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Journal articles on the topic 'VP2 mutation'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Popa-Wagner, Ruth, Florian Sonntag, Kristin Schmidt, Jason King, and Jürgen A. Kleinschmidt. "Nuclear translocation of adeno-associated virus type 2 capsid proteins for virion assembly." Journal of General Virology 93, no. 9 (2012): 1887–98. http://dx.doi.org/10.1099/vir.0.043232-0.

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Adeno-associated virus (AAV) capsid assembly occurs in the nucleus. Newly synthesized capsid proteins VP1, VP2 and VP3 contain several basic regions (BRs), which may act as nuclear localization signals (NLSs). Mutation of BR2 and BR3, located at the VP1 and VP2 N termini, marginally reduced nuclear uptake of VP1 or VP2, but not of VP3, when expressed in the context of the whole AAV type 2 (AAV2) genome. Combined mutation of BR1, BR2 and BR3 resulted in capsids with slightly reduced amounts of VP1. Expression of isolated VP1/2 N termini revealed an influence of BR3 on nuclear transport, whilst

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Yuan, Hong, Pinghua Li, Huifang Bao, et al. "Engineering viable foot-and-mouth disease viruses with increased acid stability facilitate the development of improved vaccines." Applied Microbiology and Biotechnology 104, no. 4 (2020): 1683–94. http://dx.doi.org/10.1007/s00253-019-10280-9.

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AbstractFoot-and-mouth disease virus (FMDV), the most acid-unstable virus among picornaviruses, tends to disassemble into pentamers at pH values slightly below neutrality. However, the structural integrity of intact virion is one of the most important factors that influence the induction of a protective antibody response. Thus, improving the acid stability of FMDV is required for the efficacy of vaccine preparations. According to the previous studies, a single substitution or double amino acid substitutions (VP1 N17D, VP2 H145Y, VP2 D86H, VP3 H142D, VP3 H142G, and VP1 N17D + VP2 H145Y) in the

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Chang, Xiaoran, Lisai Zhu, Junying Hu, et al. "Unveiling of Evolution Pattern for HY12 Enterovirus Quasispecies and Pathogenicity Alteration." Viruses 13, no. 11 (2021): 2174. http://dx.doi.org/10.3390/v13112174.

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Enterovirus, like the majority of RNA viruses, evolves to survive the changeable environments by a variety of strategies. Here, we showed that HY12 virus evolved to alter its characteristics and pathogenicity by employing a non-synonymous mutation. Analyses of 5′UTR, VP1 and VP2 gene sequences revealed the existence of HY12 virus in an array of mutants defined as quasispecies. The determination of diversity and complexity showed that the mutation rate and complexity of HY12 virus quasispecies increased, while the proportion of HY12 VP1 and VP2 consensus (master) sequences decreased with increa

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4

Wang, Hui, Yulu Fang, Yongtao Jia, Jiajie Tang, and Changzheng Dong. "In silico epitope prediction and evolutionary analysis reveals capsid mutation patterns for enterovirus B." PLOS ONE 18, no. 8 (2023): e0290584. http://dx.doi.org/10.1371/journal.pone.0290584.

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Enterovirus B (EVB) is a common species of enterovirus, mainly consisting of Echovirus (Echo) and Coxsackievirus B (CVB). The population is generally susceptible to EVB, especially among children. Since the 21st century, EVB has been widely prevalent worldwide, and can cause serious diseases, such as viral meningitis, myocarditis, and neonatal sepsis. By using cryo-electron microscopy, the three-dimensional (3D) structures of EVB and their uncoating receptors (FcRn and CAR) have been determined, laying the foundation for the study of viral pathogenesis and therapeutic antibodies. A limited num

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Shishido-Hara, Yukiko, Shizuko Ichinose, Kayoko Higuchi, Yoshinobu Hara, and Kotaro Yasui. "Major and Minor Capsid Proteins of Human Polyomavirus JC Cooperatively Accumulate to Nuclear Domain 10 for Assembly into Virions." Journal of Virology 78, no. 18 (2004): 9890–903. http://dx.doi.org/10.1128/jvi.78.18.9890-9903.2004.

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ABSTRACT The human polyomavirus JC (JCV) replicates in the nuclei of infected cells. Here we report that JCV virions are efficiently assembled at nuclear domain 10 (ND10), which is also known as promyelocytic leukemia (PML) nuclear bodies. The major capsid protein VP1, the minor capsid proteins VP2 and VP3, and a regulatory protein called agnoprotein were coexpressed from a polycistronic expression vector in COS-7 cells. We found that VP1 accumulated to distinct subnuclear domains in the presence of VP2/VP3 and agnoprotein, while VP1 expressed alone was distributed both in the cytoplasm and in

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Bertolotti-Ciarlet, Andrea, Sue E. Crawford, Anne M. Hutson, and Mary K. Estes. "The 3′ End of Norwalk Virus mRNA Contains Determinants That Regulate the Expression and Stability of the Viral Capsid Protein VP1: a Novel Function for the VP2 Protein." Journal of Virology 77, no. 21 (2003): 11603–15. http://dx.doi.org/10.1128/jvi.77.21.11603-11615.2003.

