OTK18, a zinc -finger protein, regulates human immunodeficiency virus type 1 long terminal repeat through two distinct regulatory regions

Masahide Horiba, Lindsey B. Martinez, James L. Buescher, Shinji Sato, Jenae Limoges, Yunquan Jiang, Clinton Jones, Tsuneya Ikezu

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19 Scopus citations


It has previously been shown by our laboratory that OTK18, a human immunodeficiency virus (HIV)-inducible zinc-finger protein, reduces progeny-virion production in infected human macrophages. OTK18 antiviral activity is mediated through suppression of Tat-induced HIV-1 long terminal repeat (LTR) promoter activity. Through the use of LTR-scanning mutant vectors, the specific regions responsible for OTK18-mediated LTR suppression have been defined. Two different LTR regions were identified as potential OTK18-binding sites by an enhanced DNA-transcription factor ELISA system; the negative-regulatory element (NRE) at -255/-238 and the Ets-binding site (EBS) at -150/-139 in the LTR. In addition, deletion of the EBS in the LTR blocked OTK18-mediated LTR suppression. These data indicate that OTK18 suppresses LTR activity through two distinct regulatory elements. Spontaneous mutations in these regions might enable HIV-1 to escape from OTK18 antiretroviral activity in human macrophages.

Original languageEnglish (US)
Pages (from-to)236-241
Number of pages6
JournalJournal of General Virology
Issue number1
StatePublished - Jan 1 2007


ASJC Scopus subject areas

  • Virology

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