The Function behind the Relation between Lipid Metabolism and Vimentin on H9N2 Subtype AIV Replication

Lu, Anran; Yang, Jing; Huang, Xiangyu; Huang, Xinmei; Yin, Guihu; Cai, Yiqin; Feng, Xiuli; Zhang, Xiaofei; Li, Yin; Liu, Qingtao

doi:10.3390/v14081814

Cited by 3 publications

(2 citation statements)

References 42 publications

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“…Viral attachment is crucial for the successful establishment of viral infection [ 33 ]. Vimentin can play a dual role in viral infection by serving as a coreceptor for SARS-CoV [ 8 ] and SARS-CoV-2 [ 9 ] to enhance viral attachment, while it can also impede the attachment of AIV by disrupting the formation of lipid rafts on the surface of host cells [ 36 ]. In this study, cell surface vimentin had no significant effect on the attachment of genotype III NDVs.…”

Section: Discussionmentioning

confidence: 99%

Cellular vimentin regulates the infectivity of Newcastle disease virus through targeting of the HN protein

Lu,

Liu,

Chen

et al. 2023

Vet Res

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The haemagglutinin-neuraminidase (HN) protein plays a crucial role in the infectivity and virulence of Newcastle disease virus (NDV). In a previous study, the mutant HN protein was identified as a crucial virulence factor for the velogenic variant NDV strain JS/7/05/Ch, which evolved from the prototypic vaccine strain Mukteswar. Furthermore, macrophages are the main susceptible target cells of NDV. However, the possible involvement of cellular molecules in viral infectivity remains unclear. Herein, we elucidate the crucial role of vimentin, an intermediate filament protein, in regulating NDV infectivity through targeting of the HN protein. Using LC‒MS/MS mass spectrometry and coimmunoprecipitation assays, we identified vimentin as a host protein that differentially interacted with prototypic and mutant HN proteins. Further analysis revealed that the variant NDV strain induced more significant rearrangement of vimentin fibres compared to the prototypic NDV strain and showed an interdependence between vimentin rearrangement and virus replication. Notably, these mutual influences were pronounced in HD11 chicken macrophages. Moreover, vimentin was required for multiple infection processes of the variant NDV strain in HD11 cells, including viral internalization, fusion, and release, while it was not necessary for those of the prototypic NDV strain. Collectively, these findings underscore the pivotal role of vimentin in NDV infection through targeting of the HN protein, providing novel targets for antiviral treatment strategies for NDV.

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Section: Discussionmentioning

confidence: 99%

Cellular vimentin regulates the infectivity of Newcastle disease virus through targeting of the HN protein

Lu,

Liu,

Chen

et al. 2023

Vet Res

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“…Vimentin regulates the activity and intracellular transport of IAVs, also exerting critical roles in the host cell response [ 80 , 89 ]. Specifically, it has been assessed that vimentin might play an important role in the regulation of lipids during H9N2 replication, providing an important antiviral target against the influenza virus [ 90 ]. Moreover, it has been shown that the integrity of IFs affects the release of H7N1 AIV progeny in mammalian cells, leading to decreased viral replication efficiency [ 91 ].…”

Section: The Involvement Of the Cellular Cytoskeleton In Influenza Vi...mentioning

confidence: 99%

Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts

De Conto

2024

Pathogens

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Influenza is one of the most prevalent causes of death worldwide. Influenza A viruses (IAVs) naturally infect various avian and mammalian hosts, causing seasonal epidemics and periodic pandemics with high morbidity and mortality. The recent SARS-CoV-2 pandemic showed how an animal virus strain could unpredictably acquire the ability to infect humans with high infection transmissibility. Importantly, highly pathogenic avian influenza A viruses (AIVs) may cause human infections with exceptionally high mortality. Because these latter infections pose a pandemic potential, analyzing the ecology and evolution features of host expansion helps to identify new broad-range therapeutic strategies. Although IAVs are the prototypic example of molecular strategies that capitalize on their coding potential, the outcome of infection depends strictly on the complex interactions between viral and host cell factors. Most of the studies have focused on the influenza virus, while the contribution of host factors remains largely unknown. Therefore, a comprehensive understanding of mammals’ host response to AIV infection is crucial. This review sheds light on the involvement of the cellular cytoskeleton during the highly pathogenic AIV infection of mammalian hosts, allowing a better understanding of its modulatory role, which may be relevant to therapeutic interventions for fatal disease prevention and pandemic management.

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Japanese encephalitis virus NS1 and NS1’ proteins induce vimentin rearrangement via the CDK1-PLK1 axis to promote viral replication

Xie,

Yang,

Yang

et al. 2024

J Virol

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The host cytoskeleton plays crucial roles in various stages of virus infection, including viral entry, transport, replication, and release. However, the specific mechanisms by which intermediate filaments are involved in orthoflavivirus infection have not been well understood. In this study, we demonstrate that the Japanese encephalitis virus (JEV) remodels the vimentin network, resulting in the formation of cage-like structures that support viral replication. Mechanistically, JEV NS1 and NS1’ proteins induce the translocation of CDK1 from the nucleus to the cytoplasm and interact with it, leading to the phosphorylation of vimentin at Ser56. This phosphorylation event recruits PLK1, which further phosphorylates vimentin at Ser83. Consequently, these phosphorylation modifications convert the typically filamentous vimentin into non-filamentous “particles” or “squiggles.” These vimentin “particles” or “squiggles” are then transported retrogradely along microtubules to the endoplasmic reticulum, where they form cage-like structures. Notably, NS1’ is more effective than NS1 in triggering the CDK1-PLK1 cascade response. Overall, our study provides new insights into how JEV NS1 and NS1’ proteins manipulate the vimentin network to facilitate efficient viral replication. IMPORTANCE Japanese encephalitis virus (JEV) is a mosquito-borne orthoflavivirus that causes severe encephalitis in humans, particularly in Asia. Despite the availability of a safe and effective vaccine, JEV infection remains a significant public health threat due to limited vaccination coverage. Understanding the interactions between JEV and host proteins is essential for developing more effective antiviral strategies. In this study, we investigated the role of vimentin, an intermediate filament protein, in JEV replication. Our findings reveal that JEV NS1 and NS1’ proteins induce vimentin rearrangement, resulting in the formation of cage-like structures that envelop the viral replication factories (RFs), thus facilitating efficient viral replication. Our research highlights the importance of the interplay between the cytoskeleton and orthoflavivirus, suggesting that targeting vimentin could be a promising approach for the development of antiviral strategies to inhibit JEV propagation.

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The Function behind the Relation between Lipid Metabolism and Vimentin on H9N2 Subtype AIV Replication

Cited by 3 publications

References 42 publications

Cellular vimentin regulates the infectivity of Newcastle disease virus through targeting of the HN protein

Cellular vimentin regulates the infectivity of Newcastle disease virus through targeting of the HN protein

Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts

Japanese encephalitis virus NS1 and NS1’ proteins induce vimentin rearrangement via the CDK1-PLK1 axis to promote viral replication

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