Mary Wilson
Well-known member
Published:September 30, 2022
DOI:https://doi.org/10.1016/j.cell.2022.09.022
Cody J. Warren [SUP]5 [/SUP]Shuiqing Yu Douglas K. Peters [SUP]6 [/SUP]Arturo Barbachano-Guerrero Qing Yang [SUP]7 [/SUP]Bridget L. Burris Gabriella Worwa I-Chueh Huang [SUP]8 [/SUP]Gregory K. Wilkerson [SUP]9 [/SUP]Tony L. Goldberg Jens H. Kuhn Sara L. Sawyer [SUP]10[/SUP]
Highlights
SHFV uses an intracellular receptor, CD163, for cellular entry
CD163 divergence in primates of some species poses a barrier to SHFV entry
All cellular proteins required for SHFV replication are functional in human cells
SHFV replication in human cells suggests potential for zoonotic transmission
SUMMARY
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.
https://www.cell.com/action/showPdf?pii=S0092-8674(22)01194-1
DOI:https://doi.org/10.1016/j.cell.2022.09.022
Cody J. Warren [SUP]5 [/SUP]Shuiqing Yu Douglas K. Peters [SUP]6 [/SUP]Arturo Barbachano-Guerrero Qing Yang [SUP]7 [/SUP]Bridget L. Burris Gabriella Worwa I-Chueh Huang [SUP]8 [/SUP]Gregory K. Wilkerson [SUP]9 [/SUP]Tony L. Goldberg Jens H. Kuhn Sara L. Sawyer [SUP]10[/SUP]
Highlights
SHFV uses an intracellular receptor, CD163, for cellular entry
CD163 divergence in primates of some species poses a barrier to SHFV entry
All cellular proteins required for SHFV replication are functional in human cells
SHFV replication in human cells suggests potential for zoonotic transmission
SUMMARY
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.
https://www.cell.com/action/showPdf?pii=S0092-8674(22)01194-1