The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.

Coxsackievirus B (CVB) is an enterovirus that most commonly causes a self-limited febrile illness in infants, but cases of severe infection can manifest in acute myocarditis. Chronic consequences of mild CVB infection are unknown, though there is an epidemiologic association between early subclinica...

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Autores principales:	Jon Sin, Jenna M Puccini, Chengqun Huang, Mathias H Konstandin, Paul E Gilbert, Mark A Sussman, Roberta A Gottlieb, Ralph Feuer
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/6a744a87bf434cc38dc1d9f8549437dd
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spelling	oai:doaj.org-article:6a744a87bf434cc38dc1d9f8549437dd2021-11-25T05:46:13ZThe impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.1553-73661553-737410.1371/journal.ppat.1004249https://doaj.org/article/6a744a87bf434cc38dc1d9f8549437dd2014-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25079373/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Coxsackievirus B (CVB) is an enterovirus that most commonly causes a self-limited febrile illness in infants, but cases of severe infection can manifest in acute myocarditis. Chronic consequences of mild CVB infection are unknown, though there is an epidemiologic association between early subclinical infections and late heart failure, raising the possibility of subtle damage leading to late-onset dysfunction, or chronic ongoing injury due to inflammatory reactions during latent infection. Here we describe a mouse model of juvenile infection with a subclinical dose of coxsackievirus B3 (CVB3) which showed no evident symptoms, either immediately following infection or in adult mice. However following physiological or pharmacologically-induced cardiac stress, juvenile-infected adult mice underwent cardiac hypertrophy and dilation indicative of progression to heart failure. Evaluation of the vasculature in the hearts of adult mice subjected to cardiac stress showed a compensatory increase in CD31+ blood vessel formation, although this effect was suppressed in juvenile-infected mice. Moreover, CVB3 efficiently infected juvenile c-kit+ cells, and cardiac progenitor cell numbers were reduced in the hearts of juvenile-infected adult mice. These results suggest that the exhausted cardiac progenitor cell pool following juvenile CVB3 infection may impair the heart's ability to increase capillary density to adapt to increased load.Jon SinJenna M PucciniChengqun HuangMathias H KonstandinPaul E GilbertMark A SussmanRoberta A GottliebRalph FeuerPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 7, p e1004249 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Jon Sin Jenna M Puccini Chengqun Huang Mathias H Konstandin Paul E Gilbert Mark A Sussman Roberta A Gottlieb Ralph Feuer The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
description	Coxsackievirus B (CVB) is an enterovirus that most commonly causes a self-limited febrile illness in infants, but cases of severe infection can manifest in acute myocarditis. Chronic consequences of mild CVB infection are unknown, though there is an epidemiologic association between early subclinical infections and late heart failure, raising the possibility of subtle damage leading to late-onset dysfunction, or chronic ongoing injury due to inflammatory reactions during latent infection. Here we describe a mouse model of juvenile infection with a subclinical dose of coxsackievirus B3 (CVB3) which showed no evident symptoms, either immediately following infection or in adult mice. However following physiological or pharmacologically-induced cardiac stress, juvenile-infected adult mice underwent cardiac hypertrophy and dilation indicative of progression to heart failure. Evaluation of the vasculature in the hearts of adult mice subjected to cardiac stress showed a compensatory increase in CD31+ blood vessel formation, although this effect was suppressed in juvenile-infected mice. Moreover, CVB3 efficiently infected juvenile c-kit+ cells, and cardiac progenitor cell numbers were reduced in the hearts of juvenile-infected adult mice. These results suggest that the exhausted cardiac progenitor cell pool following juvenile CVB3 infection may impair the heart's ability to increase capillary density to adapt to increased load.
format	article
author	Jon Sin Jenna M Puccini Chengqun Huang Mathias H Konstandin Paul E Gilbert Mark A Sussman Roberta A Gottlieb Ralph Feuer
author_facet	Jon Sin Jenna M Puccini Chengqun Huang Mathias H Konstandin Paul E Gilbert Mark A Sussman Roberta A Gottlieb Ralph Feuer
author_sort	Jon Sin
title	The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
title_short	The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
title_full	The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
title_fullStr	The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
title_full_unstemmed	The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
title_sort	impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/6a744a87bf434cc38dc1d9f8549437dd
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The impact of juvenile coxsackievirus infection on cardiac progenitor cells and postnatal heart development.

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