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

M Saifuddin1, A L Landay, M Ghassemi

  • 1Department of Immunology/Microbiology, Rush University, Chicago, Illinois 60612, USA.

AIDS Research and Human Retroviruses
|September 1, 1995
PubMed
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Human T-lymphotropic virus type I (HTLV-I) activates complement, enhancing its binding and infection of complement receptor-positive (CR+) cells. This interaction may impact viral spread and immune response in vivo.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Complement activation by viruses like HIV-1 can enhance cell binding and infection.
  • The role of complement activation in Human T-lymphotropic virus type I (HTLV-I) infection is not fully understood.

Purpose of the Study:

  • To investigate whether HTLV-I activates the complement system.
  • To determine if complement activation influences HTLV-I binding to and infection of complement receptor-positive (CR+) cells.

Main Methods:

  • Assessing HTLV-I binding to CR+ HPB-ALL cells after complement treatment.
  • Comparing HTLV-I complement activation with that of HIV-1.
  • Evaluating the effect of complement on HTLV-I infectivity in CR+ and CR- cells.

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Main Results:

  • Complement treatment increased HTLV-I binding to CR+ cells by approximately 5-fold, an effect blocked by heat inactivation, EDTA, and anti-CR2 antibodies.
  • HTLV-I is a significantly stronger complement activator than HIV-1, effective at higher dilutions.
  • Complement treatment transiently increased HTLV-I infectivity (provirus formation and p24 production) in CR+ cells but not in CR- cells.

Conclusions:

  • HTLV-I activates complement, leading to enhanced binding and transiently increased infection of CR+ cells.
  • Complement-mediated binding of HTLV-I may influence viral trafficking and immunological interactions in vivo.