Abstract:
:Production of type I IFN is the key response to viral infection. Since the discovery of type I IFNs in 1957, long double-stranded RNA formed during replication of many viruses was thought to be responsible for type I IFN induction, and for decades double-stranded RNA-activated protein kinase (PKR) was thought to be the receptor. Recently, this picture has dramatically changed. It now became evident that not PKR but two members of the Toll-like receptor (TLR) family, TLR7 and TLR9, and two cytosolic helicases, RIG-I and MDA-5, are responsible for the majority of type I IFNs induced upon recognition of viral nucleic acids. In this review, we focus on the molecular mechanisms by which those innate immune receptors detect viral infection. Based on the recent progress in the field, we now know that TLR7, TLR9, and RIG-I do not require long double-stranded RNA for type I IFN induction.
journal_name
Curr Top Microbiol Immunoljournal_title
Current topics in microbiology and immunologyauthors
Schlee M,Barchet W,Hornung V,Hartmann Gdoi
10.1007/978-3-540-71329-6_11subject
Has Abstractpub_date
2007-01-01 00:00:00pages
207-30eissn
0070-217Xissn
2196-9965journal_volume
316pub_type
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