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ABSTRACT Norwalk virus (NV) is the prototype strain of a group of noncultivable human caliciviruses responsible for epidemic outbreaks of acute gastroenteritis. The capsid protein VP1 is synthesized from a subgenomic RNA that contains two open reading frames (ORFs), ORF2 and ORF3, and the 3′ untranslated region (UTR). ORF2 and ORF3 code for the capsid protein (VP1) and a small structural basic protein (VP2), respectively. We discovered that the yields of virus-like particles (VLPs) composed of VP1 are significantly reduced when this protein is expressed from ORF2 alone. To determine how the 3′

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Stadnick, E., M. Dan, A. Sadeghi, and J. K. Chantler. "Attenuating Mutations in Coxsackievirus B3 Map to a Conformational Epitope That Comprises the Puff Region of VP2 and the Knob of VP3." Journal of Virology 78, no. 24 (2004): 13987–4002. http://dx.doi.org/10.1128/jvi.78.24.13987-14002.2004.

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ABSTRACT Ten antibody escape mutants of coxsackievirus B3 (CVB3) were used to identify nucleotide substitutions that determine viral virulence for the heart and pancreas. The P1 region, encoding the structural genes of each mutant, was sequenced to identify mutations associated with the lack of neutralization. Eight mutants were found to have a lysine-to arginine mutation in the puff region of VP2, while two had a glutamate-to-glycine substitution in the knob of VP3. Two mutants, EM1 and EM10, representing each of these mutations, were further analyzed, initially by determining their entire se

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Lim, Boon-Leong, Yongchang Cao, Tiffany Yu, and Chi-Wai Mo. "Adaptation of Very Virulent Infectious Bursal Disease Virus to Chicken Embryonic Fibroblasts by Site-Directed Mutagenesis of Residues 279 and 284 of Viral Coat Protein VP2." Journal of Virology 73, no. 4 (1999): 2854–62. http://dx.doi.org/10.1128/jvi.73.4.2854-2862.1999.

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ABSTRACT The full-length RNA genomes of a chicken embryonic fibroblast (CEF)-nonpermissive, very virulent infectious bursal disease virus (IBDV) (strain HK46) were amplified into cDNAs by reverse transcription-PCR. The full-length cDNAs were sequenced and subcloned into a eukaryotic expression vector, from which point mutations were introduced into the VP2 region by site-directed mutagenesis. The wild-type and mutated plasmids were transfected directly into CEFs to examine their ability to generate CEF-permissive recombinant viruses. Substitution of amino acid residues 279 (Asp→Asn) and 284 (A

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9

Battilani, Mara, Alessandra Scagliarini, Ernesto Tisato, et al. "Analysis of canine parvovirus sequences from wolves and dogs isolated in Italy." Journal of General Virology 82, no. 7 (2001): 1555–60. http://dx.doi.org/10.1099/0022-1317-82-7-1555.

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The VP2 genes of Italian canine parvovirus (CPV) type 2 strains isolated from dogs and wolves were sequenced and a three-dimensional model of the VP2 capsid protein was constructed. Two mutations were detected in the VP2 sequences of the Italian strains: one at residue 297 and one at residue 265. Variant 297 is the predominant CPV isolate in Europe, whereas variant 265 has never been detected before. The mutation at residue 265 causes a disruption in a G strand of the β-barrel in the VP2 protein. Data on strains isolated from wolves demonstrated that the same strain of CPV can circulate among

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Shishido-Hara, Yukiko, Yoshinobu Hara, Theresa Larson, Kotaro Yasui, Kazuo Nagashima, and Gerald L. Stoner. "Analysis of Capsid Formation of Human Polyomavirus JC (Tokyo-1 Strain) by a Eukaryotic Expression System: Splicing of Late RNAs, Translation and Nuclear Transport of Major Capsid Protein VP1, and Capsid Assembly." Journal of Virology 74, no. 4 (2000): 1840–53. http://dx.doi.org/10.1128/jvi.74.4.1840-1853.2000.

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ABSTRACT Human polyomavirus JC (JCV) can encode the three capsid proteins VP1, VP2, and VP3, downstream of the agnoprotein in the late region. JCV virions are identified in the nucleus of infected cells. In this study, we have elucidated unique features of JCV capsid formation by using a eukaryotic expression system. Structures of JCV polycistronic late RNAs (M1 to M4 and possibly M5 and M6) generated by alternative splicing were determined. VP1 would be synthesized from M2 RNA, and VP2 and VP3 would be synthesized from M1 RNA. The presence of the open reading frame of the agnoprotein or the l

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11

Hewat, Elizabeth A., Thomas C. Marlovits, and Dieter Blaas. "Structure of a Neutralizing Antibody Bound Monovalently to Human Rhinovirus 2." Journal of Virology 72, no. 5 (1998): 4396–402. http://dx.doi.org/10.1128/jvi.72.5.4396-4402.1998.

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ABSTRACT The structure of a complex between human rhinovirus 2 (HRV2) and the Fab fragment of neutralizing monoclonal antibody (MAb) 3B10 has been determined to 25-Å resolution by cryoelectron microscopy and three-dimensional reconstruction techniques. The footprint of 3B10 on HRV2 is very similar to that of neutralizing MAb 8F5, which binds bivalently across the icosahedral twofold axis. However, the 3B10 Fab fragment (Fab-3B10) is bound in an orientation, inclined at approximately 45° to the surface of the virus capsid, which is compatible only with monovalent binding of the antibody. The ca

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12

Chua, Beng Hooi, Patchara Phuektes, Sharon A. Sanders, Philip K. Nicholls, and Peter C. McMinn. "The molecular basis of mouse adaptation by human enterovirus 71." Journal of General Virology 89, no. 7 (2008): 1622–32. http://dx.doi.org/10.1099/vir.0.83676-0.

