VP‐1 quasispecies in human infection with polyomavirus BK
Identifieur interne : 001D91 ( Main/Exploration ); précédent : 001D90; suivant : 001D92VP‐1 quasispecies in human infection with polyomavirus BK
Auteurs : Chunqing Luo [États-Unis] ; Hans H. Hirsch [Suisse] ; Jeffrey Kant [États-Unis] ; Parmjeet Randhawa [États-Unis]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 2012-01.
English descriptors
- Teeft :
- Active nephropathy, Adaptive mutations, Bold line, Capsid, Capsid protein, Cell transplant recipients, Clonal sequences, Clone, Clone sequences, Coding regions, Default parameters, Epithelial cells, Error rate, Evolutionary selection pressure, Favorable prognosis, Gene region, Genome, Genomic, Genotype, Healthy individuals, Healthy subjects, Healthyviruria, Hemorrhagic cystitis, Individual loops, Infectious disease, Initial segment, Kidney transplant patients, Kidney transplant recipients, Loop region, Mouse polyomavirus, Mutation, Nephropathy, Nephropathy group, Nucleic acids, Nucleotide, Nucleotide differences, Nucleotide positions, Nucleotide substitutions, Outgroup sequence, Parent strain, Phylogenetic, Phylogenetic analysis, Phylogenetic trees, Polyomavirus, Polyomavirus type, Positive selection, Primer, Proc natl acad, Progressive multifocal encephalopathy, Progressive multifocal leukoencephalopathy, Quasispecies, Randhawa, Recombinant, Recombinant sequence, Recombinant sequences, Recombinant strains, Recombination, Reference sequences, Renal transplantation, Replication, Selection pressure, Sequence alignments, Sequence diversity, Sequencing, Sequencing primers, Sharma, Simian virus, Subgroup, Substitution, Total number, Transplant, Transplant patients, Transplantation, Transplantedviruria, Transplantedviruria group, Urine, Urine samples, Viral, Viral capsid protein, Viral genome, Viral quasispecies, Viral replication, Viremia, Virol, Virologic parameters, Viruria, Viruria genomic equivalents, Virus, Virus infections, Whole genome sequences, Whole protein, Wiley periodicals, Yogo.
Abstract
Polyomavirus BK is a recognized cause of nephropathy and hemorrhagic cystitis in kidney or allogeneic hematopoietic stem cell transplant recipients. This study explored a role of genetic variations in capsid protein VP‐1 gene as a factor in viral pathogenesis. VP‐1 was amplified from 7 healthy subjects with viruria, 7 transplant patients with viruria, and 11 patients with viremia or nephropathy. PCR products were cloned and a total of 558 clonal sequences were subjected to phylogenetic analysis using standard methods. VP‐1 quasispecies were found in 25/25 and coinfection with different genotypes in 12/25 subjects. Genotype II was found as an unexpected minority species in 5/25 individuals. Recombinant strains of uncertain biologic significance, which frequently contained genotype II and IV sequences were identified in 9/25 subjects. Viremia/nephropathy group was characterized by (a) greater sequence complexity in whole VP‐1 versus BC loop and BC loop compared to the HI loop, (b) greater intra‐strain genetic diversity in the BC loop compared to whole VP‐1 protein and HI loop, (c) more non‐synonymous substitutions (dN) in the BC loop compared to whole VP‐1 and HI loop, (e) fewer synonymous substitutions (dS) compared to healthy‐viruria group, and (f) selection pressure (dN/dS >1.0) exerted on VP‐1. In conclusion, this study documents frequent occurrence of quasispecies in a host DNA polymerase dependent virus, which is theoretically expected to show high replication fidelity. Quasispecies occur even in healthy subjects with viruria, but evolutionary selection pressure directed at the viral capsid protein (VP‐1) is seen only in patients with viremia or nephropathy. J. Med. Virol. 84:152–161, 2011. © 2011 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/jmv.22147
Affiliations:
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Hirsch</name><affiliation wicri:level="1"><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Infectious Disease, University Hospitals Basel, Institute of Medical Microbiology, Department of Biomedicine, Department of Infectious Diseases and Epidemiology, University of Basel, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author><author><name sortKey="Kant, Jeffrey" sort="Kant, Jeffrey" uniqKey="Kant J" first="Jeffrey" last="Kant">Jeffrey Kant</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Pathology, University of Pittsburgh, Pittsburgh</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Human Genetics, University of Pittsburgh, Pittsburgh</wicri:cityArea></affiliation></author><author><name sortKey="Randhawa, Parmjeet" sort="Randhawa, Parmjeet" uniqKey="Randhawa P" first="Parmjeet" last="Randhawa">Parmjeet Randhawa</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Pathology, University of Pittsburgh, Pittsburgh</wicri:cityArea></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Correspondence address: UPMC Montefiore Hospital, 3459 Fifth Avenue, Room E‐737, Pittsburgh</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">84</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="152">152</biblScope><biblScope unit="page" to="161">161</biblScope><biblScope unit="page-count">10</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-01">2012-01</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Active nephropathy</term><term>Adaptive mutations</term><term>Bold line</term><term>Capsid</term><term>Capsid