HIV-1 infection ex vivo accelerates measles virus infection by upregulating signaling lymphocytic activation molecule (SLAM) in CD4+ T Cells

Yu Ya Mitsuki, Kazutaka Terahara, Kentaro Shibusawa, Takuya Yamamoto, Takatsugu Tsuchiya, Fuminori Mizukoshi, Masayuki Ishige, Seiji Okada, Kazuo Kobayashi, Yuko Morikawa, Tetsuo Nakayama, Makoto Takeda, Yusuke Yanagi, Yasuko Tsunetsugu-Yokota

Research output: Contribution to journalArticlepeer-review

Abstract

Measles virus (MV) infection in children harboring human immunodeficiency virus type 1 (HIV-1) is often fatal, even in the presence of neutralizing antibodies; however, the underlying mechanisms are unclear. Therefore, the aim of the present study was to examine the interaction between HIV-1 and wild-type MV (MVwt) or an MV vaccine strain (MVvac) during dual infection. The results showed that the frequencies of MVwt- and MVvac-infected CD4+ T cells within the resting peripheral blood mononuclear cells (PBMCs) were increased 3- to 4-fold after HIV-1 infection, and this was associated with a marked upregulation of signaling lymphocytic activation molecule (SLAM) expression on CD4+ T cells but not on CD8+ T cells. SLAM upregulation was induced by infection with a replication-competent HIV-1 isolate comprising both the X4 and R5 types and to a lesser extent by a pseudotyped HIV-1 infection. Notably, SLAM upregulation was observed in HIV-infected as well as -uninfected CD4+ T cells and was abrogated by the removal of HLA-DR+ cells from the PBMC culture. Furthermore, SLAM upregulation did not occur in uninfected PBMCs cultured together with HIV-infected PBMCs in compartments separated by a permeable membrane, indicating that no soluble factors were involved. Rather, CD4+ T cell activation mediated through direct contact with dendritic cells via leukocyte function-associated molecule 1 (LFA-1)/intercellular adhesion molecule 1 (ICAM-1) and LFA-3/CD2 was critical. Thus, HIV-1 infection induces a high level of SLAM expression on CD4+ T cells, which may enhance their susceptibility to MV and exacerbate measles in coinfected individuals.

Original languageEnglish
Pages (from-to)7227-7234
Number of pages8
JournalJournal of virology
Volume86
Issue number13
DOIs
Publication statusPublished - Jul 2012

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Fingerprint Dive into the research topics of 'HIV-1 infection ex vivo accelerates measles virus infection by upregulating signaling lymphocytic activation molecule (SLAM) in CD4<sup>+</sup> T Cells'. Together they form a unique fingerprint.

Cite this