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A mouse-adapted strain of human enterovirus 71 (HEV71) was selected by serial passage of a HEV71 clinical isolate (HEV71-26M) in Chinese hamster ovary (CHO) cells (CHO-26M) and in newborn BALB/c mice (MP-26M). Despite improved growth in CHO cells, CHO-26M did not show increased virulence in newborn BALB/c mice compared with HEV71-26M. By contrast, infection of newborn mice with MP-26M resulted in severe disease of high mortality. Skeletal muscle was the primary site of replication in mice for both viruses. However, MP-26M infection induced severe necrotizing myositis, whereas CHO-26M infection

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Jumaa, Rawaa S. "Genetic Analysis of Field Isolates of Infectious Bursal Disease Virus in Iraqi Farms." Iraqi Journal of Veterinary Medicine 44, no. 1 (2020): 18–28. http://dx.doi.org/10.30539/ijvm.v44i1.931.

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Sixty samples of bursa of Fabricius were collected from broiler chickens suspected to be infected with infectious bursal disease virus (IBDV) in different areas of Iraq. The extracted nucleic acid was amplified using reverse transcriptase polymerase chain reaction (RT-PCR) targeting genes of segment A (Vp2, Vp3, Vp4 and Vp5 genes) and segment B (VP1 genes). The products of amplification were sent to Korea for sequencing using Sanger method. The sequencing analysis of the IBDV from the Iraqi isolates revealed that each gene had different transition and transversion (nonsense and missense of poi

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14

Lupescu, Adrian, C. Thomas Bock, Philipp A. Lang, et al. "Phospholipase A2 Activity-Dependent Stimulation of Ca2+ Entry by Human Parvovirus B19 Capsid Protein VP1." Journal of Virology 80, no. 22 (2006): 11370–80. http://dx.doi.org/10.1128/jvi.01041-06.

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ABSTRACT Recent reports demonstrated an association of human parvovirus B19 with inflammatory cardiomyopathy (iCMP), which is accompanied by endothelial dysfunction. As intracellular Ca2+ activity is a key regulator of cell function and participates in mechanisms leading to endothelial dysfunction, the present experiments explored the effects of the B19 capsid proteins VP1 and VP2. A secreted phospholipase A2 (PLA2)-like activity has been located in the VP1 unique region of the B19 minor capsid protein. As PLA2 has recently been shown to activate the store-operated or capacitative Ca2+ channel

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Tsunoda, Ikuo, Yoshiaki Wada, Jane E. Libbey, Thomas S. Cannon, Frank G. Whitby, and Robert S. Fujinami. "Prolonged Gray Matter Disease without Demyelination Caused by Theiler's Murine Encephalomyelitis Virus with a Mutation in VP2 Puff B." Journal of Virology 75, no. 16 (2001): 7494–505. http://dx.doi.org/10.1128/jvi.75.16.7494-7505.2001.

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ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups based on neurovirulence. During the acute phase, DA virus infects cells in the gray matter of the central nervous system (CNS). Throughout the chronic phase, DA virus infects glial cells in the white matter, causing demyelinating disease. Although GDVII virus also infects neurons in the gray matter, infected mice developed a severe polioencephalomyelitis, and no virus is detected in the white matter or other areas in the CNS in rare survivors. Several sequence differences between the two viruses are located

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Schirò, Giorgia, Francesco Mira, Marta Canuti, et al. "Identification and Molecular Characterization of a Divergent Asian-like Canine Parvovirus Type 2b (CPV-2b) Strain in Southern Italy." International Journal of Molecular Sciences 23, no. 19 (2022): 11240. http://dx.doi.org/10.3390/ijms231911240.

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Canine parvovirus type 2 (CPV-2) is an infectious agent relevant to domestic and wild carnivorans. Recent studies documented the introduction and spread of CPV-2c strains of Asian origin in the Italian canine population. We investigated tissue samples from a puppy collected during necropsy for the presence of viral enteropathogens and all samples tested positive only for CPV-2. The full coding sequence of a CPV-2b (VP2 426Asp) strain was obtained. This virus was related to CPV-2c strains of Asian origin and unrelated to European CPV-2b strains. The sequence had genetic signatures typical of As

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Hao, Rui, Ke Ni, Qiuling Xia, et al. "Correlation between nucleotide mutation and viral loads of human bocavirus 1 in hospitalized children with respiratory tract infection." Journal of General Virology 94, no. 5 (2013): 1079–85. http://dx.doi.org/10.1099/vir.0.047472-0.

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The human bocavirus 1 (HBoV1) parvovirus causes respiratory disease and primarily affects children. Despite its worldwide prevalence, the mechanisms of HBoV1 replication and pathogenesis remain largely undefined. In this study of 846 children hospitalized at the Children’s Hospital of Chongqing Medical University in China for respiratory tract infection between June 2009 and May 2011, HBoV1 was detected in 112 (13.2 %) by real-time quantitative PCR. The median age of HBoV1-positive patients was 10 months old. Forty-five (40.2 %) of the HBoV1 cases were monoinfections, and 67 (59.8 %) were vira

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Pan, Shunshun, Yuanzhuo Man, Xin Xu, et al. "Genetic Diversity and Recombination Analysis of Canine Parvoviruses Prevalent in Central and Eastern China, from 2020 to 2023." Microorganisms 12, no. 11 (2024): 2173. http://dx.doi.org/10.3390/microorganisms12112173.

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Canine parvovirus type-2 (CPV-2), the primary causative agent of serious canine enteric diseases, is highly contagious and associated with high fatality rates worldwide. To comprehend the current emergence of CPV-2 in central and eastern China, 130 rectal swabs from domestic or stray dogs with gastroenteritis symptoms were collected during 2020–2023. A total of 118 positive samples were detected via polymerase chain reaction, and further used to amplify and sequence the VP2 gene. Sequence analysis of the deduced amino acids of VP2 protein indicated that CPV-2c was the most prevalent variant (n

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Cao, Lin, Ran Zhang, Tingting Liu, et al. "Seneca Valley virus attachment and uncoating mediated by its receptor anthrax toxin receptor 1." Proceedings of the National Academy of Sciences 115, no. 51 (2018): 13087–92. http://dx.doi.org/10.1073/pnas.1814309115.

