. 2014 Apr;88(8):4558–4571. doi: 10.1128/JVI.03431-13

TABLE 2.

Summary of α2β1, GM1, and N-acylneuraminic acid usage for cell binding and/or infection by sialidase-sensitive (animal) rotaviruses

Virus strain	α2β1 usage^a	Untreated cells							Sialidase-treated cells
		Infectivity reduced by CTB^b	Proposed internalization pathway^c	Reduced by Neu5Acα2Me (% at 10 mM)		Reduced by Neu5Gcα2Me (% at 10 mM)		Infectivity reduced by a-GM1^d	Effect of sialidase on given property		Infectivity reduced by Neu5Acα2Me	Infectivity reduced by Neu5Gcα2Me^d
		Infectivity reduced by CTB^b	Proposed internalization pathway^c	VP8* bound^d	Infectivity	VP8* bound^d	Infect	Infectivity reduced by a-GM1^d	VP8* bound^d	Infectivity	Infectivity reduced by Neu5Acα2Me	Infectivity reduced by Neu5Gcα2Me^d
TFR-41	−	+	CE	ND	19^d	ND	0^d	ND	ND	Reduced^d	−^d	−
CRW-8	−	−	ND	41	46^e	43	66^e	ND	ND	Reduced^e,f	−^f	ND
RRV	+	−	Non-CE	ND	60^g	ND	40^e	−	ND	Reduced^h	−^d	ND
NCDV	+	−	ND	34	29^e	41	41^e	ND	Reduced	Reducedⁱ	−^d	+

Shown in references 8, 15, 18, 32, and 35. In this study, the extent of α2β1 usage was shown not to be affected by sialidase treatment of cells.

Shown by CTB infectivity inhibition in this study for UK, TFR-41, and NCDV and in references 7 and 31 for CRW-8 and RRV. STD NMR analysis showed minimal RRV VP8* binding to a-GM1 (this study).

Data are from references 11 and 13. CE, clathrin-mediated endocytosis; Non-CE, endocytosis independent of clathrin and caveolin; ND, not determined.

Shown in this study.

Shown in this study and reference 38.

Shown in this study and reference 31.

Blockade shown in this study and references 37, 38, and 67.

Shown in this study and references 27, 34, and 36.

ⁱ

Shown in this study and references 27 and 29.