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Macrophage Resistance to HIV-1 Infection Is Enhanced by the Neuropeptides VIP and PACAP

Jairo R Temerozo1, Rafael Joaquim, Eduardo G Regis

  • 1Laboratory on Thymus Research, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil.

Plos One
|July 3, 2013
PubMed

Insights

Neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) reduce HIV-1 replication in macrophages. These findings suggest VIP, PACAP, and their receptors as potential therapeutic targets for HIV-1 infection.

Area of Science:

  • Immunology
  • Virology
  • Neuroendocrinology

Background:

  • Macrophages are key in HIV-1 pathogenesis, continuously producing the virus.
  • Host factors significantly influence HIV-1 replication within macrophages.
  • Neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) affect macrophage functions via G protein-coupled receptors (VPAC1, VPAC2, PAC1).

Purpose of the Study:

  • To investigate the impact of VIP and PACAP on HIV-1 production by macrophages.
  • To elucidate the specific receptors mediating the effects of VIP and PACAP on HIV-1 replication.

Main Methods:

  • Treatment of macrophages with VIP and PACAP.
  • Assessment of HIV-1 production levels.
  • Utilized receptor antagonists and specific agonists for VPAC1, VPAC2, and PAC1.
  • Measured secretion of β-chemokines (CCL3, CCL5) and cytokine IL-10.
  • Neutralization assays for secreted factors.

Main Results:

  • VIP and PACAP synergistically or additively decrease HIV-1 production in macrophages.
  • VIP's inhibitory effect is mediated by VPAC1/2 receptors; PACAP acts via VPAC1/2 and PAC1.
  • Activation of VPAC2 or PAC1 inhibits HIV-1 production, while VPAC1 activation enhances it.
  • VIP and PACAP upregulate CCL3, CCL5, and IL-10 secretion, which mediate the antiviral effect.

Conclusions:

  • VIP and PACAP exhibit potent antiviral activity against HIV-1 in macrophages.
  • The findings highlight VPAC2 and PAC1 receptors as promising targets for novel HIV-1 therapies.
  • Targeting these neuropeptide-receptor pathways could offer alternative therapeutic strategies for HIV-1 infection.

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