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Seneca Valley virus (SVV) is an oncolytic picornavirus with selective tropism for neuroendocrine cancers. SVV mediates cell entry by attachment to the receptor anthrax toxin receptor 1 (ANTXR1). Here we determine atomic structures of mature SVV particles alone and in complex with ANTXR1 in both neutral and acidic conditions, as well as empty “spent” particles in complex with ANTXR1 in acidic conditions by cryoelectron microscopy. SVV engages ANTXR1 mainly by the VP2 DF and VP1 CD loops, leading to structural changes in the VP1 GH loop and VP3 GH loop, which attenuate interprotomer interactions

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Giraldo-Ramirez, Sebastián, Santiago Rendon-Marin, and Julián Ruiz-Saenz. "Phylogenetic, Evolutionary and Structural Analysis of Canine Parvovirus (CPV-2) Antigenic Variants Circulating in Colombia." Viruses 12, no. 5 (2020): 500. http://dx.doi.org/10.3390/v12050500.

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Canine parvovirus (CPV-2) is the causative agent of haemorrhagic gastroenteritis in canids. Three antigenic variants—CPV-2a, CPV-2b and CPV-2c—have been described, which are determined by variations at residue 426 of the VP2 capsid protein. In Colombia, the CPV-2a and CPV-2b antigenic variants have previously been reported through partial VP2 sequencing. Mutations at residues Asn428Asp and Ala514Ser of variant CPV-2a were detected, implying the appearance of a possible new CPV-2a variant in Colombia. The purpose of the present study was to characterise the full VP2 capsid protein in samples fr

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Asfor, Amin S., Vishwanatha R. A. P. Reddy, Salik Nazki, Joanna Urbaniec, Andrew J. Brodrick, and Andrew J. Broadbent. "Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro." Viruses 15, no. 1 (2022): 130. http://dx.doi.org/10.3390/v15010130.

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Infectious bursal disease virus (IBDV) vaccines do not induce sterilizing immunity, and vaccinated birds can become infected with field strains. Vaccine-induced immune selection pressure drives the evolution of antigenic drift variants that accumulate amino acid changes in the hypervariable region (HVR) of the VP2 capsid, which may lead to vaccine failures. However, there is a lack of information regarding how quickly mutations arise, and the relative contribution different residues make to immune escape. To model IBDV antigenic drift in vitro, we serially passaged a classical field strain bel

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Peters, Michelle A., David C. Jackson, Brendan S. Crabb, and Glenn F. Browning. "Mutation of chicken anemia virus VP2 differentially affects serine/threonine and tyrosine protein phosphatase activities." Journal of General Virology 86, no. 3 (2005): 623–30. http://dx.doi.org/10.1099/vir.0.80197-0.

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Novel dual-specificity protein phosphatases (DSPs), which catalyse the removal of phosphate from both phosphotyrosine and phosphoserine/phosphothreonine substrates, have recently been identified in two viruses within the family Circoviridae. Viral protein 2 (VP2) of chicken anemia virus (CAV) and ORF2 of TT virus have been shown to possess DSP activity in vitro. CAV VP2 is unusual in possessing two vicinal cysteines within the protein phosphatase signature motif. The first cysteine residue (C95) within the motif has been identified by mutagenesis as the essential catalytic cysteine. In this st

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Allison, Andrew B., Lindsey J. Organtini, Sheng Zhang, Susan L. Hafenstein, Edward C. Holmes, and Colin R. Parrish. "Single Mutations in the VP2 300 Loop Region of the Three-Fold Spike of the Carnivore Parvovirus Capsid Can Determine Host Range." Journal of Virology 90, no. 2 (2015): 753–67. http://dx.doi.org/10.1128/jvi.02636-15.

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ABSTRACTSylvatic carnivores, such as raccoons, have recently been recognized as important hosts in the evolution of canine parvovirus (CPV), a pandemic pathogen of domestic dogs. Although viruses from raccoons do not efficiently bind the dog transferrin receptor (TfR) or infect dog cells, a single mutation changing an aspartic acid to a glycine at capsid (VP2) position 300 in the prototype raccoon CPV allows dog cell infection. Because VP2 position 300 exhibits extensive amino acid variation among the carnivore parvoviruses, we further investigated its role in determining host range by analyzi

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Organtini, Lindsey J., Andrew B. Allison, Tiit Lukk, Colin R. Parrish, and Susan Hafenstein. "Global Displacement of Canine Parvovirus by a Host-Adapted Variant: Structural Comparison between Pandemic Viruses with Distinct Host Ranges." Journal of Virology 89, no. 3 (2014): 1909–12. http://dx.doi.org/10.1128/jvi.02611-14.

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Canine parvovirus type 2 (CPV-2) emerged in 1978 and spread worldwide within 2 years. Subsequently, CPV-2 was completely replaced by the variant CPV-2a, which is characterized by four specific capsid (VP2) mutations. The X-ray crystal structure of the CPV-2a capsid shows that each mutation confers small local changes. The loss of a hydrogen bond and introduction of a glycine residue likely introduce flexibility to sites that control interactions with the host receptor, antibodies, and sialic acids.

