HTLV-I activates complement leading to increased binding to complement receptor-positive cells.

Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

HTLV-I activates complement leading to increased binding to complement receptor-positive cells.

AIDS Res Hum Retroviruses. 1995 Sep;11(9):1115-22. Unique Identifier : AIDSLINE MED/96089219
Saifuddin M; Landay AL; Ghassemi M; Patki C; Spear GT; Department of Immunology/Microbiology, Rush University, Chicago,; Illinois 60612, USA.

Abstract: This investigation was performed to determine whether HTLV-I can activate complement, since previous studies show that complement activation by some viruses, including HIV-1, can enhance binding to, and infection of complement receptor-positive (CR+) cells. Complement treatment increased binding of HTLV-I to CR+ HPB-ALL cells by approximately 5-fold. In contrast, increased binding was not observed with H9 cells, which lack CR. Heat inactivation or EDTA treatment of complement blocked this increased binding while EGTA treatment only partially blocked binding. Anti-CR2 antibody significantly blocked binding of complement-treated HTLV-I to HPB-ALL cells. Since previous studies showed that HIV-1 could activate complement, activation of complement by this virus was compared with HTLV-I. It was observed that binding of HTLV-I to HPB-ALL cells was enhanced by highly dilute complement (> or = 1:810) while HIV-1 required much higher concentrations of complement (> or = 1:30), indicating that HTLV-I is a much stronger complement activator. Treatment with complement transiently increased the ability of HTLV-I to infect CR+ cell lines as judged by provirus formation (4- to 8-fold increase) and p24 production (5- to 10-fold increase). In contrast, complement treatment did not increase infection of CR- cells. In conclusion this study shows that HTLV-I activates complement leading to increased binding to, and transiently increased infection of, CR+ cells. This complement-mediated increased binding of HTLV-I may dramatically affect viral trafficking and immunological reactivity of virus in vivo.

Keywords: Antibodies, Blocking/PHARMACOLOGY Antibodies, Monoclonal/PHARMACOLOGY Cell Line Cell-Free System *Complement Activation Human HIV-1/IMMUNOLOGY HTLV-I/*IMMUNOLOGY/ISOLATION & PURIF/PHYSIOLOGY HTLV-I Antibodies/PHARMACOLOGY HTLV-I Infections/IMMUNOLOGY Proviruses/IMMUNOLOGY/ISOLATION & PURIF/PHYSIOLOGY Receptors, Complement/*METABOLISM Support, U.S. Gov't, P.H.S. Virus Replication JOURNAL ARTICLE
960530
M9651087

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1996. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1996. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .