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Non-cytolytic enterovirus
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== Note on defective interfering viruses == Non-cytolytic enteroviruses are similar to defective interfering (DI) viruses: both have deletions in their genomes. However, one difference is that DI viruses cannot replicate on their own, they are only able to replicate with the help of the lytic virus with a complete genome,<ref name="Nayak1983">{{Cite book | last = Nayak | first = D. P. | last2 = Sivasubramanian | first2 = N. | date = 1983|chapter=The Structure of Influenza Virus Defective Interfering (DI) RNAs and Their Progenitor Genes | title = Genetics of Influenza Viruses|url=https://link.springer.com/chapter/10.1007/978-3-7091-8706-7_8|language=en|location=Vienna|publisher=Springer Vienna|pages=255–279|doi=10.1007/978-3-7091-8706-7_8|isbn=9783709187081}}</ref> whereas non-cytolytic enteroviruses are thought to be able to replicate independently. Although true independent replication is not entirely certain, as in a non-cytolytic enterovirus infection, Bouin et al<ref name="Bouin2016" /> found most of the viral genomes are defective due to deletions, but they also found 0.9% of the genomes to be those of the intact lytic virus. Thus the lytic virus genome is still present in small quantities in non-cytolytic infection, and Lévêque<ref name="Leveque2017a" /> suggests that this small amount of lytic virus RNA in the cell might be helping the defective viruses to replicate. However, this low level of lytic RNA found in non-cytolytic infection is not the same as an acute lytic infection, so in that respect, it is clear that non-cytolytic enterovirus can replicate independently to the lytic virus and its lifecycle. Another difference is that defective interfering viruses have large genome deletions, typically consisting of only 5-10% of the genome of the parental lytic virus (though in the case of picornavirus DI viruses, these usually comprise 85% or more of the parental genome).<ref name="Dimmock1991">{{Cite journal | last = Dimmock | first = N.J. | date = Oct 1991 | title = The biological significance of defective interfering viruses|url=https://onlinelibrary.wiley.com/doi/abs/10.1002/rmv.1980010306|journal=Reviews in Medical Virology|language=en|volume=1|issue=3|pages=165–176|doi=10.1002/rmv.1980010306|issn=1052-9276}}</ref> By contrast, in the case of the genomic deletions of non-cytolytic enterovirus, less than 0.7% of the parental genome is lost (non-cytolytic enterovirus deletions are 7 to 49 nucleotides in size,<ref name="Kim2005b" /> and the full coxsackievirus B genome comprises around 7,400 nucleotides).<ref name="Leveque2017b" /> So non-cytolytic enterovirus still possesses most of the parental lytic virus genome, thus retaining most of the functionality.
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