T-cell receptor Vβ38.1 peptide reduces coxsackievirus-induced cardiopathology during murine acquired immunodeficiency syndrome

Ramón Tomás Sepúlveda, John Jacob Marchalonis, Ronald Ross Watson

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Infection of people with human immunodeficiency virus (HIV) as well as LP-BM5 infection in mice results in progressive deterioration of the immune system in the majority of untreated hosts. Peptide immunotherapy has been shown to be effective in the stimulation or immunoregulation of T-helper 1 (TH1) and T-helper 2 (TH2) response subsets. In murine acquired immunodeficiency syndrome (AIDS), TH1 deficiency enables the host to be susceptible to coxsackievirus infection, inducing cardiopathology in a short period. T-cell receptor (TCR) Vβ8.1 peptide, a 16-mer peptide containing the entire CDR1 segment and part of the FR2 region of human Vβ8, showed both an immunoregulating and immunostimulating effect in murine AIDS. TCR Vβ8.1 peptide acts on T cells promoting interleukin-2 production and therefore enhancing a cell-mediated immune response. It retarded development of cardiopathology due to coxsackievirus infection. Retrovirus-infected mice treated with the peptide showed a longer life span than the nontreated, retrovirus-infected animals.

Original languageEnglish (US)
Pages (from-to)489-497
Number of pages9
JournalJournal of Cardiovascular Pharmacology
Volume41
Issue number3
DOIs
StatePublished - Mar 1 2003

Keywords

  • AIDS
  • Cardiopathology
  • Coxsackievirus
  • Peptide therapy
  • T-helper 1
  • T-helper 2

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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