Analysis of viral and cellular parameters which affect the fusion process of influenza viruses

In the present investigation we studied the fusogenic process developed by influenza A, B and C viruses on cell surfaces and different factors associated with virus and cell membrane structures. The biological activity of purified virus strains was evaluated in hemagglutination, sialidase and fusion assays. Hemolysis by influenza A, B and C viruses ranging from 77.4 to 97.2 percent, from 20.0 to 65.0 percent, from 0.2 to 93.7 percent and from 9.0 to 76.1 percent was observed when human, chicken, rabbit and monkey erythrocytes, respectively, were tested at pH 5.5. At this pH, low hemolysis indexes for influenza A, B and C viruses were observed if horse erythrocytes were used as target cells for the fusion process, which could be explained by an inefficient receptor binding activity of influenza on N-glycolyl sialic acids. Differences in hemaglutinin receptor binding activity due to its specificity to N-acetyl or N-glycolyl cell surface oligosaccharides, density of these cellular receptors and level of negative charges on the cell surface may possibly explain these results, showing influence on the sialidase activity and the fusogenic process. Comparative analysis showed a lack of dependence between the sialidase and fusion activities developed by influenza B viruses. Influenza A viruses at low sialidase titers (<2) also exhibited clearly low hemolysis at pH 5.5 (15.8 percent), while influenza B viruses with similarly low sialidase titers showed highly variable hemolysis indexes (0.2 to 78.0 percent). These results support the idea that different virus and cell-associated factors such as those presented above have a significant effect on the multifactorial fusion process.

Induçäo de interferon humano de membrana aminiótica: papel de particulas defectivas interferentes / induction of human amniotic interferon by strains of paramyxovirus: Role of defective interfering particles

Resumo: A amostra Cantell de vírus parainfluenza 1 necessita de partículas defectivas interferentes (DI) para a produçäo de interferon (IFN) humano. A amostra Mill Hill do vírus da doença de Newcastle aparentemente näo as requer, embopra seja um indutor de IFN ainda mais potente. Para examinar este comportamento diverso, foram feitas passagens seriadas em ovos embrionados em baixa e alta multiciplidade de infecçäo com estes vírus, sendo que esta última propicia a formaçäo de particulas DI. Após cada passagem, o interferon humano de membrana aminiótica (IFN-MA) foi induzido e foram determinados os títulos hemaglutinante e infeccioso dos vírus e o do IFN-MA. A amostra Cantell mostrou uma reduçäo de 10.000 vezes em seu titulo infeccioso com as passagens em alta multiciplidade. Os títulos de IFN-MA produzidos foram cerca de 300 unidades por ml nas passagens em baixa multiciplidade. Contudo, a capacidade indutora desta amostra subiu de 1.200 para 4.200 unidades por ml nas passagens com alta multiplicidade. Coma amostra Mill Hill, as passagens seriadas em baixa ou alta multiplicidade de infecçäo näo modificaram os títulos infectantes ou as quantidades geradas de IFN-MA pela amostrra Cantell. Com a amostra Mill Hill, todavia, näo pode ser demonstrada a formaçäo de partículas DI, nem modificaçöes dos títulos de IFN-MA foram observados com a adiçäo de partículas DI da amostra Cantell (au)