{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T23:43:19Z","timestamp":1791157399969,"version":"4.1.0"},"reference-count":66,"publisher":"American Society for Microbiology","issue":"23","license":[{"start":{"date-parts":[[2015,12,1]],"date-time":"2015-12-01T00:00:00Z","timestamp":1448928000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>Paramyxoviruses include many important animal and human pathogens. The genome of parainfluenza virus 5 (PIV5), a prototypical paramyxovirus, encodes a V protein that inhibits viral RNA synthesis. In this work, the mechanism of inhibition was investigated. Using mutational analysis and a minigenome system, we identified regions in the N and C termini of the V protein that inhibit viral RNA synthesis: one at the very N terminus of V and the second at the C terminus of V. Furthermore, we determined that residues L16 and I17 are critical for the inhibitory function of the N-terminal region of the V protein. Both regions interact with the nucleocapsid protein (NP), an essential component of the viral RNA genome complex (RNP). Mutations at L16 and I17 abolished the interaction between NP and the N-terminal domain of V. This suggests that the interaction between NP and the N-terminal domain plays a critical role in V inhibition of viral RNA synthesis by the N-terminal domain. Both the N- and C-terminal regions inhibited viral RNA replication. The C terminus inhibited viral RNA transcription, while the N-terminal domain enhanced viral RNA transcription, suggesting that the two domains affect viral RNA through different mechanisms. Interestingly, V also inhibited the synthesis of the RNA of other paramyxoviruses, such as Nipah virus (NiV), human parainfluenza virus 3 (HPIV3), measles virus (MeV), mumps virus (MuV), and respiratory syncytial virus (RSV). This suggests that a common host factor may be involved in the replication of these paramyxoviruses.<\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            We identified two regions of the V protein that interact with NP and determined that one of these regions enhances viral RNA transcription via its interaction with NP. Our data suggest that a common host factor may be involved in the regulation of paramyxovirus replication and could be a target for broad antiviral drug development. Understanding the regulation of paramyxovirus replication will enable the rational design of vaccines and potential antiviral drugs.\n          <\/jats:p>","DOI":"10.1128\/jvi.01832-15","type":"journal-article","created":{"date-parts":[[2015,9,17]],"date-time":"2015-09-17T03:38:17Z","timestamp":1442461097000},"page":"11845-11857","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":14,"title":["Regulation of Viral RNA Synthesis by the V Protein of Parainfluenza Virus 5"],"prefix":"10.1128","volume":"89","author":[{"given":"Yang","family":"Yang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, Hubei, China"},{"name":"Department of Infectious Diseases, University of Georgia College of Veterinary Medicine, Athens, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Zengel","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, University of Georgia College of Veterinary Medicine, Athens, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minghao","family":"Sun","sequence":"additional","affiliation":[{"name":"Graduate Program in Pathobiology, Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katrina","family":"Sleeman","sequence":"additional","affiliation":[{"name":"National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Khalid Amine","family":"Timani","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason","family":"Aligo","sequence":"additional","affiliation":[{"name":"Intercollege Graduate Program in Genetics, Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Rota","sequence":"additional","affiliation":[{"name":"National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianguo","family":"Wu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, Hubei, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Biao","family":"He","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, University of Georgia College of Veterinary Medicine, Athens, Georgia, USA"},{"name":"Graduate Program in Pathobiology, Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","volume-title":"Fields virology","author":"Lamb RA","year":"2001","unstructured":"Lamb RA, Kolakofsky D. 2001. 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