Coxsackieviruses, Echoviruses, Newer Enteroviruses, and Parechoviruses

Modlin, John F.

doi:10.1016/b978-0-443-06839-3.00172-7

Cited by 9 publications

(9 citation statements)

References 308 publications

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“…coxsackievirus, echovirus, etc.) are the causative agents of 90% of cases of viral meningitis [31] . It also may argue for a different route of entry for viruses into the ear in ISSHL other than the CSF-perilymph (meningogenic) route.…”

Section: Analysis Of Evidence For and Against The Viral Hypothesismentioning

confidence: 99%

Sudden Deafness: Is It Viral?

Merchant

Durand

Adams

2008

ORL

165

120

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A number of theories have been proposed to explain the etiopathogenesis of idiopathic sudden sensorineural hearing loss (ISSHL), including viral infection, vascular occlusion, breaks of labyrinthine membranes, immune-mediated mechanisms and abnormal cellular stress responses within the cochlea. In the present paper, we provide a critical review of the viral hypothesis of ISSHL. The evidence reviewed includes published reports of epidemiological and serological studies, clinical observations and results of antiviral therapy, morphological and histopathological studies, as well as results of animal experiments. The published evidence does not satisfy the majority of the Henle-Koch postulates for viral causation of an infectious disease. Possible explanations as to why these postulates remain unfulfilled are reviewed, and future studies that may provide more insight are described. We also discuss other mechanisms that have been postulated to explain ISSHL. Our review indicates that vascular occlusion, labyrinthine membrane breaks and immune-mediated mechanisms are unlikely to be common causes of ISSHL. Finally, we review our recently proposed theory that abnormal cellular stress responses within the cochlea may be responsible for ISSHL.

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Section: Analysis Of Evidence For and Against The Viral Hypothesismentioning

confidence: 99%

Sudden Deafness: Is It Viral?

Merchant

Durand

Adams

2008

ORL

165

120

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“…Coxsackieviruses, members of the Enterovirus genus within the Picornavirus family, are common human pathogens (23). Group B coxsackieviruses (CB) are important causes of viral meningitis and myocarditis and have been implicated as a possible trigger for the onset of childhood diabetes.…”

mentioning

confidence: 99%

Single Amino Acid Changes in the Virus Capsid Permit Coxsackievirus B3 To Bind Decay-Accelerating Factor

Pan

Narayanan

Shah

et al. 2011

J Virol

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Many coxsackievirus B isolates bind to human decay-accelerating factor (DAF) as well as to the coxsackievirus and adenovirus receptor (CAR). The first-described DAF-binding isolate, coxsackievirus B3 (CB3)-RD, was obtained during passage of the prototype strain CB3-Nancy on RD cells, which express DAF but very little CAR. CB3-RD binds to human DAF, whereas CB3-Nancy does not. To determine the molecular basis for the specific interaction of CB3-RD with DAF, we produced cDNA clones encoding both CB3-RD and CB3-Nancy and mutated each of the sites at which the RD and Nancy sequences diverged. We found that a single amino acid change, the replacement of a glutamate within VP3 (VP3-234E) with a glutamine residue (Q), conferred upon CB3-Nancy the capacity to bind DAF and to infect RD cells. Readaptation of molecularly cloned CB3-Nancy to RD cells selected for a new virus with the same VP3-234Q residue. In experiments with CB3-H3, another virus isolate that does not bind measurably to DAF, adaptation to RD cells resulted in a DAF-binding isolate with a single amino acid change within VP2 (VP2-138 N to D). Both VP3-234Q and VP2-138D were required for binding of CB3-RD to DAF. In the structure of the CB3-RD-DAF complex determined by cryo-electron microscopy, both VP3-234Q and VP2-138D are located at the contact site between the virus and DAF.

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“…Currently, there is no approved agent available for treatment of enterovirus disease. Pleconaril, which was molecularly engineered to block enterovirus binding to host cells, and was studied in the setting of upper respiratory disease, aseptic meningitis and neonatal sepsis, is not yet commercially available [138]. …”

Section: Enterovirusesmentioning

confidence: 99%

Viral Product Trafficking to Mitochondria, Mechanisms and Roles in Pathogenesis

Williamson¹,

DeBiasi²,

Colberg-Poley³

2012

IDDT

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A wide variety of viruses cause significant morbidity and mortality in humans. However, targeted antiviral therapies have been developed for only a subset of these viruses, with the majority of currently licensed antiviral drugs targeting viral entry, replication or exit steps during the viral life cycle. Due to increasing emergence of antiviral drug resistant viruses, the isolation of multiple viral subtypes, and toxicities of existing therapies, there remains an urgent need for the timely development of novel antiviral agents, including those targeting host factors essential for viral replication. This review summarizes viral mitochondrial products and their effects on common mitochondria regulated pathways. These viral products and the mitochondrial pathways affected by them provide potential novel targets for the rational design of antiviral drugs. Viral products alter oxidative balance, mitochondrial permeability transition pore, mitochondrial membrane potential, electron transport and energy production. Moreover, viruses may cause the Warburg Effect, in which metabolism is reprogrammed to aerobic glycolysis as the main source of energy. Finally, viral products affect proapoptotic and antiapoptotic signaling, as well as mitochondrial innate immune signaling. Because of their importance for the generation of metabolic intermediates and energy as well as cell survival, mitochondrial pathways are targeted by multiple independent viral products. Structural modifications of existing drugs targeted to mitochondrial pathways may lead to the development of novel antiviral drugs with improved efficacy and reduced toxicity.

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Coxsackieviruses, Echoviruses, Newer Enteroviruses, and Parechoviruses

Cited by 9 publications

References 308 publications

Sudden Deafness: Is It Viral?

Sudden Deafness: Is It Viral?

Single Amino Acid Changes in the Virus Capsid Permit Coxsackievirus B3 To Bind Decay-Accelerating Factor

Viral Product Trafficking to Mitochondria, Mechanisms and Roles in Pathogenesis

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