Group B Coxsackievirus Infections in Infants Younger than Three Months of Age: A Serious Childhood Illness

Kaplan, Mark H.; Klein, Susan Blakeley; McPhee, Julia; Harper, Rita G.

doi:10.1093/clinids/5.6.1019

Cited by 229 publications

(139 citation statements)

References 45 publications

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“…Our laboratory has shown that CVB3 undergoes a burst of replication in B cells trafficking through splenic germinal centers, which are sites of active B cell proliferation (Mena et al, 1999), and both coxsackievirusinduced myocarditis and productive infection of T cells are dependent on the expression of p56 lck kinase, a signal transduction molecule involved in cellular activation (Liu et al, 2000). Thus, proliferating or highly activated cells appear to favor productive CVB infection, and we proposed (Feuer et al, 2003) that this preference may contribute to the extreme susceptibility of newborns to coxsackievirus infection and viral-induced pathology (Kaplan et al, 1983;Modlin, 1988).…”

Section: Discussionmentioning

confidence: 83%

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Feuer¹,

Pagarigan²,

Harkins³

et al. 2005

J. Neurosci.

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Type B coxsackieviruses (CVB) frequently infect the CNS and, together with other enteroviruses, are the most common cause of viral meningitis in humans. Newborn infants are particularly vulnerable, and CVB also can infect the fetus, leading to mortality, or to neurodevelopmental defects in surviving infants. Using a mouse model of neonatal CVB infection, we previously demonstrated that coxsackievirus B3 (CVB3) could infect neuronal progenitor cells in the subventricular zone (SVZ). Here we extend these findings, and we show that CVB3 targets actively proliferating (bromodeoxyuridine ϩ , Ki67 ϩ ) cells in the SVZ, including type B and type A stem cells. However, infected cells exiting the SVZ have lost their proliferative capacity, in contrast to their uninfected companions. Despite being proliferation deficient, the infected neuronal precursors could migrate along the rostral migratory stream and radial glia, to reach their final destinations in the olfactory bulb or cerebral cortex. Furthermore, infection did not prevent cell differentiation, as determined by cellular morphology and the expression of maturation markers. These data lead us to propose a model of CVB infection of the developing CNS, which may explain the neurodevelopmental defects that result from fetal infection.

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Section: Discussionmentioning

confidence: 83%

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Feuer¹,

Pagarigan²,

Harkins³

et al. 2005

J. Neurosci.

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“…Previous studies have been directed toward developing and studying coxsackievirus-induced myositis as a model for human disease (16,36,37). These models, however, may be more representative of the juvenile type of idiopathic inflammatory myopathies, for the following reasons: (a) neonatal animals and human infants are the most susceptible to coxsackievirus-induced disease, while adults are often resistant (7,11,15,38); and (b) the only controlled investigation showing serologic evidence for the role of coxsackievirus in human myositis is from the study of children with DM (2). In order to study the disease in adults, we developed a mouse myositis model using picornaviruses, which induced PM in adult mice.…”

Section: Discussionmentioning

confidence: 99%

Viral and host genetic factors influence encephalomyocarditis virus—induced polymyositis in adult mice

Miller

Love

Biswas

et al. 1987

Arthritis & Rheumatism

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Recent research findings implicate picornaviruses in the etiology of human polymyositis/dermatomyositis and suggest that genetic factors play a role in susceptibility to these diseases. We compared 2 variants of encephalomyocarditis (EMC) virus for their ability to induce polymyositis in adult mice, and evaluated what role the genetic background of the host plays in the degree of myositis induced. While BALB/c mice developed minimal myositis when infected with a diabetogenic variant (EMC‐D), the same strain inoculated with a newly isolated myopathic variant (EMC‐221A) developed viral dose—dependent elevations in muscle‐associated enzymes, bilateral limb muscle weakness, and the histopathologic changes of severe polymyositis. Mice with different genetic backgrounds showed significantly different susceptibilities to EMC‐221A. These data suggest that the severity of polymyositis induced by EMC virus is influenced by both the viral and host genomes.

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“…CV-B3 is a common causative agent of cardiac diseases, pancreatitis and acute flaccid paralysis (AFP) (Kaplan et al, 1983;Wong et al, 2011). Such diverse outcomes have been described to be due in part to the genetics/immune status of the host or the initial viral load during infection or the viral genetics or diversity in the viral population (Tracy et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Genomic characterization of coxsackievirus type B3 strains associated with acute flaccid paralysis in south-western India

Laxmivandana

Cherian

Yergolkar

et al. 2016

Journal of General Virology

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Acute flaccid paralysis (AFP) associated with coxsackievirus type B3 (CV-B3) of the species Enterovirus B is an emerging concern worldwide. Although CV-B3-associated AFP in India has been demonstrated previously, the genomic characterization of these strains is unreported. Here, CV-B3 strains detected on the basis of the partial VP1 gene in 10 AFP cases and five asymptomatic contacts identified from different regions of south-western India during 2009-2010 through the Polio Surveillance Project were considered for complete genome sequencing and characterization. Phylogenetic analysis of complete VP1 gene sequences of global CV-B3 strains classified Indian CV-B3 strains into genogroup GVI, along with strains from Uzbekistan and Bangladesh, and into a new genogroup, GVII. Genomic divergence between genogroups of the study strains was 14.4 % with significantly lower divergence (1.8 %) within GVI (n512) than that within GVII (8.5 %) (n53). The strains from both AFP cases and asymptomatic contacts, identified mainly in coastal Karnataka and Kerala, belonged to the dominant genogroup GVI, while the GVII strains were recovered from AFP cases in north interior Karnataka. All study strains carried inter-genotypic recombination with the structural region similar to reference CV-B3 strains, and 59 non-coding regions and non-structural regions closer to other enterovirus B types. Domain II structures of 59 non-coding regions, described to modulate virus replication, were predicted to have varied structural folds in the two genogroups and were attributed to differing recombination patterns. The results indicate two distinct genomic compositions of CV-B3 strains circulating in India and suggest the need for concurrent analysis of viral and host factors to further understand the varied manifestations of their infections.

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Group B Coxsackievirus Infections in Infants Younger than Three Months of Age: A Serious Childhood Illness

Cited by 229 publications

References 45 publications

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Viral and host genetic factors influence encephalomyocarditis virus—induced polymyositis in adult mice

Genomic characterization of coxsackievirus type B3 strains associated with acute flaccid paralysis in south-western India

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