Pathologic Studies of Fatal Encephalomyelitis in Children Caused by Enterovirus 71

Abstract

Our study revealed direct pathologic evidence supporting viral entry into the central nervous system (CNS) through peripheral nerves. In addition to the major motor pathway, EV71 can also enter the CNS via peripheral sensory and autonomic pathways in retrograde axonal transport.

Immune responses against enterovirus A71 infection: Implications for vaccine success

“…The role of neutrophils in EV‐A71 infection could be protective with the release of neutrophil extracellular traps as well as harmful with tissue damage as seen in other viral infections . Increased white cell counts have been associated as a risk factor for severe HFMD …”

“…127 [133][134][135] Increased white cell counts have been associated as a risk factor for severe HFMD. 110,118,131,136,137 Polymorphisms in PRR gene melanoma differentiation-associated protein 5 (MDA-5), but not toll-like receptor 3 (TLR-3) and retinoic acid-inducible gene I (RIG-I), are associated with severe EV-A71 infection. 138 Other polymorphisms reported to increase severity of EV-A71 infection include those found in IL-2, IL-6, IL-8, and IL-10.…”

Not your usual tRNA synthetase: hWARS serves as an enterovirus entry factor

“…Whether one or both forms of hWARS facilitate EV-A71 entry or that of other enteroviruses will be important to determine. This will be especially true in the context of the infection of neurons, particularly anterior horn cells, as infection of these cells results in acute flaccid paralysis and long-term neurological disability, the most feared complications of EV-A71 infection (21).…”

Cardiopulmonary failure as a result of brainstem encephalitis caused by enterovirus D68

“…Infection with EV-A71 is the most common enteroviral cause of brainstem encephalitis accompanied by cardiopulmonary failure 3 7–11. Initially, this patient was treated for cardiopulmonary failure as a result of fulminant myocarditis.…”

“…Damage to some areas of the brainstem can cause neurogenic pulmonary oedema. Regarding cardiopulmonary failure, it has been proposed that with EV-A71 infection, the mechanism may be similar to that seen with subarachnoid haemorrhage, because inflammation of the myocardium has not been found at autopsy 7 10 11 16. There are two main theories about the pathogenesis of cardiopulmonary failure secondary to subarachnoid haemorrhage: (1) catecholamines are released at the onset of subarachnoid haemorrhage, and the sympathetic nervous system stimulation induces coronary spasm; or (2) high blood concentrations of catecholamines damage the myocardium directly 17.…”