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Zoonoses: Alert Regarding Arteriviruses That Cause Monkey Hemorrhagic Fever
BN
Bertrand Neveux
10/13/2022
2 min read
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Scientists have demonstrated that the simian hemorrhagic fever virus (SHFV) is capable of infecting and replicating in human monocytes. To enter the cell, it uses the same cellular entry mechanisms as other viruses known to infect humans, such as Ebola and Lassa.
A study examined the risk of human infection with SHFV, focusing primarily on the virus’s entry and replication pathways. This is a matter of urgency: simian hemorrhagic fever is a fatal disease in macaques and is endemic in several populations of African primates, which serve as reservoir hosts. To date, there are no serological tests available to monitor human exposure in Africa, the main region where these viruses are endemic in monkeys. Furthermore, these areas are generally where interactions between primates and humans are most direct—and even aggressive—not to mention meat consumption. Thus, there is a high risk of human infection with the simian virus via zoonotic transmission.
Recent studies have also revealed the presence of these arteriviruses in great apes, chimpanzees, and gorillas. They even draw a parallel with another virus, the simian immunodeficiency virus (SIV), which brings to mind the emergence of the human immunodeficiency virus (HIV) and its rapid spread among humans in the 1970s and 1980s.
The study, published on September 30, 2022, in the journal *Cell*, warns that SHFV uses an intracellular receptor, CD163, to enter human cells. Once inside, the virus is capable of replicating in human monocytes and macrophages, and can even resist the interferon-mediated response and evade innate immunity. Until now, no arterivirus was known to infect humans. These findings raise concerns for global health and pandemic prevention. Not only is human CD163 compatible with SHFV entry into human cells, but all other cellular proteins necessary for viral replication are functional in human cells.
Thus, simian arteriviruses in nature do not require major adaptation to the human host, which is still immunologically naive to this family of viruses. There is therefore an urgent need to develop serological tests and implement surveillance measures in humans to understand the extent of population exposure in areas where the virus is endemic among primates. As the authors of this publication point out, “it is possible that people in Africa are already subclinically infected with arteriviruses. We may be facing a situation similar to what we experienced with HIV-1 infections, which spread undetected for decades before the virus was discovered in the 1980s.”
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