SEITZ, K., K. BUCZOLICH, Alžbeta DIKUNOVÁ, Pavel PLEVKA, K. POWER, T. RIIMENAPF and B. LAMP. A molecular clone of Chronic Bee Paralysis Virus (CBPV) causes mortality in honey bee pupae (Apis mellifera). Scientific reports. LONDON: NATURE PUBLISHING GROUP, 2019, vol. 9, NOV, p. 16274-16284. ISSN 2045-2322. Available from: https://dx.doi.org/10.1038/s41598-019-52822-1.
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Basic information
Original name A molecular clone of Chronic Bee Paralysis Virus (CBPV) causes mortality in honey bee pupae (Apis mellifera)
Authors SEITZ, K., K. BUCZOLICH, Alžbeta DIKUNOVÁ (703 Slovakia, belonging to the institution), Pavel PLEVKA (203 Czech Republic, guarantor, belonging to the institution), K. POWER, T. RIIMENAPF and B. LAMP.
Edition Scientific reports, LONDON, NATURE PUBLISHING GROUP, 2019, 2045-2322.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10607 Virology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 3.998
RIV identification code RIV/00216224:14740/19:00113021
Organization unit Central European Institute of Technology
Doi http://dx.doi.org/10.1038/s41598-019-52822-1
UT WoS 000494945700041
Keywords in English PHYLOGENETIC ANALYSIS; GENOME; SUSCEPTIBILITY; IDENTIFICATION; INFECTION; PROTEINS; SPREAD; L.
Tags rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Eva Dubská, učo 77638. Changed: 2/10/2023 11:07.
Abstract
Among the many diseases compromising the well-being of the honey bee (Apis mellifera) the chronic paralysis syndrome of adult honey bees is one of the best described. The causative agent, chronic bee paralysis virus (CBPV), is a positive sense, single-stranded RNA virus with a segmented genome. Segment 1 encodes three putative open reading frames (ORFs), including the RNA-dependent RNA polymerase and other non-structural protein coding regions. Segment 2 encodes four putative ORFs, which contain the genes of supposed structural proteins. In this study, we established a reverse genetic system for CBPV by molecular cloning of DNA copies of both genome segments. CBPV rescue was studied in imago and honey bee pupae infection models. Virus replication and progeny virus production was only initiated when capped RNAs of both genome segments were injected in honey bees. As injection of these clonal RNAs caused clinical symptoms similar to wild-type CBPV infection, we conclude that the novel molecular clone fulfilled Koch's postulates. Our virus clone will enable in-depth analysis of CBPV pathogenesis and help to increase knowledge about this important honey bee disease.
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