Primate hemorrhagic fever-causing arteriviruses are poised for spillover to humans

Cell. 2022 Oct 13;185(21):3980-3991.e18. doi: 10.1016/j.cell.2022.09.022. Epub 2022 Sep 30.

Abstract

Simian arteriviruses are endemic in some African primates and can cause fatal hemorrhagic fevers when they cross into primate hosts of new species. We find that CD163 acts as an intracellular receptor for simian hemorrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry that is shared with other hemorrhagic fever-causing viruses (e.g., Ebola and Lassa viruses). Further, SHFV enters and replicates in human monocytes, indicating full functionality of all of the human cellular proteins required for viral replication. Thus, simian arteriviruses in nature may not require major adaptations to the human host. Given that at least three distinct simian arteriviruses have caused fatal infections in captive macaques after host-switching, and that humans are immunologically naive to this family of viruses, development of serology tests for human surveillance should be a priority.

Keywords: CD163 receptor; arms race; arteriviruses; disease emergence; hemorrhagic fever; positive selection; primates; virus entry; virus evolution; zoonosis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arterivirus* / physiology
  • Hemorrhagic Fevers, Viral* / veterinary
  • Hemorrhagic Fevers, Viral* / virology
  • Humans
  • Macaca
  • Primates
  • Viral Zoonoses
  • Virus Internalization
  • Virus Replication