virus-heat shock protein interaction and a novel axis for innate antiviral immunityvirus-heat休克蛋白相互作用和天生的抗病毒免疫的新轴.pdfVIP
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virus-heat shock protein interaction and a novel axis for innate antiviral immunityvirus-heat休克蛋白相互作用和天生的抗病毒免疫的新轴
Cells 2012, 1, 646-666; doi:10.3390/cells1030646
OPEN ACCESS
cells
ISSN 2073-4409
/ journal / cells
Review
Virus-Heat Shock Protein Interaction and a Novel Axis for
Innate Antiviral Immunity
Mi Young Kim * and Michael Oglesbee
Department of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus,
OH 43210, USA; E-Mail: Michael.Oglesbee@
* Author to whom correspondence should be addressed; E-Mail: kim.2612@;
Tel.:+1-614-298-4211; Fax: +1-614-292-6473.
Received: 1 August 2012; in revised form: 24 August 2012 / Accepted: 27 August 2012 /
Published: 11 September 2012
Abstract: Virus infections induce heat shock proteins that in turn enhance virus gene
expression, a phenomenon that is particularly well characterized for the major inducible
70 kDa heat shock protein (hsp70). However, hsp70 is also readily induced by fever, a
phylogenetically conserved response to microbial infections, and when released from cells,
hsp70 can stimulate innate immune responses through toll like receptors 2 and 4 (TLR2 and 4).
This review examines how the virus-hsp70 relationship can lead to host protective innate
antiviral immunity, and the importance of hsp70 dependent stimulation of virus gene
expression in this host response. Beginning with the well-characterized measles
virus-hsp70 relationship and the mouse model of neuronal infection in brain, we examine
dat
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