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PI4KB on Inclusion Bodies Formed by ER Membrane Remodeling Facilitates Replication of Human Parainfluenza Virus Type 3

机译:通过ER膜重塑形成的包涵体上的PI4KB有助于复制人痹流病毒类型3

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Many positive-strand RNA viruses remodel theendomembrane to form specialized replication organelles.However, knowledge regarding whethernegative-strand RNA viruses take advantage of intracellularmembranes for replication is limited. Here weshow that a negative-strand RNA virus, human parainfluenzavirus type 3 (HPIV3), remodels the endoplasmicreticulum (ER) membrane to form inclusionbodies (IBs), whereby the phosphoprotein (P) ofHPIV3 recruits phosphatidylinositol 4-kinase beta(PI4KB) to IBs to generate PI4P, creating a PI4P-enrichedmicroenvironment to promote HPIV3 replication.In addition, we find that human respiratorysyncytial virus (HRSV) also takes advantage of theER to form IBs and that these IBs are also enrichedwith PI4P. The nucleoprotein of HRSV recruitsPI4KB to IBs. These results suggest that paramyxovirusesalso exploit the host endomembrane toform IBs and that PI4KB is recruited by viral proteinsto enrich IBs with PI4P to facilitate viral replication.
机译:许多阳性RNA病毒改造特立膜以形成专业的复制细胞器。然而,有关NEREAD-STRAND RNA病毒的知识是否利用细胞内映射进行复制。在这里,Wealow认为,一种负链RNA病毒,人对血征型3(HPIV3),重塑内皮内(ER)膜以形成包合物(IBS),其中HPIV3磷蛋白(P)新增磷脂酰肌醇4-激酶β(PI4KB)至IBS要生成PI4P,创建一个PI4P-Richedmicroenvironmentment,以促进HPIV3复制。此外,我们发现人类呼吸系统的病毒(HRSV)还利用了ARER形成IBS,并且这些IBS也富含PI4P。 HRSV的核蛋白促进了IBS至IBS。这些结果表明,副磷病毒血清缺乏宿主EndoMembrane Toform IBS,并且通过病毒蛋白抗菌剂与PI4P征集PI4KB以促进病毒复制。

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