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2019 ; 63
(2
): 51-64
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Cytosolic DNA-sensing immune response and viral infection
#MMPMID30677166
Abe T
; Marutani Y
; Shoji I
Microbiol Immunol
2019[Feb]; 63
(2
): 51-64
PMID30677166
show ga
How host cells recognize many kinds of RNA and DNA viruses and initiate innate
antiviral responses against them has not yet been fully elucidated. Over the past
decade, investigations into the mechanisms underlying these antiviral responses
have focused extensively on immune surveillance sensors that recognize
virus-derived components (such as lipids, sugars and nucleic acids). The findings
of these studies have suggested that antiviral responses are mediated by
cytosolic or intracellular compartment sensors and their adaptor molecules (e.g.,
TLR, myeloid differentiation primary response 88, retinoic acid inducible gene-I,
IFN-? promoter stimulator-1, cyclic GMP-AMP synthase and stimulator of IFN genes
axis) for the primary sensing of virus-derived nucleic acids, leading to
production of type I IFNs, pro-inflammatory cytokines and chemokines by the host
cells. Thus, host cells have evolved an elaborate host defense machinery to
recognize and eliminate virus infections. In turn, to achieve sustained viral
infection and induce pathogenesis, viruses have also evolved several
counteracting strategies for achieving immune escape by targeting immune sensors,
adaptor molecules, intracellular kinases and transcription factors. In this
review, we discuss recent discoveries concerning the role of the cytosolic
nucleic acid-sensing immune response in viral recognition and control of viral
infection. In addition, we consider the regulatory machinery of the cytosolic
nucleic acid-sensing immune response because these immune surveillance systems
must be tightly regulated to prevent aberrant immune responses to self and
non-self-nucleic acids.
|Adaptor Proteins, Signal Transducing/genetics
[MESH]
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