Neuraminidase, receptor-destroying

Keywords Ganglioside Mucins Neuraminidase Receptor binding Receptor-destroying enzyme Sialate-O-acetylesterase Virus... 

Sialic acid was the first virus receptor identified. Hirst and McClelland and Hare discovered that influenza virus is able to hemagglutinate and that adsorbed virus is eluted from erythrocytes on incubation at 37°C, indicating an enzymatic destruction of a receptor substance on the cells [1, 2]. When a similar enzymatic activity was subsequently detected in Vibrio cholerae cultures, the term receptor-destroying enzyme was introduced [3]. The substance released by the viral enzyme from soluble hemagglutination inhibitors was initially characterized as a carbohydrate of low molecular weight [4] and then identified in crystalline form as A-acetyl-o-neuraminic acid [5]. Thus, it was clear that the receptor determinant of influenza virus was sialic acid and that the viral enzyme was a neuraminidase. Furthermore, for the first time an important biological function of sialic acid had been identified. 

Sendai virus, like other myxo- and paramyxovirus, has surface glycoprotein spikes which adsorb to specific receptors on erythrocytes of most mammalian and fowl species and cause hemagglutination. The receptors on erythrocyte membranes contain neuraminic acid, as indicated by the fact that they are destroyed by neuraminidase. Haywood (3 ) demonstrated that liposomes containing gangliosides could inhibit the agglutination of erythro-... 

Influenza neuraminidase cleaves terminal sialic acid residues and destroys the receptors recognized by viral hemagglutinin, which are present on the cell surface, in progeny virions, and in respiratory secretions. This enzymatic action is essential for release of virus from infected cells. Interaction of oseltamivir carboxylate with the neuraminidase causes a conformational change within the enzyme s active site and inhibits its activity. Inhibition of neuraminidase activity leads to viral aggregation at the cell surface and reduced virus spread within the respiratory tract. 

Lukert (1972) made the interesting observation, which may not, however, be directly related to substrate specificity, that the attachment of avian, infectious bronchitis virus to monolayers of chicken embryo kidney cells was inhibited not only by the addition of free or bound sialic acid, but by sulfhydryl-containing compounds. Receptors could be destroyed by neuraminidase or p-hydroxymercuribenzoate treatment. The adsorption of Newcastle disease virus, however, was not affected by the addition of sulfhydryl compounds. 

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