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Lindberg, A. MichaelORCID iD iconorcid.org/0000-0003-3841-4826
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Publications (10 of 98) Show all publications
Simmonds, P., Gorbalenya, A. E., Harvala, H., Hovi, T., Knowles, N. J., Lindberg, A. M., . . . Zell, R. (2020). Recommendations for the nomenclature of enteroviruses and rhinoviruses. Archives of Virology, 165, 793-797
Open this publication in new window or tab >>Recommendations for the nomenclature of enteroviruses and rhinoviruses
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2020 (English)In: Archives of Virology, ISSN 0304-8608, E-ISSN 1432-8798, Vol. 165, p. 793-797Article in journal (Refereed) Published
Abstract [en]

Enteroviruses (EVs) and rhinoviruses (RVs) are significant pathogens of humans and are the subject of intensive clinical and epidemiological research and public health measures, notably in the eradication of poliovirus and in the investigation and control of emerging pathogenic EV types worldwide. EVs and RVs are highly diverse in their antigenic properties, tissue tropism, disease associations and evolutionary relationships, but the latter often conflict with previously developed biologically defined terms, such as "coxsackieviruses", "polioviruses" and "echoviruses", which were used before their genetic interrelationships were understood. This has created widespread formatting problems and inconsistencies in the nomenclature for EV and RV types and species in the literature and public databases. As members of the International Committee for Taxonomy of Viruses (ICTV) Picornaviridae Study Group, we describe the correct use of taxon names for these viruses and have produced a series of recommendations for the nomenclature of EV and RV types and their abbreviations. We believe their adoption will promote greater clarity and consistency in the terminology used in the scientific and medical literature. The recommendations will additionally provide a useful reference guide for journals, other publications and public databases seeking to use standardised terms for the growing multitude of enteroviruses and rhinoviruses described worldwide.

Place, publisher, year, edition, pages
Springer, 2020
National Category
Microbiology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-92297 (URN)10.1007/s00705-019-04520-6 (DOI)000509166800001 ()31980941 (PubMedID)
Note

Correction published in: Archives of Virology, DOI 10.1007/s00705-020-04558-x

Available from: 2020-02-21 Created: 2020-02-21 Last updated: 2020-04-28Bibliographically approved
Turkki, P., Laajala, M., Stark, M., Vandesande, H., Sallinen-Dal Maso, H., Shroff, S., . . . Marjomaki, V. (2019). Slow Infection due to Lowering the Amount of Intact versus Empty Particles Is a Characteristic Feature of Coxsackievirus B5 Dictated by the Structural Proteins. Journal of Virology, 93(20), 1-15, Article ID e01130-19.
Open this publication in new window or tab >>Slow Infection due to Lowering the Amount of Intact versus Empty Particles Is a Characteristic Feature of Coxsackievirus B5 Dictated by the Structural Proteins
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2019 (English)In: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 93, no 20, p. 1-15, article id e01130-19Article in journal (Refereed) Published
Abstract [en]

