Show simple item record

dc.contributor.authorMcDougall, William M.
dc.contributor.authorPerreira, Jill
dc.contributor.authorHung, Hui-Fang
dc.contributor.authorVertii, Anastassiia
dc.contributor.authorXiaofei, E.
dc.contributor.authorZimmerman, Wendy
dc.contributor.authorKowalik, Timothy F.
dc.contributor.authorDoxsey, Stephen J.
dc.contributor.authorBrass, Abraham L.
dc.date2022-08-11T08:09:52.000
dc.date.accessioned2022-08-23T16:46:42Z
dc.date.available2022-08-23T16:46:42Z
dc.date.issued2019-02-22
dc.date.submitted2019-03-12
dc.identifier.citation<p>iScience. 2019 Feb 22;12:270-279. doi: 10.1016/j.isci.2019.01.025. Epub 2019 Jan 21. <a href="https://doi.org/10.1016/j.isci.2019.01.025">Link to article on publisher's site</a></p>
dc.identifier.issn2589-0042 (Linking)
dc.identifier.doi10.1016/j.isci.2019.01.025
dc.identifier.pmid30716700
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40933
dc.description.abstractCongenital microcephaly occurs in utero during Zika virus (ZIKV) infection. The single-gene disorder, Majewski osteodysplastic primordial dwarfism type II (MOPDII), also leads to microcephaly and is concomitant with a decrease in the centrosomal protein, pericentrin (PCNT). This protein is a known contributor of mitotic spindle misorientation and ultimately, microcephaly. Similar to MOPDII, either viral infection or interferon (IFN)-alpha exposure reduced PCNT levels at the mitotic spindle poles. We unexpectedly found that infection of cells with any one of a diverse set of viruses, such as ZIKV, dengue virus, cytomegalovirus, influenza A virus, or hepatitis B virus, or treatment of cells with the anti-viral cytokine, IFN-alpha, produced mitotic spindle misorientation. These findings demonstrate a related mechanism for the development of microcephaly in viral infection, the host's antiviral IFN response, and primordial dwarfism.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30716700&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright 2019 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectBiological Sciences
dc.subjectCell Biology
dc.subjectPathophysiology
dc.subjectVirology
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectBiological Factors
dc.subjectCell Biology
dc.subjectCongenital, Hereditary, and Neonatal Diseases and Abnormalities
dc.subjectImmunology and Infectious Disease
dc.subjectVirology
dc.subjectVirus Diseases
dc.subjectViruses
dc.titleViral Infection or IFN-alpha Alters Mitotic Spindle Orientation by Modulating Pericentrin Levels
dc.typeJournal Article
dc.source.journaltitleiScience
dc.source.volume12
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4746&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3732
dc.identifier.contextkey14008333
refterms.dateFOA2022-08-23T16:46:42Z
html.description.abstract<p>Congenital microcephaly occurs in utero during Zika virus (ZIKV) infection. The single-gene disorder, Majewski osteodysplastic primordial dwarfism type II (MOPDII), also leads to microcephaly and is concomitant with a decrease in the centrosomal protein, pericentrin (PCNT). This protein is a known contributor of mitotic spindle misorientation and ultimately, microcephaly. Similar to MOPDII, either viral infection or interferon (IFN)-alpha exposure reduced PCNT levels at the mitotic spindle poles. We unexpectedly found that infection of cells with any one of a diverse set of viruses, such as ZIKV, dengue virus, cytomegalovirus, influenza A virus, or hepatitis B virus, or treatment of cells with the anti-viral cytokine, IFN-alpha, produced mitotic spindle misorientation. These findings demonstrate a related mechanism for the development of microcephaly in viral infection, the host's antiviral IFN response, and primordial dwarfism.</p>
dc.identifier.submissionpathoapubs/3732
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.source.pages270-279


Files in this item

Thumbnail
Name:
Publisher version
Thumbnail
Name:
1_s2.0_S2589004219300264_main.pdf
Size:
4.190Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

Copyright 2019 The Author(s).  This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Except where otherwise noted, this item's license is described as Copyright 2019 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).