Depression of early phase of HTLV-I infection in vitro mediated by human beta-interferon

C. D'Onofrio, C. F. Perno, P. Mazzetti, G. Graziani, R. Calio, E. Bonmassar

Research output: Contribution to journalArticlepeer-review

Abstract

Natural human interferon β (β-IFN) was tested during the early phase of in vitro infection with HTLV-I virus of human cord blood mononuclear cells (CBL), to evaluate whether its antiviral and immunomodulating effects might prevent spreading of infection in the host. β-IFN was found to reduce HTLV-I transmission and integration in CBL cultures. Moreover, β-IFN had no effect in preventing virus transmission and integration in K562 and a very limited effect in HL60 and Molt-4 human tumour lines, suggesting a cell-type specific mode of action. β-IFN induced a 'priming' response on CBL, since overnight pretreatment of recipient cells or one single treatment at the onset of the coculture were almost equally effective in protecting against HTLV-I infection. During the early days post infection (p.i.), IFN-treated CBL showed a pattern of phenotypic markers that was closer to that of non-infected CBL. In contrast, untreated CBL exposed to HTLV-I showed a percent increase of Tac+, M3+ and Leu 11+ subpopulations. Cell-mediated immune responses of CBL were depressed after coculturing with HTLV-I producer MT-2 cells. β-IFN was able to boost the cell-mediated cytotoxicity of fresh and infected CBL against both K562 and MT-2 target cells. Leukocyte blastogenesis in mixed lymphocyte/tumour cell cultures, evaluated in terms of 3H-thymidine incorporation during the first week p.i., was also enhanced by IFN when macrophages and lymphocytes were reconstituted at an optimal 1:20 ratio. It is conceivable that this overall enhancement of the immune response induced by β-IFN could contribute to reduce HTLV-I infection in vitro.

Original languageEnglish
Pages (from-to)481-488
Number of pages8
JournalBritish Journal of Cancer
Volume57
Issue number5
Publication statusPublished - 1988

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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