Abstract
Hantavirus can cause hemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus pulmonary syndrome (HPS) in America, with high mortality and unknown mechanisms. Innate immunity is the host’s first-line defense to bridge the acquired immunity against viral infections. However, hantavirus has evolved various strategies in both molecular and cellular aspects to evade the host’s natural immune surveillance. The Interferon-I (IFN-I) signaling pathway, a central link of host defense, induces various antiviral proteins to control the infection. This paper summarizes the molecular mechanisms of hantavirus evasion mechanisms of the IFN signaling pathway and cellular processes such as regulated cell death and cell stress. Besides, hantavirus could also evade immune surveillance evasion through cellular mechanisms, such as upregulating immune checkpoint molecules interfering with viral infections. Understanding hantavirus’s antiviral immune evasion mechanisms will deepen our understanding of its pathogenesis and help us develop more effective methods to control and eliminate hantavirus.
Highlights
Specialty section: This article was submitted to Virology, a section of the journal Frontiers in Microbiology
This paper summarizes the molecular mechanisms of hantavirus evasion mechanisms of the IFN signaling pathway and cellular processes such as regulated cell death and cell stress
It has been demonstrated that the virus RNA rather than the virion proteins acts as pathogen-associated molecular patterns (PAMPs) to trigger innate immune activation during hantavirus infection (Zhang et al, 2014; Kell et al, 2020)
Summary
The repeated outbreaks of diseases caused by hantavirus have seriously threatened human health. Liu et al (2021) showed for the first time that a significant portion of CD8+ T cells in patients at the acute phase of severe HFRS harbored HTNV nucleocapsid protein, and confirmed that primary human CD8+ T cells were permissive to HTNV infection in vitro and supported the complete viral replication cycle using electoral microscopy. It has been demonstrated that the virus RNA rather than the virion proteins acts as pathogen-associated molecular patterns (PAMPs) to trigger innate immune activation during hantavirus infection (Zhang et al, 2014; Kell et al, 2020). A recent study has described that primary monocytes and endothelial cells infected by PUUV could even activate mucosal-associated invariant T (MAIT) cells, which might increase the cytolytic potential of MAIT cells and exert its antiviral effect (Maleki et al, 2021). Understanding the anti-virus immune escape mechanisms of hantavirus will deepen our understanding of the pathogenesis of hantavirus and help us develop more effective methods to control and eliminate hantavirus
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