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Order Picornavirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Next, Dalsgaard et al. (1997) reported the insertion of a 17-aa epitope DGAVQPDGGQPAVRNER from the N-terminal part of the VP2 capsid protein of mink enteritis virus (MEV), corresponding to aa residues 3–19 from VP2 of canine parvovirus (CPV) and the successful expression of the epitope on the surface of the chimeric CPMV when propagated in cowpea. The efficacy of the chimeric virus was established by the demonstration that one subcutaneous injection of 1 mg of the chimera in mink conferred protection against clinical disease and virtually abolished shedding of virus after challenge with virulent MEV. Remarkably, the epitope used occurred in three different virus species—MEV, CPV, and feline panleukopenia virus (FPLV) from the family Parvoviridae, order Piccovirales (Chapter 9), and thus the same vaccine could be used in three economically important viral hosts—mink, dogs, and cats, respectively (Dalsgaard et al. 1997). In fact, Langeveld et al. (2001) found that the CPMV chimeras carrying the same 17-aa epitope corresponding to aa residues 3–19 from VP2 of the CPV, inserted between aa 22 and 23 of the CPMV S protein, provided complete protection of dogs from clinical disease and CPV shedding in vivo. Furthermore, the fine character of immune response (Nicholas et al. 2002) and the effect of priming/booster immunization protocols (Nicholas et al. 2003) on immune response to CPV in mice were characterized.
Critical Appraisal of Animal Models for Antibiotic Toxicity
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Patricia D. Williams, Girard H. Hottendorf
Animals: Male and female adult mongrel cats, weighing between 2.1 and 4.2 kg when started on the study, were immunized against feline panleukopenia and feline rhinotracheitis and conditioned for at least 4 weeks prior to use. Thecats were divided into groups of five according to body weight and sex.
TANK-binding kinase 1 as a novel therapeutic target for viral diseases
Published in Expert Opinion on Therapeutic Targets, 2019
The human T lymphotropic virus type 1 (HTLV-1) accomplishes its life cycle through its oncoprotein Tax. Tax inhibits the K63-linked ubiquitination of STING to disrupt the interaction between STING and TBK1. Additionally, Tax binds to TBK1 and blocks its kinase activity [101,102]. Several viral proteins disturb the activity of TBK1 through the steric hindrance. For example, NS2 of feline panleukopenia virus (FPV) [103] and papain-like protease (PLpro) of severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) [104], interact directly with TBK1 to prevent the formation of STING containing complexes. Furthermore, Porcine epidemic diarrhea virus (PEDV)-encoded nucleocapsid (N) protein [105] and the open reading frame 11 (ORF11) of murine gammaherpesvirus 68 (MHV-68) [106] perturb the interaction between TBK1 and IRF3 by direct targeting TBK1.