Infection of human T lymphoid cells by human herpesvirus 6 is blocked by two unrelated protein tyrosine kinase inhibitors, biochanin A and herbimycin

M. Cirone, C. Zompetta, D. Tarasi, L. Frati, A. Faggioni

Research output: Contribution to journalArticle

Abstract

Human herpesvirus 6 is a T lymphotropic herpesvirus that causes exanthem subitum in infants and is considered a potential cofactor in AIDS etiopathogenesis and progression owing to its in vivo and in vitro interactions with human immunodeficiency virus. We report that no differences in phosphorylation on tyrosine residues of cellular proteins were detectable at early times following HHV-6 infection in comparison to uninfected cells. On the contrary, several cellular proteins appeared phosphorylated on tyrosine at 24-48 hr postinfection. In addition, when tyrosine phosphorylation induced by HHV-6 infection was inhibited by the tyrosine kinase inhibitor biochanin A, the infection of HSB-2 cells was also coordinately reduced, as judged by inhibition of cytopathic effect and by inhibition of early and late viral antigen expression. Similar results were obtained with a second unrelated tyrosine kinase inhibitor, herbimycin. The inhibitors seem to act at a late stage of the viral infectious cycle, since neither viral binding nor internalization were affected. Thus, our results indicate that HHV-6 infection leads to the phosphorylation of protein tyrosine kinases, which may play a role in the course of viral infection, probably by participating in the cytopathic effect induced by the virus.

Original languageEnglish
Pages (from-to)1629-1634
Number of pages6
JournalAIDS Research and Human Retroviruses
Volume12
Issue number17
Publication statusPublished - Nov 20 1996

ASJC Scopus subject areas

  • Immunology
  • Virology

Fingerprint Dive into the research topics of 'Infection of human T lymphoid cells by human herpesvirus 6 is blocked by two unrelated protein tyrosine kinase inhibitors, biochanin A and herbimycin'. Together they form a unique fingerprint.

  • Cite this