Inhibition of HIV-1 replication by anti-trans-activation responsive polyamide nucleotide analog

Antiviral Res. 2002 Oct;56(1):13-27. doi: 10.1016/s0166-3542(02)00024-4.

Abstract

Efficient replication and gene expression of human immunodeficiency virus-1 (HIV-1) involves specific interaction of the viral protein Tat, with its trans-activation responsive element (TAR) which forms a highly stable stem-loop structure. We have earlier shown that a 15-mer polyamide nucleotide analog (PNA) targeted to the loop and bulge region of TAR blocks Tat-mediated transactivation of the HIV-1 LTR both in vitro and in cell culture (Mayhood et al., Biochemistry 39 (2000) 11532). In this communication, we have designed four anti-TAR PNAs of different length such that they either complement the entire loop and bulge region (PNA(TAR-16) and PNA(TAR-15)) or are short of few sequences in the loop (PNA(TAR-13)) or in both the loop and bulge (PNA(TAR-12)), and examined their functional efficacy in vitro as well as in HIV-1 infected cell cultures. All four anti-TAR PNAs showed strong affinity for TAR RNA, while their ability to block in vitro reverse transcription was influenced by their length. In marked contrast to PNA(TAR-12) and PNA(TAR-13), the two longer PNA(TARs) were able to efficiently sequester the targeted site on TAR RNA, thereby substantially inhibiting Tat-mediated transactivation of the HIV-1 LTR. Further, a substantial inhibition of virus production was noted with all the four anti-TAR PNA, with PNA(TAR-16) exhibiting a dramatic reduction of HIV-1 production by nearly 99%. These results point to PNA(TAR-16) as a potential anti-HIV agent.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Anti-HIV Agents / chemistry
  • Anti-HIV Agents / metabolism
  • Anti-HIV Agents / pharmacology*
  • Base Sequence
  • Cells, Cultured
  • Gene Products, tat / metabolism*
  • HIV Long Terminal Repeat / genetics
  • HIV Long Terminal Repeat / physiology
  • HIV-1 / drug effects*
  • HIV-1 / physiology
  • Humans
  • Lymphocytes / virology
  • Peptide Nucleic Acids / chemistry
  • Peptide Nucleic Acids / metabolism
  • Peptide Nucleic Acids / pharmacology*
  • RNA, Viral / metabolism
  • Transcriptional Activation
  • Transfection
  • Virus Replication / drug effects*
  • tat Gene Products, Human Immunodeficiency Virus

Substances

  • Anti-HIV Agents
  • Gene Products, tat
  • Peptide Nucleic Acids
  • RNA, Viral
  • tat Gene Products, Human Immunodeficiency Virus