Enterovirus B species typically cause a rapid cytolytic infection leading to efficient release of progeny viruses. However, they are also capable of persistent infections in tissues, which are suggested to contribute to severe chronic states such as myocardial inflammation and type 1 diabetes. In order to understand the factors contributing to differential infection strategies, we constructed a chimera by combining the capsid proteins from fast-cytolysis-causing echovirus 1 (EV1) with nonstructural proteins from coxsackievirus B5 (CVB5), which shows persistent infection in RD cells. The results showed that the chimera behaved similarly to parental EV1, leading to efficient cytolysis in both permissive A549 and semipermissive RD cells. In contrast to EV1 and the chimera, CVB5 replicated slowly in permissive cells and showed persistent infection in semipermissive cells. However, there was no difference in the efficiency of uptake of CVB5 in A549 or RD cells in comparison to the chimera or EV1. CVB5 batches constantly contained significant amounts of empty capsids, also in comparison to CVBS's close relative CVB3. During successive passaging of batches containing only intact CVB5, increasing amounts of empty and decreasing amounts of infective capsids were produced. Our results demonstrate that the increase in the amount of empty particles and the lowering of the amount of infective particles are dictated by the CVB5 structural proteins, leading to slowing down of the infection between passages. Furthermore, the key factor for persistent infection is the small amount of infective particles produced, not the high number of empty particles that accumulate. IMPORTANCE Enteroviruses cause several severe diseases, with lytic infections that lead to rapid cell death but also persistent infections that are more silent and lead to chronic states of infection. Our study compared a cytolytic echovirus 1 infection to persistent coxsackievirus B5 infection by making a chimera with the structural proteins of echovirus 1 and the nonstructural proteins of coxsackievirus B5. Coxsackievirus 85 infection was found to lead to the production of a high number of empty viruses (empty capsids) that do not contain genetic material and are unable to continue the infection. Coinciding with the high number of empty capsids, the amount of infective virions decreased. This characteristic property was not observed in the constructed chimera virus, suggesting that structural proteins are in charge of these phenomena. These results shed light on the mechanisms that may cause persistent infections. Understanding events leading to efficient or inefficient infections is essential in understanding virus-caused pathologies.

Place, publisher, year, edition, pages
American Society of Microbiology, 2019
Keywords
enterovirus, infection kinetics, viral nonstructural proteins, viral structural proteins, virus-host interactions
National Category
Microbiology
Research subject
Ecology, Microbiology
Identifiers
urn:nbn:se:lnu:diva-89707 (URN)10.1128/JVI.01130-19 (DOI)000488281200032 ()31375587 (PubMedID)
Available from: 2019-10-18 Created: 2019-10-18 Last updated: 2019-10-18Bibliographically approved
Zell, R., Delwart, E., Gorbalenya, A. E., Hovi, T., King, A. M., Knowles, N. J., . . . Yamashita, T. (2017). ICTV Virus Taxonomy Profile: Picornaviridae. Journal of General Virology, 98(10), 2421-2422
Open this publication in new window or tab >>ICTV Virus Taxonomy Profile: Picornaviridae
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2017 (English)In: Journal of General Virology, ISSN 0022-1317, E-ISSN 1465-2099, Vol. 98, no 10, p. 2421-2422Article in journal (Refereed) Published
Abstract [en]

The family Picornaviridae comprises small non-enveloped viruses with RNA genomes of 6.7 to 10.1 kb, and contains > 30 genera and > 75 species. Most of the known picornaviruses infect mammals and birds, but some have also been detected in reptiles, amphibians and fish. Many picornaviruses are important human and veterinary pathogens and may cause diseases of the central nervous system, heart, liver, skin, gastrointestinal tract or upper respiratory tract. Most picornaviruses are transmitted by the faecal-oral or respiratory routes. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the taxonomy of the Picornaviridae, which is available at www. ictv. global/report/picornaviridae.

Place, publisher, year, edition, pages
Microbiology Society, 2017
Keywords
Picornaviridae, ICTV, taxonomy, poliovirus, foot-and-mouth disease virus, rhinovirus, enterovirus
National Category
Microbiology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-69753 (URN)10.1099/jgv.0.000911 (DOI)000417310000004 ()28884666 (PubMedID)2-s2.0-85031033462 (Scopus ID)
Available from: 2018-01-12 Created: 2018-01-12 Last updated: 2019-09-06Bibliographically approved
Mullapudi, E., Novacek, J., Palkova, L., Kulich, P., Lindberg, A. M., van Kuppeveld, F. J. M. & Plevka, P. (2016). Structure and Genome Release Mechanism of the Human Cardiovirus Saffold Virus 3. Journal of Virology, 90(17), 7628-7639
Open this publication in new window or tab >>Structure and Genome Release Mechanism of the Human Cardiovirus Saffold Virus 3
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2016 (English)In: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 90, no 17, p. 7628-7639Article in journal (Refereed) Published
Abstract [en]

