期刊
JOURNAL OF VIROLOGY
卷 80, 期 6, 页码 2760-2770出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.80.6.2760-2770.2006
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资金
- NCI NIH HHS [T32 CA009385, CA68485, P30 CA068485, CA09385] Funding Source: Medline
- NIAID NIH HHS [T32 AI007474, AI07474, R01 AI032539, T32 AI007281, AI007281, AI32539] Funding Source: Medline
- NIDDK NIH HHS [P30 DK020593, DK20593] Funding Source: Medline
Reovirus infection is initiated by interactions between the attachment protein sigma 1 and cell surface carbohydrate and junctional adhesion molecule A (JAM-A). Expression of a JAM-A mutant lacking a cytoplasmic tail in nonpermissive cells conferred full susceptibility to reovirus infection, suggesting that cell surface molecules other than JAM-A mediate viral internalization following attachment. The presence of integrin-binding sequences in reovirus outer capsid protein lambda 2, which serves as the structural base for sigma 1, suggests that integrins mediate reovirus endocytosis. A beta 1 integrin-specific antibody, but not antibodies specific for other integrin subunits, inhibited reovirus infection of HeLa cells. Expression of a beta 1 integrin cDNA, along with a cDNA encoding JAM-A, in nonpermissive chicken embryo fibroblasts conferred susceptibility to reovirus infection. Infectivity of reovirus was significantly reduced in beta 1-deficient mouse embryonic stem cells in comparison to isogenic cells expressing PI. However, reovirus bound equivalently to cells that differed in levels of beta 1 expression, suggesting that beta 1 integrins are involved in a postattachment entry step. Concordantly, uptake of reovirus virions into beta 1-deficient cells was substantially diminished in comparison to viral uptake into beta 1-expressing cells. These data provide evidence that beta 1 integrin facilitates reovirus internalization and suggest that viral entry occurs by interactions of reovirus virions with independent attachment and entry receptors on the cell surface.
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