title: HTLV-I activates complement leading to increased binding to complement receptor-positive cells.
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.
authors.affiliation: Department of Immunology/Microbiology, Rush University, Chicago, Illinois 60612, USA.
authors.forename: M
authors.initials: M
authors.lastname: Saifuddin
authors.forename: A L
authors.initials: AL
authors.lastname: Landay
authors.forename: M
authors.initials: M
authors.lastname: Ghassemi
authors.forename: C
authors.initials: C
authors.lastname: Patki
authors.forename: G T
authors.initials: GT
authors.lastname: Spear
mesh_terms: D019138:Antibodies, Blocking / Q000494:pharmacology; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D002460:Cell Line; D002474:Cell-Free System; D003167:Complement Activation; D015497:HIV-1 / Q000276:immunology; D015481:HTLV-I Antibodies / Q000494:pharmacology; D015490:HTLV-I Infections / Q000276:immunology; D015368:Human T-lymphotropic virus 1 / Q000276:immunology* / Q000302:isolation & purification / Q000502:physiology; D006801:Humans; D011533:Proviruses / Q000276:immunology / Q000302:isolation & purification / Q000502:physiology; D011951:Receptors, Complement / Q000378:metabolism*; D014779:Virus Replication
chemical_list: D019138:Antibodies, Blocking; D000911:Antibodies, Monoclonal; D015481:HTLV-I Antibodies; D011951:Receptors, Complement