In order to initiate an infection, viruses need to deliver their genomes into cells. This involves uncoating the genome and transporting it to the cytoplasm. The process of genome delivery is not well understood for nonenveloped viruses. We address this gap in our current knowledge by studying the uncoating of the nonenveloped human cardiovirus Saffold virus 3 (SAFV-3) of the family Picornaviridae. SAFVs cause diseases ranging from gastrointestinal disorders to meningitis. We present a structure of a native SAFV-3 virion determined to 2.5 angstrom by X-ray crystallography and an 11-angstrom-resolution cryo-electron microscopy reconstruction of an "altered" particle that is primed for genome release. The altered particles are expanded relative to the native virus and contain pores in the capsid that might serve as channels for the release of VP4 subunits, N termini of VP1, and the RNA genome. Unlike in the related enteroviruses, pores in SAFV-3 are located roughly between the icosahedral 3- and 5-fold axes at an interface formed by two VP1 and one VP3 subunit. Furthermore, in native conditions many cardioviruses contain a disulfide bond formed by cysteines that are separated by just one residue. The disulfide bond is located in a surface loop of VP3. We determined the structure of the SAFV-3 virion in which the disulfide bonds are reduced. Disruption of the bond had minimal effect on the structure of the loop, but it increased the stability and decreased the infectivity of the virus. Therefore, compounds specifically disrupting or binding to the disulfide bond might limit SAFV infection. IMPORTANCE A capsid assembled from viral proteins protects the virus genome during transmission from one cell to another. However, when a virus enters a cell the virus genome has to be released from the capsid in order to initiate infection. This process is not well understood for nonenveloped viruses. We address this gap in our current knowledge by studying the genome release of Human Saffold virus 3. Saffold viruses cause diseases ranging from gastrointestinal disorders to meningitis. We show that before the genome is released, the Saffold virus 3 particle expands, and holes form in the previously compact capsid. These holes serve as channels for the release of the genome and small capsid proteins VP4 that in related enteroviruses facilitate subsequent transport of the virus genome into the cell cytoplasm.

National Category
Microbiology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-57044 (URN)10.1128/JVI.00746-16 (DOI)000382306800004 ()27279624 (PubMedID)2-s2.0-84983560201 (Scopus ID)
Available from: 2016-10-05 Created: 2016-10-04 Last updated: 2017-11-30Bibliographically approved
Sabin, C., Fuzik, T., Skubnik, K., Palkova, L., Lindberg, A. M. & Plevka, P. (2016). Structure of Aichi Virus 1 and Its Empty Particle: Clues to Kobuvirus Genome Release Mechanism. Journal of Virology, 90(23), 10800-10810
Open this publication in new window or tab >>Structure of Aichi Virus 1 and Its Empty Particle: Clues to Kobuvirus Genome Release Mechanism
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2016 (English)In: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 90, no 23, p. 10800-10810Article in journal (Refereed) Published
Abstract [en]

Aichi virus 1 (AiV-1) is a human pathogen from the Kobuvirus genus of the Picornaviridae family. Worldwide, 80 to 95% of adults have antibodies against the virus. AiV-1 infections are associated with nausea, gastroenteritis, and fever. Unlike most picornaviruses, kobuvirus capsids are composed of only three types of subunits: VP0, VP1, and VP3. We present here the structure of the AiV-1 virion determined to a resolution of 2.1 angstrom using X-ray crystallography. The surface loop puff of VP0 and knob of VP3 in AiV-1 are shorter than those in other picornaviruses. Instead, the 42-residue BC loop of VP0 forms the most prominent surface feature of the AiV-1 virion. We determined the structure of AiV-1 empty particle to a resolution of 4.2 angstrom using cryo-electron microscopy. The empty capsids are expanded relative to the native virus. The N-terminal arms of capsid proteins VP0, which mediate contacts between the pentamers of capsid protein protomers in the native AiV-1 virion, are disordered in the empty capsid. Nevertheless, the empty particles are stable, at least in vitro, and do not contain pores that might serve as channels for genome release. Therefore, extensive and probably reversible local reorganization of AiV-1 capsid is required for its genome release. IMPORTANCE Aichi virus 1 (AiV-1) is a human pathogen that can cause diarrhea, abdominal pain, nausea, vomiting, and fever. AiV-1 is identified in environmental screening studies with higher frequency and greater abundance than other human enteric viruses. Accordingly, 80 to 95% of adults worldwide have suffered from AiV-1 infections. We determined the structure of the AiV-1 virion. Based on the structure, we show that antiviral compounds that were developed against related enteroviruses are unlikely to be effective against AiV-1. The surface of the AiV-1 virion has a unique topology distinct from other related viruses from the Picornaviridae family. We also determined that AiV-1 capsids form compact shells even after genome release. Therefore, AiV-1 genome release requires large localized and probably reversible reorganization of the capsid.

