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

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 hem-orrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry that is shared with other hemor-rhagic 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 sur-veillance should be a priority.

Automated summary

The study found that simian arteriviruses can use CD163 as an intracellular receptor to enter and replicate in human monocytes, indicating that they may not require major adaptations to infect human hosts. Given the potential fatal infections caused by simian arteriviruses in captive macaques and the lack of immunity in humans, developing serology tests for human surveillance should be a priority.