Key result
Skeletal muscle denervation markedly increases Coxsackie A2 virus replication and tissue destruction in mice.
Why the study?
The role of synaptic transmission in preventing susceptibility of mature skeletal muscle to Coxsackievirus infection was unclear.
May link denervation to heightened enteroviral muscle susceptibility; hypothesis-generating for human myocarditis or myositis, needs prospective validation.
Coxsackie A viruses can infect denervated but not innervated mature skeletal muscles. The role of synaptic transmission in preventing susceptibility to Coxsackievirus infection was studied by surgically denervating leg muscles of mice or injecting the muscles with botulinum toxin to block quantal release of acetylcholine. Control muscles were injected with heat-inactivated toxin. Subsequent injection of Coxsackie A2 virus resulted in extensive virus replication and tissue destruction in the denervated and botulinum toxin-treated muscles, while the control muscles showed only minimal changes. This suggests that the susceptibility of skeletal muscle to Coxsackievirus infection is regulated by synaptic transmission.
No takes yet. Share an insight, caveat, or question.
Andrew et al. (1984) studied Coxsackie A 2 virus infection. Surgical denervation or botulinum toxin injection vs. Heat-inactivated toxin was evaluated on Virus replication and tissue destruction. Surgical denervation or botulinum toxin injection in mice skeletal muscles resulted in extensive Coxsackie A2 virus replication and tissue destruction compared to heat-inactivated toxin.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: