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A neuron-specific role for autophagy in antiviral defense against herpes simplex virus.

Abstract：

:Type I interferons (IFNs) are considered to be the universal mechanism by which viral infections are controlled. However, many IFN-stimulated genes (ISGs) rely on antiviral pathways that are toxic to host cells, which may be detrimental in nonrenewable cell types, such as neurons. We show that dorsal root ganglionic (DRG) neurons produced little type I IFNs in response to infection with a neurotropic virus, herpes simplex type 1 (HSV-1). Further, type I IFN treatment failed to completely block HSV-1 replication or to induce IFN-primed cell death in neurons. We found that DRG neurons required autophagy to limit HSV-1 replication both in vivo and in vitro. In contrast, mucosal epithelial cells and other mitotic cells responded robustly to type I IFNs and did not require autophagy to control viral replication. These findings reveal a fundamental difference in the innate antiviral strategies employed by neurons and mitotic cells to control HSV-1 infection.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Yordy B,Iijima N,Huttner A,Leib D,Iwasaki A

doi

10.1016/j.chom.2012.07.013

subject

Has Abstract

pub_date

2012-09-13 00:00:00

pages

334-45

issue

3

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(12)00273-9

journal_volume

12

pub_type

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