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KREMEN1 Is a Host Entry Receptor for a Major Group of Enteroviruses.

Abstract：

:Human type A Enteroviruses (EV-As) cause diseases ranging from hand-foot-and-mouth disease to poliomyelitis-like disease. Although cellular receptors are identified for some EV-As, they remain elusive for the majority of EV-As. We identify the cell surface molecule KREMEN1 as an entry receptor for coxsackievirus A10 (CV-A10). Whereas loss of KREMEN1 renders cells resistant to CV-A10 infection, KREMEN1 overexpression enhances CV-A10 binding to the cell surface and increases susceptibility to infection, indicating that KREMEN1 is a rate-limiting factor for CV-A10 infection. Furthermore, the extracellular domain of KREMEN1 binds CV-A10 and functions as a neutralizing agent during infection. Kremen-deficient mice are resistant to CV-A10-induced lethal paralysis, emphasizing the relevance of Kremen for infection in vivo. KREMEN1 is also essential for infection by a phylogenetic and pathogenic related group of EV-As. Collectively these findings highlight the importance of KREMEN1 for these emerging pathogens and its potential as an antiviral therapeutic target.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Staring J,van den Hengel LG,Raaben M,Blomen VA,Carette JE,Brummelkamp TR

doi

10.1016/j.chom.2018.03.019

subject

Has Abstract

pub_date

2018-05-09 00:00:00

pages

636-643.e5

issue

5

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(18)30148-3

journal_volume

23

pub_type

杂志文章

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