National Category
Microbiology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-59721 (URN)10.1128/JVI.01601-16 (DOI)000389904500030 ()2-s2.0-85000963069 (Scopus ID)
Available from: 2017-01-10 Created: 2017-01-10 Last updated: 2017-11-29Bibliographically approved
Sävneby, A., Luthman, J., Nordenskjold, F., Andersson, B. & Lindberg, A. M. (2016). The Transcriptome of Rhabdomyosarcoma Cells Infected with Cytolytic and Non-Cytolytic Variants of Coxsackievirus B2 Ohio-1. PLoS ONE, 11(10), Article ID e0164548.
Open this publication in new window or tab >>The Transcriptome of Rhabdomyosarcoma Cells Infected with Cytolytic and Non-Cytolytic Variants of Coxsackievirus B2 Ohio-1
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2016 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 10, article id e0164548Article in journal (Refereed) Published
Abstract [en]

The transcriptomes of cells infected with lytic and non-lytic variants of coxsackievirus B2 Ohio-1 (CVB2O) were analyzed using next generation sequencing. This approach was selected with the purpose of elucidating the effects of lytic and non-lytic viruses on host cell transcription. Total RNA was extracted from infected cells and sequenced. The resulting reads were subsequently mapped against the human and CVB2O genomes. The amount of intracellular RNA was measured, indicating lower proportions of human RNA in the cells infected with the lytic virus compared to the non-lytic virus after 48 hours. This may be explained by reduced activity of the cellular transcription/translation machinery in lytic enteroviral replication due to activities of the enteroviral proteases 2A and/or 3C. Furthermore, differential expression in the cells infected with the two virus variants was identified and a number of transcripts were singled out as possible answers to the question of how the viruses interact with the host cells, resulting in lytic or non-lytic infections.

National Category
Microbiology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-58203 (URN)10.1371/journal.pone.0164548 (DOI)000386204000039 ()2-s2.0-84992035054 (Scopus ID)
Available from: 2016-11-18 Created: 2016-11-18 Last updated: 2018-11-01Bibliographically approved
Jonsson, N., Sävneby, A., Gullberg, M., Evertsson, K., Klingel, K. & Lindberg, A. M. (2015). Efficient replication of recombinant Enterovirus B types, carrying different P1 genes in the coxsackievirus B5 replicative backbone. Virus genes, 50(3), 351-357
Open this publication in new window or tab >>Efficient replication of recombinant Enterovirus B types, carrying different P1 genes in the coxsackievirus B5 replicative backbone
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2015 (English)In: Virus genes, ISSN 0920-8569, E-ISSN 1572-994X, Vol. 50, no 3, p. 351-357Article in journal (Refereed) Published
Abstract [en]

