流感病毒表面抗原抗体对病毒释放的抑制作用。
Inhibition of virus release by antibodies to surface antigens of influenza viruses.
作者信息
Dowdle W R, Downie J C, Laver W G
出版信息
J Virol. 1974 Feb;13(2):269-75. doi: 10.1128/JVI.13.2.269-275.1974.
Abstract
When influenza virus was mixed with antisera to its surface subunits before inoculation of cell cultures, anti-hemagglutinin antibodies neutralized infectivity but anti-neuraminidase did not. When the antisera were added after infection of cell cultures, anti-hemagglutinin and anti-neuraminidase antibodies were equally effective in reducing virus titers in culture fluids. Decreased virus titers were not due to interference of antibody with assay and were not accompanied by a reduction in the synthesis of hemagglutinin and neuraminidase subunits. Both antisera also effectively prevented in vitro virus spread. Inhibition of virus release by neuraminidase antibody appeared unrelated to its antienzyme property. Hydrolysis of N-acetyl neuraminic acid residues of infected host cells proceeded unimpaired in the presence of subunit antisera. Anti-hemagglutinin and anti-neuraminidase antibodies may act to prevent virus release by binding newly formed virus subunits to each other and to anti-genically altered cell membranes.
摘要
在接种细胞培养物之前，将流感病毒与针对其表面亚基的抗血清混合时，抗血凝素抗体可中和感染性，但抗神经氨酸酶抗体则不能。当在细胞培养物感染后加入抗血清时，抗血凝素和抗神经氨酸酶抗体在降低培养液中的病毒滴度方面同样有效。病毒滴度降低并非由于抗体对检测的干扰，且血凝素和神经氨酸酶亚基的合成也未减少。两种抗血清还均能有效阻止病毒在体外传播。神经氨酸酶抗体对病毒释放的抑制作用似乎与其抗酶特性无关。在亚基抗血清存在的情况下，受感染宿主细胞的N - 乙酰神经氨酸残基的水解未受影响。抗血凝素和抗神经氨酸酶抗体可能通过将新形成的病毒亚基彼此结合以及与抗原性改变的细胞膜结合来阻止病毒释放。
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