48]   Evolutionary pattern of human immunodeficiency virus (HIV) replication and distribution in lymph nodes following primary infection: Implications for antiviral therapy [J].
Pantaleo, G ;
Cohen, OJ ;
Schacker, T ;
Vaccarezza, M ;
Graziosi, C ;
Rizzardi, GP ;
Kahn, J ;
Fox, CH ;
Schnittman, SM ;
Schwartz, DH ;
Corey, L ;
Fauci, AS .
NATURE MEDICINE, 1998, 4 (03) :341-345
[49]   HIV GLYCOPROTEIN-41 AND COMPLEMENT FACTOR-H INTERACT WITH EACH OTHER AND SHARE FUNCTIONAL AS WELL AS ANTIGENIC HOMOLOGY [J].
PINTER, C ;
SICCARDI, AG ;
LOPALCO, L ;
LONGHI, R ;
CLIVIO, A .
AIDS RESEARCH AND HUMAN RETROVIRUSES, 1995, 11 (08) :971-980
[50]  
REYNES M, 1985, J IMMUNOL, V135, P2687