Clinical Characteristics of Enterovirus A71 Neurologic Disease During an Outbreak in Children in Colorado, 2018

Messacar, Kevin; Spence‐Davizon, Emily; Osborne, Christina; Press, Craig; Schreiner, Teri; Martin, Jan; Messer, Ricka; Maloney, John; Burakoff, Alexis; Barnes, Meghan; Rogers, Shannon; Lopez, Adriana; Routh, Janell; Gerber, Susan I.; Oberste, M. Steven; Nix, Allan; Abzug, Mark J.; Tyler, Ken; Herlihy, Rachel; Dominguez, Samuel R.

doi:10.2139/ssrn.3417873

Cited by 4 publications

(4 citation statements)

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“…WNV appears to be a particularly notable cause of AFM occurring in adults, but this syndrome appears distinct from childhood AFM. In addition, recent descriptions of AFM cases associated with EV-A71 suggest that these cases have distinct clinical presentations and a different outcome from those associated with EV-D68 (Messacar et al, in review) [50]. Under the CSTE guidelines, 120 confirmed cases of AFM from 34 states were documented in 2014, 149 cases in 39 states (and the District of Columbia) in 2016, and 233 cases in 41 states in 2018 [32,33,34,35,51].…”

Section: Enterovirus D68 (Ev-d68)-associated Acute Flaccid Myelitimentioning

confidence: 99%

Understanding Enterovirus D68-Induced Neurologic Disease: A Basic Science Review

Hixon

Frost

Rudy

et al. 2019

Viruses

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In 2014, the United States (US) experienced an unprecedented epidemic of enterovirus D68 (EV-D68)-induced respiratory disease that was temporally associated with the emergence of acute flaccid myelitis (AFM), a paralytic disease occurring predominantly in children, that has a striking resemblance to poliomyelitis. Although a definitive causal link between EV-D68 infection and AFM has not been unequivocally established, rapidly accumulating clinical, immunological, and epidemiological evidence points to EV-D68 as the major causative agent of recent seasonal childhood AFM outbreaks in the US. This review summarizes evidence, gained from in vivo and in vitro models of EV-D68-induced disease, which demonstrates that contemporary EV-D68 strains isolated during and since the 2014 outbreak differ from historical EV-D68 in several factors influencing neurovirulence, including their genomic sequence, their receptor utilization, their ability to infect neurons, and their neuropathogenicity in mice. These findings provide biological plausibility that EV-D68 is a causal agent of AFM and provide important experimental models for studies of pathogenesis and treatment that are likely to be difficult or impossible in humans.

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Section: Enterovirus D68 (Ev-d68)-associated Acute Flaccid Myelitimentioning

confidence: 99%

Understanding Enterovirus D68-Induced Neurologic Disease: A Basic Science Review

Hixon

Frost

Rudy

et al. 2019

Viruses

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“…Через несколько лет реиннервированные увеличенные двигательные единицы могут подвергаться дегенерации в результате метаболического стресса, как это описано и при полиомиелите [14]. Пациенты, у которых причиной ОВМ был энтеровирус А-71, имели более легкую клиническую картину по сравнению с теми, у кого заболевание было вызвано энтеровирусом D-68 [36]. После перенесенного заболевания неврологическое восстановление пациентов вариабельно и часто неполное.…”

Section: консервативное лечениеunclassified

Nerve transfer in children with acute flaccid myelitis for restoration of upper limb function (literature review)

Agranovich,

Komolkin

2024

Neuromuscular Diseases

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The term “acute flaccid myelitis” is used to describe a condition characterized by acute flaccid paralysis of the limb, as well as damage to the motor neurons of the spinal cord. The absence of specific treatment, severe neurological deficit that persists in 75–95 % of patients in the long term indicates its severity.The aim of the work is to describe acute flaccid myelitis in children, modern methods of treatment, and estimate the effectiveness of nerve transfers for restoration of the upper limb function.The search for publications was carried out in the PubMed/MEDLINE, Google Scholar databases from 2003 to 2022, and data from the US Centers for Disease Control and Prevention (https://www.cdc.gov) were used. There were analyzed surgical treatments of 57 children with paresis of the upper extremities due to AFM (105 nerve transfers). Restoration of shoulder function (neurotization of n. axillaris, n. suprascapularis) was performed in 57 (54.3 %) patients, elbow flexion (neurotization of n. musculocutaneus) in 37 (35.2 %), elbow extension in 9 (8.5 %) (neurotization of the branch of n. radialis to m. triceps brachii), fingers flexion in 1 (1 %) (neurotization of the n. interosseus anterior branch), fingers extension in 1 (1 %) (neurotization of n. interosseus posterior).The review demonstrated the effectiveness of nerve transfers in children with paresis of the upper extremities due to acute flaccid myelitis who were operated up to 1 year from the onset of the disease.

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“…Notably, 93% of laboratory-confirmed deaths due to HFMD between 2008 and 2012 in China were associated with EVA71 [7]. A recent observational cohort study from Colorado identified that EVA71 accounts for 58% of child cases of enterovirus-induced neurological disease [110]. EVA71 can occasionally cause severe neurological complications, including brainstem encephalitis, aseptic meningitis, and acute flaccid paralysis, which are considered to be a major factor in most fatal cases [111].…”

Section: Autophagy Is Involved In Eva71-induced Nervous System Injurymentioning

confidence: 99%

Dysregulated autophagy contributes to the pathogenesis of enterovirus A71 infection

Zhang

2020

Cell Biosci

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Enterovirus A71 (EVA71) infection continues to remain a vital threat to global public health, especially in the Asia–Pacific region. It is one of the most predominant pathogens that cause hand, foot, and mouth disease (HFMD), which occurs mainly in children below 5 years old. Although EVA71 prevalence has decreased sharply in China with the use of vaccines, epidemiological studies still indicate that EVA71 infection involves severe and even fatal HFMD cases. As a result, it remains more fundamental research into the pathogenesis of EVA71 as well as to develop specific anti-viral therapy. Autophagy is a conserved, self-degradation system that is critical for maintaining cellular homeostasis. It involves a variety of biological functions, such as development, cellular differentiation, nutritional starvation, and defense against pathogens. However, accumulating evidence has indicated that EVA71 induces autophagy and hijacks the process of autophagy for their optimal infection during the different stages of life cycle. This review provides a perspective on the emerging evidence that the “positive feedback” between autophagy induction and EVA71 infection, as well as its potential mechanisms. Furthermore, autophagy may be involved in EVA71-induced nervous system impairment through mediating intracranial viral spread and dysregulating host regulator involved self-damage. Autophagy is a promising therapeutic target in EVA71 infection.

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Clinical Characteristics of Enterovirus A71 Neurologic Disease During an Outbreak in Children in Colorado, 2018

Cited by 4 publications

References 0 publications

Understanding Enterovirus D68-Induced Neurologic Disease: A Basic Science Review

Understanding Enterovirus D68-Induced Neurologic Disease: A Basic Science Review

Nerve transfer in children with acute flaccid myelitis for restoration of upper limb function (literature review)

Dysregulated autophagy contributes to the pathogenesis of enterovirus A71 infection

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