Structural highlights
Function
SPIKE_ADE02 Forms spikes that protrude from each vertex of the icosahedral capsid. Interacts with host coxsackievirus and adenovirus receptor CXADR located at the cell tight junctions to provide virion initial attachment to target cell. The fiber protein binds to CXADR with a higher affinity than CXADR binds to itself, thereby blocking the cell-cell adhesion function of CXADR dimers and leading to local disruption of the tight junction. Fiber protein present on neo-synthesized particles may thus disrupt the junctional integrity in order to facilitate further neighboring cells infection. Fiber proteins are shed during virus entry, when virus is still at the cell surface. Fiber shedding is dependent on viral CXADR drifting motion and subsequent binding to immobile integrins. Heparan sulfate might also play a role in virus binding.[1] [2] [3] [4]
Evolutionary Conservation
Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.
References
- ↑ Dechecchi MC, Tamanini A, Bonizzato A, Cabrini G. Heparan sulfate glycosaminoglycans are involved in adenovirus type 5 and 2-host cell interactions. Virology. 2000 Mar 15;268(2):382-90. PMID:10704346 doi:http://dx.doi.org/10.1006/viro.1999.0171
- ↑ Walters RW, Freimuth P, Moninger TO, Ganske I, Zabner J, Welsh MJ. Adenovirus fiber disrupts CAR-mediated intercellular adhesion allowing virus escape. Cell. 2002 Sep 20;110(6):789-99. PMID:12297051
- ↑ Burckhardt CJ, Suomalainen M, Schoenenberger P, Boucke K, Hemmi S, Greber UF. Drifting motions of the adenovirus receptor CAR and immobile integrins initiate virus uncoating and membrane lytic protein exposure. Cell Host Microbe. 2011 Aug 18;10(2):105-17. doi: 10.1016/j.chom.2011.07.006. PMID:21843868 doi:http://dx.doi.org/10.1016/j.chom.2011.07.006
- ↑ Wang K, Huang S, Kapoor-Munshi A, Nemerow G. Adenovirus internalization and infection require dynamin. J Virol. 1998 Apr;72(4):3455-8. PMID:9525681
