Seneca Valley Virus Exploits TEM8, a Collagen Receptor Implicated in Tumor Growth

Evans, David J.; Wasinger, Alexa M; Brey, Robert N.; Dunleavey, James M.; Croix, Brad St.; Bann, James G.

doi:10.3389/fonc.2018.00506

Cited by 20 publications

(15 citation statements)

References 55 publications

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“…SVA was first discovered in human fetal retinal cell culture medium in 2002, which may be derived from contaminants in fetal bovine serum or porcine trypsin (Reddy et al, 2007). After that, it was developed as a virus oncolytic agent in human cancer therapy but not associated with sporadic cases of vesicular disease in pigs (Koppers-Lalic and Hoeben, 2011;Poirier et al, 2013;Evans et al, 2018). In 2007, the first positive case of SVA related to porcine idiopathic vesicular disease was reported in Canada (Pasma et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons

et al. 2022

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Senecavirus A (SVA) is a new type of virus related to swine vesicular disease, which results in enormous economic losses worldwide. At present, the host transcriptional responses to SVA infection, host-SVA interactions, and the mechanism of SVA in innate immune modulation are not well understood. This study explores the gene expression profiles of PK-15 cells at 0, 6, 12, 18, 24, 36 h SVA post-infection by RNA sequencing. Our analysis identified 61, 510, 1,584, 2,460, and 2,359 differentially expressed genes (DEGs) in the comparison groups S6 vs. Control, S12 vs. Control, S18 vs. Control, S24 vs. Control, S36 vs. Control, respectively. The reproducibility and repeatability of the results were validated by RT-qPCR, and all DEGs exhibited expression patterns consistent with the RNA-seq results. According to GO enrichment analysis and KEGG pathway analysis of DEGs in different periods after SVA infection, we found that SVA infection significantly modified the host cell gene-expression patterns and the host cells responded in highly specific manners, including response to signal reception and transmission, external biotic stimulus, response to the virus and host immune defense response. Notably, we observed the specific induction of type III interferon IFN-λ1 and IFN-λ3, which indicated that type III interferon plays an important antiviral function in PK-15 cells. Furthermore, our results showed that SVA might be recognized by RIG-I/MDA-5 receptors first after infecting PK-15 cells and then activates downstream IRF7-mediated signaling pathways, causing an increase in the expression of type III interferon. This study could provide important insights into the modulation of host metabolism during SVA infection and provide a strong theoretical basis for a better understanding of the pathogenic mechanism and immune escape mechanism of SVA.

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Section: Introductionmentioning

confidence: 99%

Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons

et al. 2022

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“…Interestingly, the protein interacts with Tumor Endothelial Marker 8 (TEM-8). This type I transmembrane receptor is known to be over-expressed in inflammatory processes and in cancer 59 ; it is one of the receptors for the Bacillus anthracis protective antigen toxin and the Seneca Valley Virus 60,61 ; it has also been shown to modulate lymphocyte maturation and ECM remodelling 62,63 . Thus, the interaction between SmERp60 and TEM-8 suggests either a role for this receptor in host-pathogen interaction or a doorway for the parasite to hijack the host immune system.…”

Section: Discussionmentioning

confidence: 99%

A comparative analysis of secreted protein disulfide isomerases from the tropical co-endemic parasites Schistosoma mansoni and Leishmania major

Miele

Badaoui

Maugliani

et al. 2019

Sci Rep

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The human parasites Schistosoma mansoni and Leishmania major are co-endemic and a major threat to human health. Though displaying different tissue tropisms, they excrete/secrete similar subsets of intracellular proteins that, interacting with the host extracellular matrix (ECM), help the parasites invading the host. We selected one of the most abundant proteins found in the secretomes of both parasites, protein disulfide isomerase (PDI), and performed a comparative screening with surface plasmon resonance imaging (SPRi), looking for ECM binding partners. Both PDIs bind heparan sulfate; none of them binds collagens; each of them binds further ECM components, possibly linked to the different tropisms. We investigated by small-angle X-ray scattering both PDIs structures and those of a few complexes with host partners, in order to better understand the differences within this conserved family fold. Furthermore, we highlighted a previously undisclosed moonlighting behaviour of both PDIs, namely a concentration-dependent switch of function from thiol-oxidoreductase to holdase. Finally, we have tried to exploit the differences to look for possible compounds able to interfere with the redox activity of both PDI.

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“…Recently a novel biomarker called tumor endothelial marker 8 (TEM 8) has been confirmed to act as a receptor for SVV, facilitating in viral entry in tumor cells. TEM 8 pre-screening can potentially form an important strategy to select patients for SVV therapeutic clinical trials [ 128 ].…”

Section: Seneca Valley Virusmentioning

confidence: 99%

Clinical Application of Oncolytic Viruses: A Systematic Review

Cook

Chauhan

2020

IJMS

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Leveraging the immune system to thwart cancer is not a novel strategy and has been explored via cancer vaccines and use of immunomodulators like interferons. However, it was not until the introduction of immune checkpoint inhibitors that we realized the true potential of immunotherapy in combating cancer. Oncolytic viruses are one such immunotherapeutic tool that is currently being explored in cancer therapeutics. We present the most comprehensive systematic review of all oncolytic viruses in Phase 1, 2, and 3 clinical trials published to date. We performed a systematic review of all published clinical trials indexed in PubMed that utilized oncolytic viruses. Trials were reviewed for type of oncolytic virus used, method of administration, study design, disease type, primary outcome, and relevant adverse effects. A total of 120 trials were found; 86 trials were available for our review. Included were 60 phase I trials, five phase I/II combination trials, 19 phase II trials, and two phase III clinical trials. Oncolytic viruses are feverously being evaluated in oncology with over 30 different types of oncolytic viruses being explored either as a single agent or in combination with other antitumor agents. To date, only one oncolytic virus therapy has received an FDA approval but advances in bioengineering techniques and our understanding of immunomodulation to heighten oncolytic virus replication and improve tumor kill raises optimism for its future drug development.

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Seneca Valley Virus Exploits TEM8, a Collagen Receptor Implicated in Tumor Growth

Cited by 20 publications

References 55 publications

Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons

Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons

A comparative analysis of secreted protein disulfide isomerases from the tropical co-endemic parasites Schistosoma mansoni and Leishmania major

Clinical Application of Oncolytic Viruses: A Systematic Review

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