No evidence of a death-like function for species B1 human adenovirus type 3 E3-9K during A549 cell line infection

Persistent Link:
http://hdl.handle.net/10150/610099
Title:
No evidence of a death-like function for species B1 human adenovirus type 3 E3-9K during A549 cell line infection
Author:
Frietze, Kathryn; Campos, Samuel; Kajon, Adriana
Affiliation:
Infectious Disease Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM, USA; Department of Immunobiology, BIO5 Institute, University of Arizona, Keating Building Rm 423, 1657 E. Helen St, Tucson, 85721-0240, AZ, USA; Department of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, NM, 87131-0001, USA
Issue Date:
2012
Publisher:
BioMed Central
Citation:
Frietze et al. BMC Research Notes 2012, 5:429 http://www.biomedcentral.com/1756-0500/5/429
Journal:
BMC Research Notes
Rights:
© 2012 Frietze et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
BACKGROUND:Subspecies B1 human adenoviruses (HAdV-B1) are prevalent respiratory pathogens. Compared to their species C (HAdV-C) counterparts, relatively little work has been devoted to the characterization of their unique molecular biology. The early region 3 (E3) transcription unit is an interesting target for future efforts because of its species-specific diversity in genetic content among adenoviruses. This diversity is particularly significant for the subset of E3-encoded products that are membrane glycoproteins and may account for the distinct pathobiology of the different human adenovirus species. In order to understand the role of HAdV-B-specific genes in viral pathogenesis, we initiated the characterization of unique E3 genes. As a continuation of our efforts to define the function encoded in the highly polymorphic ORF E3-10.9K and testing the hypothesis that the E3-10.9K protein orthologs with a hydrophobic domain contribute to the efficient release of viral progeny, we generated HAdV-3 mutant viruses unable to express E3-10.9K ortholog E3-9K and examined their ability to grow, disseminate, and egress in cell culture.RESULTS:No differences were observed in the kinetics of infected cell death, and virus progeny release or in the plaque size and dissemination phenotypes between cells infected with HAdV-3 E3-9K mutants or the parental virus. The ectopic expression of E3-10.9K orthologs with a hydrophobic domain did not compromise cell viability.CONCLUSIONS:Our data show that despite the remarkable similarities with HAdV-C E3-11.6K, HAdV-B1 ORF E3-10.9K does not encode a product with a "death-like" biological activity.
EISSN:
1756-0500
DOI:
10.1186/1756-0500-5-429
Keywords:
Adenovirus; E3 region; Genetic polymorphism; Virus egress
Version:
Final published version
Additional Links:
http://www.biomedcentral.com/1756-0500/5/429

Full metadata record

DC FieldValue Language
dc.contributor.authorFrietze, Kathrynen
dc.contributor.authorCampos, Samuelen
dc.contributor.authorKajon, Adrianaen
dc.date.accessioned2016-05-20T08:58:33Z-
dc.date.available2016-05-20T08:58:33Z-
dc.date.issued2012en
dc.identifier.citationFrietze et al. BMC Research Notes 2012, 5:429 http://www.biomedcentral.com/1756-0500/5/429en
dc.identifier.doi10.1186/1756-0500-5-429en
dc.identifier.urihttp://hdl.handle.net/10150/610099-
dc.description.abstractBACKGROUND:Subspecies B1 human adenoviruses (HAdV-B1) are prevalent respiratory pathogens. Compared to their species C (HAdV-C) counterparts, relatively little work has been devoted to the characterization of their unique molecular biology. The early region 3 (E3) transcription unit is an interesting target for future efforts because of its species-specific diversity in genetic content among adenoviruses. This diversity is particularly significant for the subset of E3-encoded products that are membrane glycoproteins and may account for the distinct pathobiology of the different human adenovirus species. In order to understand the role of HAdV-B-specific genes in viral pathogenesis, we initiated the characterization of unique E3 genes. As a continuation of our efforts to define the function encoded in the highly polymorphic ORF E3-10.9K and testing the hypothesis that the E3-10.9K protein orthologs with a hydrophobic domain contribute to the efficient release of viral progeny, we generated HAdV-3 mutant viruses unable to express E3-10.9K ortholog E3-9K and examined their ability to grow, disseminate, and egress in cell culture.RESULTS:No differences were observed in the kinetics of infected cell death, and virus progeny release or in the plaque size and dissemination phenotypes between cells infected with HAdV-3 E3-9K mutants or the parental virus. The ectopic expression of E3-10.9K orthologs with a hydrophobic domain did not compromise cell viability.CONCLUSIONS:Our data show that despite the remarkable similarities with HAdV-C E3-11.6K, HAdV-B1 ORF E3-10.9K does not encode a product with a "death-like" biological activity.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.biomedcentral.com/1756-0500/5/429en
dc.rights© 2012 Frietze et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)en
dc.subjectAdenovirusen
dc.subjectE3 regionen
dc.subjectGenetic polymorphismen
dc.subjectVirus egressen
dc.titleNo evidence of a death-like function for species B1 human adenovirus type 3 E3-9K during A549 cell line infectionen
dc.typeArticleen
dc.identifier.eissn1756-0500en
dc.contributor.departmentInfectious Disease Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM, USAen
dc.contributor.departmentDepartment of Immunobiology, BIO5 Institute, University of Arizona, Keating Building Rm 423, 1657 E. Helen St, Tucson, 85721-0240, AZ, USAen
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, NM, 87131-0001, USAen
dc.identifier.journalBMC Research Notesen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
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