protein</term><term>Cell transplant recipients</term><term>Clonal sequences</term><term>Clone</term><term>Clone sequences</term><term>Coding regions</term><term>Default parameters</term><term>Epithelial cells</term><term>Error rate</term><term>Evolutionary selection pressure</term><term>Favorable prognosis</term><term>Gene region</term><term>Genome</term><term>Genomic</term><term>Genotype</term><term>Healthy individuals</term><term>Healthy subjects</term><term>Healthyviruria</term><term>Hemorrhagic cystitis</term><term>Individual loops</term><term>Infectious disease</term><term>Initial segment</term><term>Kidney transplant patients</term><term>Kidney transplant recipients</term><term>Loop region</term><term>Mouse polyomavirus</term><term>Mutation</term><term>Nephropathy</term><term>Nephropathy group</term><term>Nucleic acids</term><term>Nucleotide</term><term>Nucleotide differences</term><term>Nucleotide positions</term><term>Nucleotide substitutions</term><term>Outgroup sequence</term><term>Parent strain</term><term>Phylogenetic</term><term>Phylogenetic analysis</term><term>Phylogenetic trees</term><term>Polyomavirus</term><term>Polyomavirus type</term><term>Positive selection</term><term>Primer</term><term>Proc natl acad</term><term>Progressive multifocal encephalopathy</term><term>Progressive multifocal leukoencephalopathy</term><term>Quasispecies</term><term>Randhawa</term><term>Recombinant</term><term>Recombinant sequence</term><term>Recombinant sequences</term><term>Recombinant strains</term><term>Recombination</term><term>Reference sequences</term><term>Renal transplantation</term><term>Replication</term><term>Selection pressure</term><term>Sequence alignments</term><term>Sequence diversity</term><term>Sequencing</term><term>Sequencing primers</term><term>Sharma</term><term>Simian virus</term><term>Subgroup</term><term>Substitution</term><term>Total number</term><term>Transplant</term><term>Transplant patients</term><term>Transplantation</term><term>Transplantedviruria</term><term>Transplantedviruria group</term><term>Urine</term><term>Urine samples</term><term>Viral</term><term>Viral capsid protein</term><term>Viral genome</term><term>Viral quasispecies</term><term>Viral replication</term><term>Viremia</term><term>Virol</term><term>Virologic parameters</term><term>Viruria</term><term>Viruria genomic equivalents</term><term>Virus</term><term>Virus infections</term><term>Whole genome sequences</term><term>Whole protein</term><term>Wiley periodicals</term><term>Yogo</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Polyomavirus BK is a recognized cause of nephropathy and hemorrhagic cystitis in kidney or allogeneic hematopoietic stem cell transplant recipients. This study explored a role of genetic variations in capsid protein VP‐1 gene as a factor in viral pathogenesis. VP‐1 was amplified from 7 healthy subjects with viruria, 7 transplant patients with viruria, and 11 patients with viremia or nephropathy. PCR products were cloned and a total of 558 clonal sequences were subjected to phylogenetic analysis using standard methods. VP‐1 quasispecies were found in 25/25 and coinfection with different genotypes in 12/25 subjects. Genotype II was found as an unexpected minority species in 5/25 individuals. Recombinant strains of uncertain biologic significance, which frequently contained genotype II and IV sequences were identified in 9/25 subjects. Viremia/nephropathy group was characterized by (a) greater sequence complexity in whole VP‐1 versus BC loop and BC loop compared to the HI loop, (b) greater intra‐strain genetic diversity in the BC loop compared to whole VP‐1 protein and HI loop, (c) more non‐synonymous substitutions (dN) in the BC loop compared to whole VP‐1 and HI loop, (e) fewer synonymous substitutions (dS) compared to healthy‐viruria group, and (f) selection pressure (dN/dS >1.0) exerted on VP‐1. In conclusion, this study documents frequent occurrence of quasispecies in a host DNA polymerase dependent virus, which is theoretically expected to show high replication fidelity. Quasispecies occur even in healthy subjects with viruria, but evolutionary selection pressure directed at the viral capsid protein (VP‐1) is seen only in patients with viremia or nephropathy. J. Med. Virol. 84:152–161, 2011. © 2011 Wiley Periodicals, Inc.</div></front></TEI><affiliations><list><country><li>Suisse</li><li>États-Unis</li></country><region><li>Pennsylvanie</li></region></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Luo, Chunqing" sort="Luo, Chunqing" uniqKey="Luo C" first="Chunqing" last="Luo">Chunqing Luo</name></region><name sortKey="Kant, Jeffrey" sort="Kant, Jeffrey" uniqKey="Kant J" first="Jeffrey" last="Kant">Jeffrey Kant</name><name sortKey="Kant, Jeffrey" sort="Kant, Jeffrey" uniqKey="Kant J" first="Jeffrey" last="Kant">Jeffrey Kant</name><name sortKey="Randhawa, Parmjeet" sort="Randhawa, Parmjeet" uniqKey="Randhawa P" first="Parmjeet" last="Randhawa">Parmjeet Randhawa</name><name sortKey="Randhawa, Parmjeet" sort="Randhawa, Parmjeet" uniqKey="Randhawa P" first="Parmjeet" last="Randhawa">Parmjeet Randhawa</name><name sortKey="Randhawa, Parmjeet" sort="Randhawa, Parmjeet" uniqKey="Randhawa P" first="Parmjeet" last="Randhawa">Parmjeet Randhawa</name></country><country name="Suisse"><noRegion><name sortKey="Hirsch, Hans H" sort="Hirsch, Hans H" uniqKey="Hirsch H" first="Hans H." last="Hirsch">Hans H. 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