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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Virology. 2015 Jul 1;484:288–304. doi: 10.1016/j.virol.2015.06.006

Figure 6. Model of adult heart failure in juvenile CVB-infected mice.

Figure 6

(A) A population of CPCs susceptible to CVB infection resides within the myocardium. Upon augmented cardiac stress, oxygen demand increases within the heart tissue. CPCs are recruited to drive angiogenesis and neovascularization which increases vascular density in the muscle allowing for efficient perfusion of oxygenated blood. (B) When the heart undergoes mild CVB infection, CPCs are preferentially targeted by the virus resulting in a depletion of the CPC population; however the myocardium is otherwise normal. Following cardiac stress, the limited number of remaining CPCs cannot sufficiently stimulate blood vessel formation and the myocardium becomes ischemic. The lack of vascularization causes the heart to become hypertrophic resulting in scar formation and cardiac dysfunction.