Recombination is an important feature in theevolution of the Enterovirus genus. Phylogenetic studies ofenteroviruses have revealed that the capsid genomic region(P1) is type specific, while the parts of the genome codingfor the non-structural proteins (P2–P3) are species specific.Hence, the genome may be regarded as consisting of twomodules that evolve independently. In this study, it wasinvestigated whether the non-structural coding part of thegenome in one type could support replication of a virus witha P1 region from another type of the same species. A cas-sette vector (pCas) containing a full-length cDNA copy ofcoxsackievirus B5 (CVB5) was used as a replicative back-bone. The P1 region of pCas was replaced with the corre-sponding part from coxsackievirus B3Nancy(CVB3N),coxsackievirus B6Schmitt(CVB6S), and echovirus 7Wal-lace(E7W), all members of theEnterovirus Bspecies. Thereplication efficiency after transfection with clone-derivedin vitro transcribed RNA was studied and compared withthat of pCas. All the recombinant viruses replicated with similar efficiencies and showed threshold cycle (Ct) values,tissue culture infectivity dose 50 %, and plaque-forming unittiters comparable to viruses generated from the pCas con-struct. In addition to this, a clone without the P1 region wasalso constructed, and Western Blot and immunofluorescencestaining analysis showed that the viral genome could betranslated and replicated despite the lack of the structuralprotein-coding region. To conclude, the replicative back-bone of the CVB5 cassette vector supports replication ofintraspecies constructs with P1 regions derived from othermembers of theEnterovirus Bspecies. In addition to this,the replicative backbone can be both translated and repli-cated without the presence of a P1 region.

National Category
Biochemistry and Molecular Biology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-41538 (URN)10.1007/s11262-015-1177-x (DOI)000355233000001 ()25663145 (PubMedID)2-s2.0-84929956418 (Scopus ID)
Available from: 2015-04-01 Created: 2015-04-01 Last updated: 2017-12-04Bibliographically approved
Zhu, L., Wang, X., Ren, J., Porta, C., Wenham, H., Ekström, J.-O., . . . Stuart, D. I. (2015). Structure of Ljungan virus provides insight into genome packaging of this picornavirus. Nature Communications, 6, Article ID 8316.
Open this publication in new window or tab >>Structure of Ljungan virus provides insight into genome packaging of this picornavirus
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2015 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 6, article id 8316Article in journal (Refereed) Published
Abstract [en]

Picornaviruses are responsible for a range of human and animal diseases, but how their RNA genome is packaged remains poorly understood. A particularly poorly studied group within this family are those that lack the internal coat protein, VP4. Here we report the atomic structure of one such virus, Ljungan virus, the type member of the genus Parechovirus B, which has been linked to diabetes and myocarditis in humans. The 3.78-angstrom resolution cryo-electron microscopy structure shows remarkable features, including an extended VP1 C terminus, forming a major protuberance on the outer surface of the virus, and a basic motif at the N terminus of VP3, binding to which orders some 12% of the viral genome. This apparently charge-driven RNA attachment suggests that this branch of the picornaviruses uses a different mechanism of genome encapsidation, perhaps explored early in the evolution of picornaviruses.

Keywords
Biological sciences, Biophysics, Virology
National Category
Microbiology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-47715 (URN)10.1038/ncomms9316 (DOI)000364920600001 ()26446437 (PubMedID)2-s2.0-84943631507 (Scopus ID)
Available from: 2015-12-04 Created: 2015-12-04 Last updated: 2017-12-01Bibliographically approved
Israelsson, S., Sävneby, A., Ekström, J.-O., Jonsson, N., Edman, K. & Lindberg, A. M. (2014). Improved replication efficiency of echovirus 5 after transfection of colon cancer cells using an authentic 5' RNA genome end methodology. Investigational new drugs, 32(6), 1063-1070
Open this publication in new window or tab >>Improved replication efficiency of echovirus 5 after transfection of colon cancer cells using an authentic 5' RNA genome end methodology
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2014 (English)In: Investigational new drugs, ISSN 0167-6997, E-ISSN 1573-0646, Vol. 32, no 6, p. 1063-1070Article in journal (Refereed) Published
Abstract [en]

