Document 0542
 DOCN  M9650542
 TI    HTLV-I activates complement leading to increased binding to complement
       receptor-positive cells.
 DT    9605
 AU    Saifuddin M; Landay AL; Ghassemi M; Patki C; Spear GT; Department of
       Immunology/Microbiology, Rush University, Chicago,; Illinois 60612, USA.
 SO    AIDS Res Hum Retroviruses. 1995 Sep;11(9):1115-22. Unique Identifier :
       AIDSLINE MED/96089219
 AB    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.
 DE    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

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).