Selective autophagy receptor SQSTM1/ p62 inhibits Seneca Valley virus replication by targeting viral VP1 and VP3

Wen, Wei; Li, Xiangmin; Yin, Mengge; Wang, Haoyuan; Qin, Li; Li, Hui; Liu, Wenqiang; Zhao, Zekai; Zhao, Qiongqiong; Chen, Huanchun; Hu, Junjie; Qian, Ping

doi:10.1080/15548627.2021.1897223

Cited by 55 publications

(50 citation statements)

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“…There were also several chaperons showing positive correlation with viral genes, such as clusterin (clu), which has antiapoptotic activity and is directly targeted by the Influenza A virus nucleoprotein (Tripathi et al 2013). Another protein of interest is sequestosome-1 (sqstm1), a receptor required for selected autophagy that inhibits Seneca valley virus and avian influenza replication (Wen et al 2021; Liu et al 2021).…”

Section: Resultsmentioning

confidence: 99%

Understanding host response to infectious salmon anaemia virus in an Atlantic salmon cell line using single-cell RNA sequencing

Gervais

Gratacap

Papadopoulou

et al. 2022

Preprint

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Background: Infectious Salmon Anaemia Virus (ISAV) is an Orthomixovirus that currently represents a large problem for salmonid aquaculture worldwide. Prevention and treatment methods are only partially effective. Genetic selection and genome engineering strategies have potential to develop ISAV resistant salmon stocks. However, this requires a detailed understanding of the genomic regulation of ISAV pathogenesis. Here, we used single cell RNA sequencing on a salmonid cell line to provide a high dimensional insight into the transcriptional landscape that underpin host-virus interactions during ISAV infection at the single cell level. Results: Salmon head kidney 1 (SHK-1) cells were single-cell RNA sequenced before challenge, and at 24h, 48h, and 96h post-ISAV challenge. The results revealed marked changes in the host transcriptome at 48h and 96h post-infection, even in uninfected cells, potentially suggesting paracrine signalling. This paracrine activation of uninfected cells seemed to be unspecific, involving pathways such as mRNA sensing, ubiquitination or proteasome, and also the up-regulation of the mitochondrial ribosome genes. At 24h post infection, cells showed expression signatures consistent with viral entry, with up-regulation of genes such as PI3K, FAK or JNK. At 48h and 96h, infected cells showed a clear anti-viral response, characterised by the expression of IFNA2 or IRF2. Conclusions: This study has increased our understanding of the cellular response of Atlantic salmon during ISAV infection, and revealed potential host-virus interactions at the cellular level. The results highlight the value of single-cell sequencing to characterise cell culture models of viral infection, and the results can be exploited in future functional studies to increase the resistance of Atlantic salmon to ISAV.

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Section: Resultsmentioning

confidence: 99%

Understanding host response to infectious salmon anaemia virus in an Atlantic salmon cell line using single-cell RNA sequencing

Gervais

Gratacap

Papadopoulou

et al. 2022

Preprint

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“…Maggioli et al [16] found that SVA VP3 can elicit neutralizing antibodies at an early stage of virus infection. A recent study has shown that SVA VP3 protein is also involved in cell autophagy [17]. These findings indicate that picornavirus VP3 proteins play critical roles in the viral infection of the host.…”

Section: Introductionmentioning

confidence: 85%

Identification of a B-Cell Epitope in the VP3 Protein of Senecavirus A

Chen

Wang

et al. 2021

Viruses

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Senecavirus A (SVA) is a member of the genus Senecavirus of the family Picornaviridae. SVA-associated vesicular disease (SAVD) outbreaks have been extensively reported since 2014–2015. Characteristic symptoms include vesicular lesions on the snout and feet as well as lameness in adult pigs and even death in piglets. The capsid protein VP3, a structural protein of SVA, is involved in viral replication and genome packaging. Here, we developed and characterized a mouse monoclonal antibody (mAb) 3E9 against VP3. A motif 192GWFSLHKLTK201 was identified as the linear B-cell epitope recognized by mAb 3E9 by using a panel of GFP-tagged epitope polypeptides. Sequence alignments show that 192GWFSLHKLTK201 was highly conserved in all SVA strains. Subsequently, alanine (A)-scanning mutagenesis indicated that W193, F194, L196, and H197 were the critical residues recognized by mAb 3E9. Further investigation with indirect immunofluorescence assay indicated that the VP3 protein was present in the cytoplasm during SVA replication. In addition, the mAb 3E9 specifically immunoprecipitated the VP3 protein from SVA-infected cells. Taken together, our results indicate that mAb 3E9 could be a powerful tool to work on the function of the VP3 protein during virus infection.

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“…Activation of autophagy by rapamycin will also disrupt the autophagy process induced by SVA ( 9 , 54 ). Interestingly, this phenomenon seems to be species-specific ( 55 ). Autophagy inducers can inhibit the process of virus-induced autophagy in multiple human cell lines, resulting in reduced SVA replication levels.…”

Section: Sva Infection-induced Cell Death Including Apoptosis Autopha...mentioning

confidence: 99%

“…However, SVA can promote the proliferation and spread of the virus by inducing autophagy in porcine cells. The molecular mechanisms of these species-specific differences need to be further characterized ( 9 , 53 , 55 ).…”

Section: Sva Infection-induced Cell Death Including Apoptosis Autopha...mentioning

confidence: 99%

“…SQSTM1/p62 is an autophagy receptor that can present ubiquitinated substrates to autophagosomes to complete phagocytosis and an important component of the cellular antiviral mechanism ( 56 , 57 ). In SVA-infected cells, overexpressed SQSTM1 promotes virus degradation by targeting SVA’s capsid proteins VP1 and VP3, ultimately inhibiting the spread of SVA ( 55 ). However, current studies have found that the 3Cpro protease of SVA can inhibit SQSTM1-mediated selective autophagy by cleaving SQSTM1, eliminating its antiviral effect ( 55 ).…”

Section: Sva Infection-induced Cell Death Including Apoptosis Autopha...mentioning

confidence: 99%

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Senecavirus A as an Oncolytic Virus: Prospects, Challenges and Development Directions

Luo

Wang

et al. 2022

Front. Oncol.

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Oncolytic viruses have the capacity to selectively kill infected tumor cells and trigger protective immunity. As such, oncolytic virotherapy has become a promising immunotherapy strategy against cancer. A variety of viruses from different families have been proven to have oncolytic potential. Senecavirus A (SVA) was the first picornavirus to be tested in humans for its oncolytic potential and was shown to penetrate solid tumors through the vascular system. SVA displays several properties that make it a suitable model, such as its inability to integrate into human genome DNA and the absence of any viral-encoded oncogenes. In addition, genetic engineering of SVA based on the manipulation of infectious clones facilitates the development of recombinant viruses with improved therapeutic indexes to satisfy the criteria of safety and efficacy regulations. This review summarizes the current knowledge and strategies of genetic engineering for SVA, and addresses the current challenges and future directions of SVA as an oncolytic agent.

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Selective autophagy receptor SQSTM1/ p62 inhibits Seneca Valley virus replication by targeting viral VP1 and VP3

Cited by 55 publications

References 50 publications

Understanding host response to infectious salmon anaemia virus in an Atlantic salmon cell line using single-cell RNA sequencing

Understanding host response to infectious salmon anaemia virus in an Atlantic salmon cell line using single-cell RNA sequencing

Identification of a B-Cell Epitope in the VP3 Protein of Senecavirus A

Senecavirus A as an Oncolytic Virus: Prospects, Challenges and Development Directions

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