Human and most animal rotavirus strains do not require the presence of sialic acid on the cell surface for efficient infectivity.

Abstract

The outer capsid spike protein VP4 is the main rotavirus cell attachment protein, but the cellular receptor used by rotavirus to establish a productive infection remains unknown. Sialic acid (SA) residues on the cell surface have been shown to be required for efficient binding and infectivity of animal rotaviruses (ARVs), but not of human rotaviruses (HRVs). Since the SA dependence of only a limited number of strains has been tested to date, in this study a larger number of strains were tested to further investigate the involvement of SA in rotavirus infectivity. Following treatment of African green monkey kidney cell (MA104) monolayers with neuraminidase, productive infection of rotavirus was measured by immunofluorescence. The infectivity of all 14 HRVs tested was SA-independent. Ten of 15 ARVs tested were SA-independent, while only five were SA-dependent. These results indicate that most ARVs, like HRVs, infect permissive cells in an SA-independent manner, probably by a common cellular receptor.

Human Milk Contains Novel Glycans That Are Potential Decoy Receptors for Neonatal Rotaviruses

“…5G; data compiled in supplemental Table S5). Together with the data from the virus binding to the CFG glycan microarray, our results show that the bovine G10[P11] strain B223 does not recognize any sialylated glycans in agreement with previous observations (74).…”

“…Recent observations show that not all rotaviruses require a sialic acid determinant for binding (49,74,93). Based on the studies reported here, it is important that the so-called neuraminidase-insensitive or sialic-acid-independent rotaviruses be analyzed for their glycan binding specificities on similar shotgun glycan microarrays comprising milk glycans or glycans released from cells or tissues susceptible to rotavirus infection.…”

Analysis by rotavirus gene 6 reverse transcriptase-polymerase chain reaction assay of rotavirus-positive gastroenteritis cases observed during the vaccination phase of the Rotavirus Efficacy and Safety Trial (REST)

“…The median clinical severity score of RVGE cases among placebo recipients was 10 (range, [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19], which is indicative of moderate-to-severe RVGE. The median score reduction between the wild-type RVGE cases among placebo recipients and vaccine-type RVGE among vaccine recipients was 6 (95% confidence interval [CI]: 4, 7); whereas, the median score reduction between the wild-type RVGE cases among placebo recipients and wild-type RVGE among vaccine recipients was 4 (95% CI: -1, 7).…”

“…The plaque assay was utilized in REST because RV5 readily forms plaques in susceptible cell monolayers upon direct inoculation, whereas wild-type rotaviruses do not. 19 Hence, it was used to determine vaccine-type or wild-type rotavirus strains. 5 In the plaque assay, a rotavirus particle is able to form a plaque when an intact virus particle infects a cell, replicates, and then lyses that cell.…”

“…5 In the plaque assay, a rotavirus particle is able to form a plaque when an intact virus particle infects a cell, replicates, and then lyses that cell. 19 However, it is important to note that the plaque assay may not always detect fully intact, infectious rotavirus particles present in all samples; the virus in the stool may not replicate in cell culture because some stool specimens are cytotoxic and inhibitors prevent replication of fully intact, infectious rotavirus particles. With this caveat, the plaque assay was thought to only detect infectious vaccine virus but if the vaccine-virus in the stool sample was not infectious (or failed to grow in the plaque assay), then it was assumed that no vaccine-virus was present in the sample.…”