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Honkimaa, Anni, Bryn Kimura, Amir-Babak Sioofy-Khojine, et al. "Genetic Adaptation of Coxsackievirus B1 during Persistent Infection in Pancreatic Cells." Microorganisms 8, no. 11 (2020): 1790. http://dx.doi.org/10.3390/microorganisms8111790.

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Coxsackie B (CVB) viruses have been associated with type 1 diabetes. We have recently observed that CVB1 was linked to the initiation of the autoimmune process leading to type 1 diabetes in Finnish children. Viral persistency in the pancreas is currently considered as one possible mechanism. In the current study persistent infection was established in pancreatic ductal and beta cell lines (PANC-1 and 1.1B4) using four different CVB1 strains, including the prototype strain and three clinical isolates. We sequenced 5′ untranslated region (UTR) and regions coding for structural and non-structural

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Lawal, U. N., and M. B. Bello. "Molecular characterization of the VP2 protein of BGM-70 adapted low passaged UPM190 infectious bursal disease virus isolate." Sokoto Journal of Veterinary Sciences 21, no. 3 (2023): 111–18. http://dx.doi.org/10.4314/sokjvs.v21i3.2.

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The study evaluated the genetic profile of a low passaged BGM-70 adapted very virulent infectious bursal disease virus (vvIBDV) isolated in Malaysia in the year 2004 based on the VP2 hypervariable region. Embryonated chicken eggs were first used to propagate UPM190 12 times before being low passaged in BGM-70 cell line 7 times yielding UMP190BGMP7 whose VP2 nucleotide and amino acid sequences were determined and compared with reference sequences after Sanger sequencing of the low passage virus. The nucleotide and amino acid sequences of UPM190BGMP7 virus were similar with the sequences of viru

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Wen, Yinghui, Zhengxu Tang, Kunli Wang, et al. "Epidemiological and Molecular Investigation of Feline Panleukopenia Virus Infection in China." Viruses 16, no. 12 (2024): 1967. https://doi.org/10.3390/v16121967.

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The feline panleukopenia virus (FPV) is a highly contagious virus that affects cats worldwide, characterized by leukopenia, high temperature and diarrhea. Recently, the continuous prevalence and variation of FPV have attracted widespread concern. The aim of this study was to investigate the isolation, genetic evolution, molecular characterization and epidemiological analysis of FPV strains among cats and dogs in China from 2019 to 2024. The 41 FPV strains, including 38 feline strains and 3 canine strains, were isolated from rectal swab samples by inoculating monolayer FK81 cells and performing

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Abere, Bizunesh, Hongzhao Zhou, Masahiro Shuda, et al. "Replication Kinetics for a Reporter Merkel Cell Polyomavirus." Viruses 14, no. 3 (2022): 473. http://dx.doi.org/10.3390/v14030473.

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Merkel cell polyomavirus (MCV) causes one of the most aggressive human skin cancers, but laboratory studies on MCV replication have proven technically difficult. We report the first recombinase-mediated MCV minicircle (MCVmc) system that generates high levels of circularized virus, allowing facile MCV genetic manipulation and characterization of viral gene expression kinetics during replication. Mutations to Fbw7, Skp2, β-TrCP and hVam6p interaction sites, or to the stem loop sequence for the MCV-encoded miRNA precursor, markedly increase viral replication, whereas point mutation to an origin-

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Hoang, Minh, Cheng-Nan Wu, Chuen-Fu Lin, et al. "Genetic characterization of feline panleukopenia virus from dogs in Vietnam reveals a unique Thr101 mutation in VP2." PeerJ 8 (October 12, 2020): e9752. http://dx.doi.org/10.7717/peerj.9752.

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Background Canine parvovirus type 2 (CPV-2) and feline parvovirus (FPV) are known as the main causes of several serious diseases and have a severe impact on puppies and kittens, respectively. FPV and new CPV-2 variants are all able to infect cats, causing diseases indistinguishable from feline panleukopenia. However, FPV only replicates efficiently in feline cells in vitro and replicates in dogs in the thymus and bone marrow without being shed in feces. In our previous study, the genotypes of six parvoviral isolates were unable to be identified using a SimpleProbe® real-time PCR assay. Methods

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Yuan, Shilin, Guiming Li, Ying Wang, et al. "Identification of Positively Charged Residues in Enterovirus 71 Capsid Protein VP1 Essential for Production of Infectious Particles." Journal of Virology 90, no. 2 (2015): 741–52. http://dx.doi.org/10.1128/jvi.02482-15.

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ABSTRACTEnterovirus 71 (EV71), a positive-stranded RNA virus, is the major cause of hand, foot, and mouth disease (HFMD) in children, which can cause severe central nervous system disease and death. The capsids of EV71 consist of 60 copies of each of four viral structural proteins (VP1 to VP4), with VP1, VP2, and VP3 exposed on the surface and VP4 arranged internally. VP1 plays a central role in particle assembly and cell entry. To gain insight into the role of positively charged residues in VP1 function in these processes, a charged-to-alanine scanning analysis was performed using an infectio

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Peters, Michelle A., Brendan S. Crabb, Elizabeth A. Washington, and Glenn F. Browning. "Site-directed mutagenesis of the VP2 gene of Chicken anemia virus affects virus replication, cytopathology and host-cell MHC class I expression." Journal of General Virology 87, no. 4 (2006): 823–31. http://dx.doi.org/10.1099/vir.0.81468-0.

