Peptide-based inhibitor of host factor involved in HIV-1 replication

The Need

The emergence of HIV-1 infection continues to pose significant challenges in healthcare worldwide. Current treatment approaches primarily target viral components, leading to the development of drug resistance over time. There is a pressing need for innovative therapeutic strategies that disrupt the HIV-1 lifecycle by targeting host cell factors, thereby reducing the likelihood of drug resistance and improving treatment efficacy.

The Technology

Our groundbreaking discovery focuses on the role of Human lysyl-tRNA synthetase (LysRS) in facilitating various stages of the HIV-1 lifecycle. Normally housed in a multi-synthetase complex (MSC) in the cytoplasm for its housekeeping function of tRNA aminoacylation, LysRS undergoes a conformational change upon HIV-1 infection. This change enables it to enter the nucleus and interact with viral components, thereby influencing viral transcription and infectivity. Leveraging this mechanism, we have identified an N-terminal peptide (N36) capable of modulating LysRS conformation, leading to reduced HIV-1 Gag protein expression and infectivity.

Commercial Applications

  • Development of novel anti-HIV therapeutics targeting host cell factors.
  • Potential inclusion in combination therapy regimens to enhance treatment efficacy and mitigate drug resistance.
  • Application in HIV-1 research and drug discovery to elucidate the role of host cell factors in viral replication.


  • Unique approach: Targeting host cell factors presents a novel strategy to combat HIV-1 infection, reducing the likelihood of drug resistance.
  • Enhanced treatment efficacy: By disrupting multiple stages of the HIV-1 lifecycle, our technology has the potential to improve patient outcomes.
  • Reduced viral infectivity: Modulating LysRS conformation with N36 peptide results in decreased HIV-1 Gag protein expression, ultimately reducing viral infectivity.

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