Crystallization and preliminary X-ray diffraction studies of Seneca Valley Virus-001, a new member of the<i>Picornaviridae</i>family

Venkataraman, Sangita; Reddy, Seshidhar P.; Loo, Jackie; Idamakanti, Neeraja; Hallenbeck, Paul L.; Reddy, Vijay

doi:10.1107/s1744309108006921

Cited by 27 publications

(14 citation statements)

References 13 publications

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“…The genome of SVA is approximately 7.2 kb in length, which contains a single open reading frame (ORF). The ORF encoding a polyprotein of 2181 amino acids, consists of 12 proteins (Lpro, VP1, VP2, VP3, VP4, 2A, 2B, 2C, 3A, 3B, 3C, and 3D) [1][2][3]. Structural biology analysis revealed that the B-cell epitopes of SVA mainly exist in VP2 and VP3 proteins (in our laboratory).…”

Section: Introductionmentioning

confidence: 66%

Comparison of the Pathogenicity of Two Different Branches of Senecavirus a Strain in China

Zhang

Hao

et al. 2020

Pathogens

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Senecavirus A (SVA), an emerging infectious disease, is associated with the porcine idiopathic vesicular disease. Here, the pathogenesis of different strains of SVA was investigated in growing-finishing pigs. We aimed to evaluate the replication characteristics, virus particle morphology, clinical signs, and vesicular lesions in comparison with two different strains of SVA. The animals were infected with SVA HB-CH-2016 or CH/AH-02/2017 by intranasal routes (3 mL, 109TCID50/mL) and monitored daily for 14 days post-inoculation (dpi) for clinical signs and vesicular lesions. Viremia or viral shedding was detected in the blood, fecal swab, and nasal swab samples. Results showed no distinct differences in plaque size, replication ability, and characteristic virions between SVA HB-CH-2016 and CH/AH-02/2017 strains. Animal experimental results showed that both SVA CH/AH-02/2017 and SVA HB-CH-2016 could infect pigs. However, an obvious difference in the pathogenicity and dynamics of infection was observed between SVA HB-CH-2016 and CH/AH-02/2017 strains. The pathogenesis of SVA CH/AH-02/2017 was similar to that of published results of USA strains, whereas the SVA HB-CH-2016 strain had low pathogenicity to pigs. Clinical signs and vesicular lesions were observed in SVA CH/AH-02/2017-infected pigs. Additionally, the different branches of SVA should be capable of inducing broad cross-reactive neutralizing antibodies, which play an important role in clearing the SVA virus. This study of animal models for SVA infection will be beneficial to develop vaccines and antivirals.

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Section: Introductionmentioning

confidence: 66%

Comparison of the Pathogenicity of Two Different Branches of Senecavirus a Strain in China

Zhang

Hao

et al. 2020

Pathogens

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“…Seneca Valley Virus (SVV-001) is a replication-competent oncolytic picornavirus, discovered as a contaminant of a laboratory adenovirus preparation (4–7). The replicative potential of SVV-001 has been studied in a large number of human cancer lines.…”

Section: Introductionmentioning

confidence: 99%

Phase I Clinical Study of Seneca Valley Virus (SVV-001),a Replication-Competent Picornavirus, in Advanced Solid Tumors with Neuroendocrine Features

Rudin

Poirier

Senzer

et al. 2011

Clinical Cancer Research

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114

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Purpose Seneca Valley Virus (SVV-001) is a novel naturally occurring replication-competent picornavirus with potent and selective tropism for neuroendocrine cancer cell types, including small cell lung cancer. We conducted a first-in-human, first-in-class phase I clinical trial of this agent in patients with cancers with neuroendocrine features, including small cell lung cancer. Experimental Design Clinical evaluation of single intravenous doses in patients with cancers with neuroendocrine features was performed across five log-increments from 107 to 1011 vp/kg. Toxicity, viral titers and clearance, neutralizing antibody development, and tumor response were assessed. Results A total of 30 patients were treated with SVV-001, including six with small cell carcinoma at the lowest dose of 107 vp/kg. SVV-001 was well tolerated, with no dose-limiting toxicities observed in any dose cohort. Viral clearance was documented in all subjects and correlated temporally with development of antiviral antibodies. Evidence of in vivo intratumoral viral replication was observed among patients with small cell carcinoma, with peak viral titers estimated to be >103-fold higher than the administered dose. One patient with previously progressive chemorefractory small cell lung cancer remained progression-free for 10 months after SVV-001 administration, and is alive over 3 years after treatment. Conclusions Intravenous SVV-001 administration in patients is well tolerated at doses up to 1011 vp/kg, with predictable viral clearance kinetics, intratumoral viral replication, and evidence of antitumor activity in patients with small cell lung cancer. Phase II clinical evaluation in small cell lung cancer is warranted, and has been initiated.

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“…The SVV-001 was crystallized in a R3 space group with unit cell dimensions a = b =311.5Å, c =1526.4Å, α=β=90°, γ=120° and it’s structure was determined at 2.3Å resolution by molecular replacement using MEV capsid as the model (Venkataraman et al, 2008). The unit cell of SVV-001 is unusual because of a long c -axis (1526Å) that is nearly 4.9 times the lengths of a or b axis (311Å) and hence accommodates six virus particles.…”

Section: Methodsmentioning

confidence: 99%

Structure of Seneca Valley Virus-001: An Oncolytic Picornavirus Representing a New Genus

Reddy²,

et al. 2008

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SUMMARY The crystal structure of Seneca Valley Virus-001, SVV-001, the representative member of a new genus “Senecavirus” is reported at 2.3Å resolution. SVV-001 is the first naturally occurring non-pathogenic picornavirus seen to mediate selective cytotoxicity towards tumor cells with neuroendocrine cancer features. The non-segmented (+) ssRNA genome of SVV-001 shares closest sequence similarity with the genomes of the members of Cardiovirus. The overall tertiary structure of VP1-VP4 subunits is conserved with the exception of loops, especially those of VP1 that show large deviations relative to the members of the Cardioviruses. The surface loops of VP1 and VP2 are predicted to mediate cell tropism of SVV-001. In addition, the organization of the packaged nucleic acid density indicates that certain regions of VP2 and VP4 interact closely with the packaged nucleic acid.

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Crystallization and preliminary X-ray diffraction studies of Seneca Valley Virus-001, a new member of thePicornaviridaefamily

Cited by 27 publications

References 13 publications

Comparison of the Pathogenicity of Two Different Branches of Senecavirus a Strain in China

Comparison of the Pathogenicity of Two Different Branches of Senecavirus a Strain in China

Phase I Clinical Study of Seneca Valley Virus (SVV-001),a Replication-Competent Picornavirus, in Advanced Solid Tumors with Neuroendocrine Features

Structure of Seneca Valley Virus-001: An Oncolytic Picornavirus Representing a New Genus

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