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Chicken anemia virus (CAV) is an immunosuppressive pathogen of chickens. To further examine the role of viral protein 2 (VP2), which possesses dual-specificity protein phosphatase (DSP) activity, in viral cytopathogenicity and its influence on viral growth and virulence, an infectious genomic clone of CAV was subjected to site-directed mutagenesis. Substitution mutations C87R, R101G, K102D and H103Y were introduced into the DSP catalytic motif and R129G, Q131P, R/K/K150/151/152G/A/A, D/E161/162G/G, L163P, D169G and E186G into a region predicted to have a high degree of secondary structure. All

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Hao, Xiangqi, Yanchao Li, Xiangyu Xiao, Bo Chen, Pei Zhou, and Shoujun Li. "The Changes in Canine Parvovirus Variants over the Years." International Journal of Molecular Sciences 23, no. 19 (2022): 11540. http://dx.doi.org/10.3390/ijms231911540.

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Canine parvovirus (CPV-2) is one of the most important pathogens in dogs, and despite the continual development of vaccines against CPV-2, CPV-2 is still circulating in the canine population. The CPV-2a/2b/2c variant has replaced the original CPV-2 virus and seems to exhibit accelerated transmission. Although CPV-2 infection has been frequently reported, no studies have summarized information of CPV-2 variants currently circulating worldwide. To track the evolution of CPV-2, we downloaded and analyzed all VP2 sequences from the NCBI database (from 1978 to 2022). We found that CPV-2c shows a te

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Wang, Xiuwan, Maura Carrai, Kate Van Brussel, et al. "Low Intrahost and Interhost Genetic Diversity of Carnivore Protoparvovirus 1 in Domestic Cats during a Feline Panleukopenia Outbreak." Viruses 14, no. 7 (2022): 1412. http://dx.doi.org/10.3390/v14071412.

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Feline panleukopenia (FPL), a highly contagious and frequently fatal disease of cats, is caused by Feline parvovirus (FPV) and Canine parvovirus (CPV). We characterised the diversity of these Carnivore protoparvovirus 1 variants in 18 faecal samples collected from domestic cats with FPL during an outbreak, using targeted parvoviral DNA metagenomics to a mean depth of >10,000 × coverage per site. All samples comprised FPV alone. Compared with the reference FPV genome, isolated in 1967, 44 mutations were detected. Ten of these were nonsynonymous, including 9 in nonstructural genes and one in

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Nour, Islam, Julia R. Blakey, Sonsiray Alvarez-Narvaez, and Sujit K. Mohanty. "Whole Genome Sequencing of Infectious Bursal Disease Viruses Isolated from a Californian Outbreak Unravels the Underlying Virulence Markers and Highlights Positive Selection Incidence." Viruses 15, no. 10 (2023): 2044. http://dx.doi.org/10.3390/v15102044.

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Outbreaks of the immunosuppressive infectious bursal disease (IBD) are frequently reported worldwide, despite the vaccination regimes. A 2009 Californian IBD outbreak caused by rA and rB isolates was described as very virulent (vv) IBD virus (IBDV); however, molecular factors beyond this virulence were not fully uncovered. Therefore, segments of both isolates were amplified, successfully cloned, whole genome sequenced by Next Generation Sequencing, genotyped, and the leading virulence factors were entirely investigated in terms of phylogenetic and amino acid analysis and protein modeling for p

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Jnaoui, Karima, Muriel Minet, and Thomas Michiels. "Mutations That Affect the Tropism of DA and GDVII Strains of Theiler's Virus In Vitro Influence Sialic Acid Binding and Pathogenicity." Journal of Virology 76, no. 16 (2002): 8138–47. http://dx.doi.org/10.1128/jvi.76.16.8138-8147.2002.

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ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) is a natural pathogen of the mouse. The different strains of TMEV are divided into two subgroups according to the pathology they provoke. The neurovirulent strains GDVII and FA induce an acute fatal encephalitis, while persistent strains, like DA and BeAn, cause a chronic demyelinating disease associated with viral persistence in the central nervous system. Different receptor usage was proposed to account for most of the phenotype difference between neurovirulent and persistent strains. Persistent but not neurovirulent strains were shown

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Hu, Wen, Xin Xu, Qiang Liu, et al. "Molecular characterisation and genetic diversity of canine parvovirus type 2 prevalent in Central China." Journal of Veterinary Research 64, no. 3 (2020): 347–54. http://dx.doi.org/10.2478/jvetres-2020-0056.

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AbstractIntroductionCanine parvovirus (CPV) disease is one of the most threatening to domestic and wild dogs.Material and MethodsA total of 132 clinical samples were isolated from domestic dogs with diarrhoea from Henan, Hubei, Jiangsu, and Anhui provinces from 2016 to 2017, and 56 were positive for CPV-2 by PCR. A phylogenetic tree was constructed for the isolate sequences incorporating 53 non-Chinese reference strains.ResultsVP2 sequences showed the strains mainly to be new CPV-2a/2b and CPV-2c genotypes. The Ala5Gly, Phe267Tyr, Ser297Ala, Tyr324Ile, Gln370Arg, Asn426Asp or Asn426Glu, and Th

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Pikuła, Anna, Katarzyna Domańska-Blicharz, Rytis Cepulis, and Krzysztof Śmietanka. "Identification of infectious bursal disease virus with atypical VP2 amino acid profile in Latvia." Journal of Veterinary Research 61, no. 2 (2017): 145–49. http://dx.doi.org/10.1515/jvetres-2017-0018.

