Many viruses have been shown to upregulate host autophagic processes during the course of infection. Originally this process was thought to be a response mechanism of the host cell in order to engulf viral particles and destroy them to prevent viral spread and host cell death. However, certain viruses have been shown to strategically hijack the autophagic pathway to evade host immunity and increase viral replication. Coxsackievirus B (CVB) is a non-enveloped picornavirus that most commonly causes a self-limited febrile illness in young children, but in rare severe cases can progress to myocarditis, pancreatitis, or meningo-encephalitis. It has also been associated with late-onset idiopathic dilated cardiomyopathy. CVB type 3 (CVB3) has previously been documented to upregulate host autophagic machinery upon infection, and we report here that the virus can infect cardiac stem cells and other muscle progenitors and allow itself to be engulfed in autophagosomes which later get shed from the surface of the host cell. This is a novel method of viral dissemination especially for a “naked” virus which would typically escape the infected host by triggering cytolysis. However, cytolytic viruses subsequently become exposed to neutralizing antibodies. The fact that CVB3 can hide itself in host membranes presents several fascinating possibilities. Not only could the ejected autophagosome mask the virus from adaptive immunity, but it may also bypass receptor-mediated endocytosis and infect cell-types that might lack CVB3 receptors. This mode of viral escape represents a unique evolutionary adaptation which obscures the line dividing enveloped and non-enveloped viruses.