1. Common and unique mechanisms of filamentous actin formation by viruses of the genus Orthorubulavirus
- Author
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Yusuke Matsumoto, Machiko Nishio, and Keisuke Ohta
- Subjects
RHOA ,viruses ,macromolecular substances ,Plasma protein binding ,Mumps virus ,Simian ,medicine.disease_cause ,Filamentous actin ,Virus ,Cell Line ,Viral Proteins ,03 medical and health sciences ,Virology ,medicine ,Animals ,Humans ,Rubulavirus ,030304 developmental biology ,0303 health sciences ,biology ,030306 microbiology ,GTPase-Activating Proteins ,Rubulavirus Infections ,General Medicine ,biology.organism_classification ,Actins ,Parainfluenza Virus 2, Human ,Cell culture ,Host-Pathogen Interactions ,Parainfluenza Virus 5 ,biology.protein ,rhoA GTP-Binding Protein ,Protein Binding - Abstract
We previously found that infection with human parainfluenza virus type 2 (hPIV-2), a member of the genus Orthorubulavirus, family Paramyxoviridae, causes filamentous actin (F-actin) formation to promote viral growth. In the present study, we investigated whether similar regulation of F-actin formation is observed in infections with other rubulaviruses, such as parainfluenza virus type 5 (PIV-5) and simian virus 41 (SV41). Infection with these viruses caused F-actin formation and RhoA activation, which promoted viral growth. These results indicate that RhoA-induced F-actin formation is important for efficient growth of these rubulaviruses. Only SV41 and hPIV-2 V and P proteins bound to Graf1, while the V and P proteins of PIV-5, mumps virus, and hPIV-4 did not bind to Graf1. In contrast, the V proteins of these rubulaviruses bound to both inactive RhoA and profilin 2. These results suggest that there are common and unique mechanisms involved in regulation of F-actin formation by members of the genus Orthorubulavirus.
- Published
- 2020