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AbstractIntroduction: Infectious bursal disease virus (IBDV) is a causative agent of immunosuppressive disorder resulting in significant losses to the world poultry industry. This study describes the molecular characterisation of an atypical IBDV from a field outbreak that occurred in vaccinated chicken flocks in Latvia in 2011.Material and Methods: Ten bursae of Fabricius from each flock were collected for laboratory examination. Virus isolation was performed in embryonated eggs and CEF culture. The RT-PCR aimed at hypervariable domain of VP2 gene combined with sequencing was performed for de

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Hu, Wen, Liangyan Zheng, Xin Xu, et al. "Genetic characterisation and local genotypes of canine parvovirus strains collected from pet dogs in central and eastern China during 2018–2019." Journal of Veterinary Research 64, no. 4 (2020): 477–86. http://dx.doi.org/10.2478/jvetres-2020-0076.

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AbstractIntroductionCanine parvovirus type-2 (CPV-2) causes acute infectious diseases in puppies, which show high morbidity and mortality. Better effect of vaccination against these diseases could be achieved with deeper knowledge of CPV-2 genotype dissemination and mutation history. This study investigated CPV-2–positive samples collected recently over a wide region of China.Material and MethodsA total of 118 faecal samples from dogs identified as CPV-positive were collected from veterinary clinics in central and eastern China. Overall, 16 strains collected from Anhui, 29 from Henan, and 16 f

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Lee, Donald W., Andrew B. Allison, Kaitlyn B. Bacon, Colin R. Parrish, and Susan Daniel. "Single-Particle Tracking Shows that a Point Mutation in the Carnivore Parvovirus Capsid Switches Binding between Host-Specific Transferrin Receptors." Journal of Virology 90, no. 9 (2016): 4849–53. http://dx.doi.org/10.1128/jvi.03204-15.

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Determining how viruses infect new hosts via receptor-binding mechanisms is important for understanding virus emergence. We studied the binding kinetics of canine parvovirus (CPV) variants isolated from raccoons—a newly recognized CPV host—to different carnivore transferrin receptors (TfRs) using single-particle tracking. Our data suggest that CPV may utilize adhesion-strengthening mechanisms during TfR binding and that a single mutation in the viral capsid at VP2 position 300 can profoundly alter receptor binding and infectivity.

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Yang, Yuqing, Yi Geng, Ping Ouyang, et al. "Identification of a Feline Panleukopenia Virus from Captive Giant Pandas (Ailuropoda melanoleuca) and Its Phylogenetic Analysis." Transboundary and Emerging Diseases 2023 (May 19, 2023): 1–8. http://dx.doi.org/10.1155/2023/7721487.

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The host range of feline panleukopenia virus (FPV) is expanding and is a serious threat to both captive and free-range endangered wildlife. The FPV named FPV-am2020 was isolated from fecal samples from four diarrheal captive giant pandas in 2020, and pathogenicity and phylogenetic analysis were conducted in this study. Three-month-old cats challenged with FPV-am2020 experienced 100% mortality. The complete FPV-am2020 sequence was determined and comprised 5277 base pairs (bp), 36.76% GC content, and two open reading frames. According to the phylogenetic analysis of whole genome sequences and VP

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Celma, Cristina C. P., and Polly Roy. "A Viral Nonstructural Protein Regulates Bluetongue Virus Trafficking and Release." Journal of Virology 83, no. 13 (2009): 6806–16. http://dx.doi.org/10.1128/jvi.00263-09.

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ABSTRACT Bluetongue virus (BTV), a nonenveloped insect-borne virus, is released from infected cells by multiple pathways. Unlike other nonenveloped viruses, in addition to cell lysis the newly synthesized virus particles also appear to use a unique “budding” process. The nonstructural protein NS3, the only membrane protein encoded by BTV in infected cells, has been implicated in this process, since it appears to interact not only with the outermost viral capsid protein VP2 but also with a component of the cellular ESCRT pathway. However, to date it had not been possible to obtain direct eviden

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Wu, Qianqian, Xin Xu, Qinxi Chen, et al. "Genetic Analysis of Avian Gyrovirus 2 Variant-Related Gyrovirus Detected in Farmed King Ratsnake (Elaphe carinata): The First Report from China." Pathogens 8, no. 4 (2019): 185. http://dx.doi.org/10.3390/pathogens8040185.

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Avian gyrovirus 2 (AGV2), which is similar to chicken infectious anemia virus, is a new member of the genus Gyrovirus. AGV2 has been detected not only in chicken but also in human tissues and feces. This study analyzed 91 samples (8 from liver tissue and 83 from fecal samples) collected from king ratsnakes (Elaphe carinata) from 7 separate farms in Hubei and Henan, China, for AGV2 DNA using PCR. The results demonstrated a low positive rate of AGV2 (6.59%, 6/91) in the snakes, and all the positive samples were collected from the same farm. The AGV2 strain HB2018S1 was sequenced, and its 2376 nt

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QI, Xiao-le, Zhen LU, Nian WANG, et al. "Analysis of the function of D279N mutation of VP2 of infectious bursal disease virus." Journal of Integrative Agriculture 14, no. 12 (2015): 2618–25. http://dx.doi.org/10.1016/s2095-3119(14)60933-3.

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Pei, Jie, Rui-Lun Liu, Zhi-Hui Yang, et al. "Identification of Critical Amino Acids of Coxsackievirus A10 Associated with Cell Tropism and Viral RNA Release during Uncoating." Viruses 15, no. 10 (2023): 2114. http://dx.doi.org/10.3390/v15102114.

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Coxsackievirus A10 (CV-A10) is a prevailing causative agent of hand–foot–mouth disease, necessitating the isolation and adaptation of appropriate strains in cells allowed for human vaccine development. In this study, amino acid sequences of CV-A10 strains with different cell tropism on RD and Vero cells were compared. Various amino acids on the structural and non-structural proteins related to cell tropism were identified. The reverse genetic systems of several CV-A10 strains with RD+/Vero− and RD+/Vero+ cell tropism were developed, and a set of CV-A10 recombinants were produced. The binding,

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Yu, Zuhua, Wenjie Wang, Chuan Yu, et al. "Molecular Characterization of Feline Parvovirus from Domestic Cats in Henan Province, China from 2020 to 2022." Veterinary Sciences 11, no. 7 (2024): 292. http://dx.doi.org/10.3390/vetsci11070292.

