Macrophage-associated wound healing contributes to African green monkey SIV pathogenesis control

Fredrik Barrenas1,2, Kevin Raehtz3,4, Cuiling Xu5

  • 1Department of Microbiology, University of Washington, Seattle, WA, USA.

Nature Communications
|November 10, 2019
PubMed

Insights

African green monkeys (AGMs) resist simian immunodeficiency virus (SIV) by activating conserved wound healing mechanisms. This process, involving fibronectin and TGF-β, prevents immune exhaustion seen in AIDS-susceptible rhesus macaques (RMs).

Area of Science:

  • Immunology
  • Virology
  • Systems Biology

Background:

  • Natural hosts of simian immunodeficiency virus (SIV) avoid AIDS despite lifelong infection.
  • Rhesus macaques (RMs) are susceptible to simian AIDS.
  • African green monkeys (AGMs) are natural SIV hosts that do not develop AIDS.

Purpose of the Study:

  • To investigate the mechanisms by which AGMs resist SIV-induced immunodeficiency.
  • To compare gene expression profiles in SIV-infected AGMs and RMs.

Main Methods:

  • Developed Conserved Gene Signature Analysis (CGSA), a systems biology approach.
  • Compared RNA sequencing data from rectal tissues of SIV-infected AGMs and RMs.
  • Analyzed gene expression profiles, focusing on wound healing and immune response pathways.

Main Results:

  • AGMs rapidly activate and maintain conserved, evolutionarily regenerative wound healing mechanisms in mucosal tissue.
  • Fibronectin, a wound healing protein, exhibits distinct tissue distribution and abundance kinetics in AGMs.
  • AGM monocytes display an embryonic development and repair/regeneration signature with reduced inflammatory gene expression compared to RMs, featuring TGF-β.

Conclusions:

  • AGMs employ a regenerative wound healing process to maintain mucosal integrity during SIV infection.
  • This regenerative response likely prevents the inflammatory insults that lead to immune exhaustion in SIV-susceptible species like RMs.
  • The findings offer insights into host-pathogen interactions and potential strategies for preventing SIV/HIV pathogenesis.