Oncolytic virotherapy is a promising novel form of cancer treatment, but the therapeutic efficiency needs improvement. A potential strategy to enhance the therapeutic effect of oncolytic viruses is to use infectious nucleic acid as therapeutic agent to initiate an oncolytic infection, without administrating infectious viral particles. Here we demonstrate improved viral replication activation efficiency when transfecting cells with 5’ end authentic in vitro transcribed enterovirus RNA as compared to genomic RNA with additional non-genomic 5’ nucleotides generated by conventional cloning methods. We used echovirus 5 (E5) as an oncolytoc model virus due to its ability to replicate in and completely destroy five out of six colon cancer cell lines and kill artificial colon cancer tumors (HT29 spheroids), as shown here. An E5 infectious cDNA clone including a hammerhead ribozyme sequence was used to generate in vitro transcripts with native 5’ genome ends. In HT29 cells, activation of virus replication is approximately 20-fold more efficient for virus genome transcripts with native 5’ genome ends compared to E5 transcripts generated from a standard cDNA clone. This replication advantage remains when viral progeny release starts by cellular lysis 22 h post transfection. Hence, a native 5’ genomic end improves infection activation efficacy of infectious nucleic acid, potentially enhancing its therapeutic effect when used for cancer treatment. The clone design with a hammerhead ribozyme is likely to be applicable to a variety of oncolytic positive sense RNA viruses for the purpose of improving the efficacy of oncolytic virotherapy.

Keywords
Picornavirus, RNA virus, Enterovirus, Oncolytic virotherapy, Hammerhead ribozyme, Infectious nucleic acid
National Category
Biochemistry and Molecular Biology
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-41541 (URN)10.1007/s10637-014-0136-z (DOI)000345142300002 ()2-s2.0-84938677294 (Scopus ID)
Available from: 2015-04-01 Created: 2015-04-01 Last updated: 2017-12-04Bibliographically approved
Jääskeläinen, A. J., Kolehmainen, P., Voutilainen, L., Hauffe, H. C., Kallio-Kokko, H., Lappalainen, M., . . . Vapalahti, O. (2013). Evidence of ljungan virus specific antibodies in humans and rodents, Finland.. Journal of Medical Virology, 85(11), 2001-2008
Open this publication in new window or tab >>Evidence of ljungan virus specific antibodies in humans and rodents, Finland.
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2013 (English)In: Journal of Medical Virology, ISSN 0146-6615, E-ISSN 1096-9071, Vol. 85, no 11, p. 2001-2008Article in journal (Refereed) Published
Abstract [en]

Ljungan virus (LV, genus Parechovirus, family Picornaviridae) is considered currently to be a rodent-borne virus. Despite suggested human disease associations, its zoonotic potential remains unclear. To date, LV antibody prevalence in both humans and rodents has not been studied. In this study, two different LV immunofluorescence assays (LV IFAs) were developed with LV genotypes 1 (LV strain 87-012G) and 2 (LV strain 145SLG), and cross-neutralization and -reaction studies were carried out with LV strain 145SLG. Finally, a panel of 37 Finnish sera was screened for anti-LV antibodies using two different LV IFAs (LV 145SLG and LV 87-012G) and a neutralization (NT) assay (LV 145SLG), and 50 samples from Myodes glareolus by LV IFA (LV 145SLG). The LV seroprevalence study showed 38% and 18% positivity in humans and M. glareolus, respectively. LV IFAs and NT assays were compared, and the results were in good agreement. The data are the first evidence of humans and rodents coming into contact with LV in Finland. Additional studies are required in order to acquire a better understanding of the prevalence, epidemiological patterns and possible disease association of LV infections.

National Category
Microbiology Infectious Medicine
Research subject
Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-30618 (URN)10.1002/jmv.23681 (DOI)000329198500020 ()23852812 (PubMedID)2-s2.0-84883055074 (Scopus ID)
Available from: 2013-11-20 Created: 2013-11-20 Last updated: 2017-12-06Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0003-3841-4826

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