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

M. Saifuddin, A. L. Landay, M. Ghassemi, C. Patki, G. T. Spear

Research output: Contribution to journalArticlepeer-review


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 (≥1:810) while HIV-1 required much higher concentrations of complement (≥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.

Original languageEnglish (US)
Pages (from-to)1115-1122
Number of pages8
JournalAIDS Research and Human Retroviruses
Issue number9
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Infectious Diseases


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