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Carnivore protoparvovirus-1, feline parvovirus (FPV), and canine parvovirus (CPV) continue to spread in companion animals all over the world. As a result, FPV and CPV underwent host-to-host transfer in carnivorous wild-animal hosts. Here, a total of 82 fecal samples of suspected cat FPV infections were collected from Henan Province from 2020 to 2022. The previously published full-length sequence primers of VP2 and NS1 genes were used to amplify the targeted genes of these samples, and the complete gene sequences of 11 VP2 and 21 NS1 samples were obtained and analyzed. Analysis showed that the

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Ahmed, Rony, Md Oli, Md Jahan, et al. "Circulation of the reassorted very virulent genotype of infectious bursal disease virus isolated from vaccinated broiler chickens in Bangladesh." Journal of Advanced Veterinary and Animal Research 11, no. 3 (2024): 534. http://dx.doi.org/10.5455/javar.2024.k803.

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Objective: The methodology employed in this research was designed to identify and characterize the infectious bursal disease virus (IBDV) at the molecular level, originating from recent outbreaks in Bangladesh. Materials and Methods: The IBDV outbreak farm was investigated, and bursa of Fabricius (BF) specimens were acquired from infected chickens. Initially, viruses in the processed samples were detected in chicken embryo fibroblast (CEF) cells, and the RT-PCR method was used to confirm IBDV. The positive samples were injected through chorioallantoic membrane route into the embryo of a 10-day

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Jantafong, Tippawan, Sakchai Ruenphet, Harold R. Garner, and Krit Ritthipichai. "Tracing the Genetic Evolution of Canine Parvovirus Type 2 (CPV-2) in Thailand." Pathogens 11, no. 12 (2022): 1460. http://dx.doi.org/10.3390/pathogens11121460.

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Canine parvovirus type 2 (CPV-2) is responsible for hemorrhagic gastroenteritis in dogs worldwide. High genomic substitution rates in CPV-2 contribute to the progressive emergence of novel variants with increased ability to evade the host immune response. Three studies have analyzed the genomic mutations of CPV-2 variants in Thailand. These investigations were independently conducted at different timepoints. Thus, a retrospective integrated analysis of CPV-2 genomic mutations has not been fully performed. Our study aimed at evaluating the evolutionary changes in CPV-2 in Thailand from 2003 to

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Mira, Francesco, Marta Canuti, Giuseppa Purpari, et al. "Molecular Characterization and Evolutionary Analyses of Carnivore Protoparvovirus 1 NS1 Gene." Viruses 11, no. 4 (2019): 308. http://dx.doi.org/10.3390/v11040308.

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Carnivore protoparvovirus 1 is the etiological agent of a severe disease of terrestrial carnivores. This unique specie encompasses canine parvovirus type 2 (CPV-2) and feline panleukopenia virus (FPLV). Studies widely analyzed the main capsid protein (VP2), but limited information is available on the nonstructural genes (NS1/NS2). This paper analyzed the NS1 gene sequence of FPLV and CPV strains collected in Italy in 2009–2017, along with worldwide related sequences. Differently from VP2, only one NS1 amino-acid residue (248) clearly and constantly distinguished FPLV from CPV-2, while five pos

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Wang, Ming-Yang, Shi-Bo Zhao, Shu-Yi Wang, Meng-Hua Du, Sheng-Li Ming, and Lei Zeng. "Feline Panleukopenia Virus ZZ202303 Strain: Molecular Characterization and Structural Implications of the VP2 Gene Phylogenetic Divergence." International Journal of Molecular Sciences 26, no. 10 (2025): 4573. https://doi.org/10.3390/ijms26104573.

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Feline panleukopenia virus (FPV), the etiological agent of a highly contagious multispecies disease, demonstrates concerning phylogenetic divergence that compromises vaccine cross-protection. This study aimed to characterize a novel FPV strain through integrated virological and molecular analyses to assess epidemiological implications. From seven clinical specimens obtained from feline hosts with panleukopenia in Henan Province, China, we isolated FPV ZZ202303 using an F81 cell culture coupled with PCR verification, demonstrating potent cytopathic effects (TCID50: 10−5.72/0.1 mL) and rapid rep

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Jia, Qingmei, James M. Hogle, Tsutomu Hashikawa, and Akio Nomoto. "Molecular Genetic Analysis of Revertants from a Poliovirus Mutant That Is Specifically Adapted to the Mouse Spinal Cord." Journal of Virology 75, no. 23 (2001): 11766–72. http://dx.doi.org/10.1128/jvi.75.23.11766-11772.2001.

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ABSTRACT SA virus, a mutant of the Mahoney strain of type 1 poliovirus (PV1/Mahoney), replicates specifically in the spinal cords of mice and causes paralysis, although the PV1/Mahoney strain does not show any mouse neurovirulence (Q. Jia, S. Ohka, K. Iwasaki, K. Tohyama, and A. Nomoto, J. Virol. 73:6041–6047, 1999). The key mutation site for the mouse neurovirulence of SA was mapped to nucleotide (nt) 928 of the genome (A to G), resulting in the amino acid substitution of Met for Ile at residue 62 within the capsid protein VP4 (VP4062). A small-plaque phenotype of SA appears to be indicative

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