Soluble gC1q-R/p33, a cell protein that binds to the globular "Heads" of C1q, effectively inhibits the growth of HIV-1 strains in cell cultures

J. Szabó, L. Cervenák, F. D. Tóth, Z. Prohászka, L. Horváth, K. Kerekes, Z. Beck, A. Bácsi, A. Erdei, E. I.B. Peerschke, G. Füst, B. Ghebrehiwet

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10 Citations (Scopus)


Clq and the outer envelope protein of HIV, gpl20, have several structural and functional similarities. Therefore, it is plausible to assume that proteins that are able to interact with Clq may also interact with isolated gp 120 as well as the whole HIV-1 virus. Based on this hypothesis, we studied the potential ability of the recombinant form of the 33-kDa protein, which binds to the globular "heads" of Clq (gClq-R/p33), to inhibit the growth of different HIV-1 strains in cell cultures. gClq-R/p33 was found to effectively and dose-dependently inhibit the production of one T-lymphotropic (X4) and one macrophage-tropic (R5) strain in human T cell lines (MT-4 and H9) and human monocyte-derived macrophage cultures, respectively. At a concentration range of 5-25 μg/ml, gClq-R caused a marked and prolonged suppression of virus production. The extent of inhibition was enhanced when gClq-R was first incubated with and then removed from the target cell cultures before virus infection, compared to that when the cells were infected with gClq-R-HIV mixtures. The extent of inhibition was comparable to that of the Leu3a anti-CD4 antibody. Addition of gClq-R to the cell cultures on day 1 or 2 after infection induced markedly less inhibition of HIV-1 growth than pretreatment of the cells just before or together with the infective HIV strains. In ELISA experiments, gClq-R did not bind to a solid-phase recombinant gp120 while strong and dose-dependent binding of gClq-R to solid-phase CD4 was observed. Our present findings indicate that gClq-R is an effective inhibitor of HIV-1 infection, which prevents viral entry by blocking the interaction between CD4 and gp120. Since gClq-R is a human protein, it is most probably not antigenic in humans. It would seem logical, therefore, to consider gClq-R or its fragments involved in the CD4 binding as potential therapeutic agents.

Original languageEnglish
Pages (from-to)222-231
Number of pages10
JournalClinical Immunology and Immunopathology
Issue number2
Publication statusPublished - Dec 1 2001



  • CD4
  • GClq receptor
  • HIV-1
  • Inhibition
  • Viral entry

ASJC Scopus subject areas

  • Immunology and Allergy
  • Pathology and Forensic Medicine
  • Immunology

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