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.

中文翻译：

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正腮红病毒属病毒形成丝状肌动蛋白的共同和独特机制。

我们以前发现人类感染人类副流感病毒2型（hPIV-2），正痘病毒属，副粘病毒科的成员，导致丝状肌动蛋白（F-肌动蛋白）形成，以促进病毒的生长。在本研究中，我们调查了在其他风疹病毒（如副流感病毒5型（PIV-5）和猿猴病毒41（SV41））感染中是否观察到类似的F-肌动蛋白形成调控。这些病毒感染导致F-肌动蛋白形成和RhoA活化，从而促进了病毒的生长。这些结果表明，RhoA诱导的F-肌动蛋白的形成对于这些风疹病毒的有效生长很重要。只有SV41和hPIV-2 V和P蛋白与Graf1结合，而PIV-5，腮腺炎病毒和hPIV-4的V和P蛋白不与Graf1结合。相反，