Host-cell-dependent role of actin cytoskeleton during the replication of a human strain of influenza A virus

• Published in: Archives of virology Vol. 153; no. 7; pp. 1209 - 1221
• Main Authors: Arcangeletti, M. C, De Conto, F, Ferraglia, F, Pinardi, F, Gatti, R, Orlandini, G, Covan, S, Motta, F, Rodighiero, I, Dettori, G, Chezzi, C
• Format: Journal Article
• Language: English
• Published: Vienna Vienna : Springer Vienna 01-07-2008; Springer Vienna; Springer; Springer Nature B.V
• Subjects: Actins - antagonists & inhibitors; Actins - metabolism; Animals; Biological and medical sciences; Biomedical and Life Sciences; Biomedicine; Cell Line; Cytochalasin D - pharmacology; Cytoskeleton; Cytoskeleton - metabolism; Cytoskeleton - virology; Dogs; Fundamental and applied biological sciences. Psychology; Infections; Infectious Diseases; Influenza A virus; Influenza A virus - physiology; Macaca mulatta; Medical Microbiology; Microbiology; Microscopy, Confocal; Miscellaneous; Original Article; Physiology; Viral infections; Virology; Virus Replication; Viruses; West Nile virus; Italy; Influenza Virus; Actin Cytoskeleton; Actin Network; Cortical Actin; Influenza; Virus; Human; Influenzavirus A; Influenza A virus; Actin; Orthomyxoviridae; Cytoskeleton; Replication; Strain
• ISSN: 0304-8608; 1432-8798
• DOI: 10.1007/s00705-008-0103-0

This study was aimed at investigating the possible involvement of the actin cytoskeleton in the modulation of host permissiveness to A/NWS/33 human influenza virus infection in two mammalian (MDCK and LLC-MK2) cell lines in vitro. During the early stages of infection, no appreciable association between incoming NWS/33 virions and cortical actin was detectable in the permissive MDCK model by confocal microscopy, while extensive colocalization and a slower infection progression were observed in LLC-MK2 cells. In the latter model, we also demonstrated the inability of the virus to carry out multiple replication cycles, irrespective of the presence of cleaved HA subunits in the released virions. Treatment with the actin-depolymerizing agent cytochalasin D significantly increased the infection efficiency in LLC-MK2 cells, while a detrimental effect was observed in the MDCK cell line. Our data suggest a selective role of the actin network in inducing a restriction to influenza virus replication, mostly depending on its molecular organization, the host cell type and virus replication phase.