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<p>Newcastle disease virus (NDV) is an avian paramyxovirus known to infect more than 250 bird species across the globe. NDV is enveloped and carries a negative-sense RNA genome that codes for six structural proteins and two accessory proteins expressed through a unique co-transcriptional RNA editing mechanism. One of the accessory viral proteins, V protein, is multifunctional and a well-known interferon (IFN) antagonist. The overexpression of V protein is known to enhance viral production kinetics during NDV infection. In this study, we elucidated the events that lead to this augmented viral replication. The V protein overexpression downregulated the expression of host RNA sensor, namely MDA5. Furthermore, during the over-expression of V protein in NDV infected cells, the V protein aggregated in the perinuclear region, co-localizing and binding with the replicating dsRNA. Our structural studies and in silico predictions suggest that V protein binding with dsRNA interferes and competes with MDA5 for binding to dsRNA, eventually disrupting the IFN induction and facilitating the viral replication. This study reports a novel mechanism of host immune evasion by the accessory V protein.</p>

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Accessory viral protein, V, of Newcastle Disease Virus binds dsRNA to facilitate immune evasion

  • 期刊论文

  • 发表日期：

    2025年1月18日

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  • Sunny Deval,
  • Vaishnavi Senthil Nathan,
  • Sangita Venkataraman,
  • P. L. Rao,
  • Prajna Parimita Kar,
  • Anand Srivastava,
  • Madhuri Subbiah

摘要

Newcastle disease virus (NDV) is an avian paramyxovirus known to infect more than 250 bird species across the globe. NDV is enveloped and carries a negative-sense RNA genome that codes for six structural proteins and two accessory proteins expressed through a unique co-transcriptional RNA editing mechanism. One of the accessory viral proteins, V protein, is multifunctional and a well-known interferon (IFN) antagonist. The overexpression of V protein is known to enhance viral production kinetics during NDV infection. In this study, we elucidated the events that lead to this augmented viral replication. The V protein overexpression downregulated the expression of host RNA sensor, namely MDA5. Furthermore, during the over-expression of V protein in NDV infected cells, the V protein aggregated in the perinuclear region, co-localizing and binding with the replicating dsRNA. Our structural studies and in silico predictions suggest that V protein binding with dsRNA interferes and competes with MDA5 for binding to dsRNA, eventually disrupting the IFN induction and facilitating the viral replication. This study reports a novel mechanism of host immune evasion by the accessory V protein.