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Non-cytolytic enterovirus
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== The spread of non-cytolytic enterovirus infection in the host == Non-cytolytic enterovirus, though defective due to deletions in its genome, appears capable of propagating itself within the host. This is demonstrated when cultured non-cytolytic enterovirus is injected intraperitoneally into mice: the infection travels to the heart, and then produces a persistent non-cytolytic infection in the heart tissues.<ref>{{Cite web|url=https://www.youtube.com/watch?v=3Ro7UlhSD-w&t=7m57s | title = How Does a Lytic Enterovirus Persist and Cause Chronic Disease? Enterovirus Session, International Symposium on Viruses in CFS & Post-viral Fatigue, Maryland, US, June 2008. Timecode: 7:57. | last=Chapman | first = Nora | date = 2008 | website = YouTube | archive-url=|archive-date=|url-status=|access-date=}}</ref> Non-cytolytic enterovirus is able to propagate because although the virus is defective, its genome is still packaged into capsids to make virions which can transport the non-cytolytic infection to other cells. Evidence for this virion mode of propagation comes from the fact that when cultured non-cytolytic [[Coxsackie B virus|coxsackievirus B3]] is introduced to a cell line, infection of those cells can be prevented by CVB3 neutralizing antibody. Non-cytolytic enterovirus virions may be transmitted to other cells by means of extracellular vesicles, the formation of cell protrusions, and intercellular bridges.<ref name="Genoni2017">{{Cite journal | last = Genoni | first = Angelo | last2 = Canducci | first2 = Filippo | last3 = Rossi | first3 = Agostino | last4 = Broccolo | first4 = Francesco | last5 = Chumakov | first5 = Konstantin | last6 = Bono | first6 = Giorgio | last7 = Salerno-Uriarte | first7 = Jorge | last8 = Salvatoni | first8 = Alessandro | last9 = Pugliese | first9 = Alberto | date = 2017-07-10 | title = Revealing enterovirus infection in chronic human disorders: An integrated diagnostic approach|url=http://www.nature.com/articles/s41598-017-04993-y|journal=Scientific Reports|language=en|volume=7|issue=1|pages=|doi=10.1038/s41598-017-04993-y|issn=2045-2322|pmc=5504018|pmid=28694527|quote=In persistently infected cultures, virus transmission may occur through the release of extracellular vesicles, formation of cell protrusions and intercellular bridges. This exit mode may facilitate virus dissemination in vivo in the presence of a robust immune response.|via=}}</ref> Interestingly, when non-cytolytic enteroviral RNA is packed into virions, as well as virions containing the normal positive ssRNA genome, negative ssRNA is also encapsidated in almost as many virions. Thus in non-cytolytic infection, virions containing the negative ssRNA anti-genome are found, which is very unusual, and this is a signature of non-cytolytic infection.<ref>{{Cite web|url=https://www.youtube.com/watch?v=3Ro7UlhSD-w&t=6m57s | title = How Does a Lytic Enterovirus Persist and Cause Chronic Disease? Enterovirus Session, International Symposium on Viruses in CFS & Post-viral Fatigue, Maryland, US, June 2008. Timecode: 6:57. | last=Chapman | first = Nora | date = 2008 | website = YouTube | archive-url=|archive-date=|url-status=|access-date=}}</ref><ref name="Kim2005a">{{Cite journal | last = Kim | first = K.-S. | last2 = Tracy | first2 = S. | last3 = Tapprich | first3 = W. | last4 = Bailey | first4 = J. | last5 = Lee | first5 = C.-K. | last6 = Kim | first6 = K. | last7 = Barry | first7 = W.H. | last8 = Chapman | first8 = N.M. | date = Jun 2005 | title = 5'-Terminal deletions occur in coxsackievirus B3 during replication in murine hearts and cardiac myocyte cultures and correlate with encapsidation of negative-strand viral RNA|url=https://www.ncbi.nlm.nih.gov/pubmed/15890942/|journal=Journal of Virology|volume=79|issue=11 | pages = 7024–7041|doi=10.1128/JVI.79.11.7024-7041.2005|issn=0022-538X|pmc=1112132|pmid=15890942|quote=The detection of the largest capsid protein, VP1, by Western blot analysis in cells inoculated with CVB3/TD8 and TD50, together with the ablation of detectable CVB3/TD RNA in cells infected with virus in the presence of anti-CVB3 neutralizing antibody, strongly suggests that CVB3/TD strains are normally encapsidated and transmitted.|via=}}</ref>
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