Gentsch J R, Pacitti A F
J Virol. 1985 Nov;56(2):356-64. doi: 10.1128/JVI.56.2.356-364.1985.
The effect of pretreatment of murine L cells with bacterial neuraminidases on type 3 reovirus attachment was examined. We observed that such treatments resulted in a 60 to 80% decrease of subsequent attachment of 35S-labeled type 3 reovirus in a time- and dose-dependent manner. This result was specific for removal of cell surface sialic acid residues since the specific neuraminidase inhibitor 2-deoxy-2,3-dehydro-n-acetyl neuraminic acid completely prevented the observed effect. Although the total amount of radiolabeled virus bound to neuraminidase-treated cells was greatly reduced, unlabeled reovirus competed only slightly less efficiently for the attachment of 35S-labeled reovirus to neuraminidase-treated versus mock-treated L cells, suggesting that the specificity of the virus interaction with cellular receptor sites was only slightly diminished. Saturation experiments with mock-treated cells or with cells treated with Vibrio cholerae or with V. cholerae plus Arthrobacter ureafaciens neuraminidases indicated that the number of specific cellular receptor sites for type 3 reovirus were reduced by about 47%. We determined that under the neuraminidase digestion conditions used in this experiment we were able to remove a maximum 75% of the total N-acetylneuraminic acid of L cells. Our results also demonstrated that glycoproteins bearing a large amount of sialic acid containing oligosaccharides as well as purified N-acetylneuraminic acid, N-glycolylneuraminic acid, and N-acetylneuraminyl lactose were inhibitors of attachment, while proteins containing no sialic acid or negligible amounts of sialic acid did not inhibit attachment. High concentrations of various monosaccharides and lactose had no effect on reovirus attachment, in agreement with the recent results of Armstrong and his collaborators (Armstrong et al., Virology, 138:37-48, 1984). These data are also supported by the observation that gangliosides are inhibitors of viral attachment (Armstrong et al., Virology, 138:37-48, 1984). Taken together, our results suggest that cell surface sialic acid-containing glycoconjugates are involved in type 3 reovirus binding to murine L cells.
研究了用细菌神经氨酸酶预处理鼠L细胞对3型呼肠孤病毒附着的影响。我们观察到,这种处理导致随后35S标记的3型呼肠孤病毒的附着以时间和剂量依赖的方式减少了60%至80%。由于特异性神经氨酸酶抑制剂2-脱氧-2,3-脱氢-N-乙酰神经氨酸完全阻止了观察到的效应,所以该结果是细胞表面唾液酸残基去除的特异性结果。尽管与神经氨酸酶处理过的细胞结合的放射性标记病毒的总量大大减少,但未标记的呼肠孤病毒在与模拟处理的L细胞相比时,对35S标记的呼肠孤病毒附着的竞争效率仅略有降低,这表明病毒与细胞受体位点相互作用的特异性仅略有降低。对模拟处理的细胞或用霍乱弧菌或霍乱弧菌加尿素节杆菌神经氨酸酶处理的细胞进行的饱和实验表明,3型呼肠孤病毒的特异性细胞受体位点数量减少了约47%。我们确定,在本实验所用的神经氨酸酶消化条件下,我们能够去除L细胞中最多75%的总N-乙酰神经氨酸。我们的结果还表明,带有大量含唾液酸寡糖的糖蛋白以及纯化的N-乙酰神经氨酸、N-糖基神经氨酸和N-乙酰神经氨酰乳糖是附着的抑制剂,而不含唾液酸或唾液酸含量可忽略不计的蛋白质则不抑制附着。高浓度的各种单糖和乳糖对呼肠孤病毒附着没有影响,这与阿姆斯特朗及其合作者最近的结果一致(阿姆斯特朗等人,《病毒学》,138:37-48,1984)。神经节苷脂是病毒附着的抑制剂这一观察结果也支持了这些数据(阿姆斯特朗等人,《病毒学》,138:37-48,1984)。综上所述,我们的结果表明,细胞表面含唾液酸的糖缀合物参与了3型呼肠孤病毒与鼠L细胞的结合。