Department of Microbiology, School of Medicine, Wakayama Medical University, 811-1, Kimiidera, Wakayama, 641-8509, Japan.
Arch Virol. 2020 Apr;165(4):799-807. doi: 10.1007/s00705-020-04565-y. Epub 2020 Feb 25.
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.
我们之前发现,副黏病毒科副黏液病毒属的人类副流感病毒 2 型(hPIV-2)感染会导致丝状肌动蛋白(F-actin)形成,从而促进病毒生长。在本研究中,我们调查了其他副黏液病毒(如副流感病毒 5 型(PIV-5)和猿猴病毒 41 型(SV41))感染中是否观察到类似的 F-actin 形成调节。这些病毒的感染导致 F-actin 形成和 RhoA 激活,从而促进了病毒的生长。这些结果表明,RhoA 诱导的 F-actin 形成对于这些副黏液病毒的有效生长很重要。只有 SV41 和 hPIV-2 的 V 和 P 蛋白与 Graf1 结合,而 PIV-5、腮腺炎病毒和 hPIV-4 的 V 和 P 蛋白则不与 Graf1 结合。相比之下,这些副黏液病毒的 V 蛋白与无活性的 RhoA 和 Profilin 2 均结合。这些结果表明,在副黏液病毒属成员中,F-actin 形成的调节存在共同和独特的机制。