microcephaly/protease

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Suggested mechanisms for Zika virus causing microcephaly: what do the genomes tell us?

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Zika virus (ZIKV) is an emerging human pathogen. Since its arrival in the Western hemisphere, from Africa via Asia, it has become a serious threat to pregnant women, causing microcephaly and other neuropathies in developing fetuses. The mechanisms behind these teratogenic effects are unknown,

Increased activity of unlinked Zika virus NS2B/NS3 protease compared to linked Zika virus protease.

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Zika virus (ZIKV) is a flavivirus spread by daytime-active Aedes spp. mosquitoes such as A. aegypti and A. albopictus. Previously thought to be a mild infection, the latest ZIKV outbreak in the Americas is causally associated with more severe symptoms as well as severe birth defects, such as

Identification of novel small molecule inhibitors against NS2B/NS3 serine protease from Zika virus.

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Zika flavivirus infection during pregnancy appears to produce higher risk of microcephaly, and also causes multiple neurological problems such as Guillain-Barré syndrome. The Zika virus is now widespread in Central and South America, and is anticipated to become an increasing risk in the southern

Zika Virus Targeting by Screening Inhibitors against NS2B/NS3 Protease.

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Zika flavivirus is suspected to cause Guillain-Barre syndrome in adults and microcephaly, along with other congenital abnormalities in infants. Presently, no vaccines or therapeutics are available. Here, we report novel compounds identified by high-throughput virtual screening of Maybridge chemical

Zika Virus NS3 Protease Pharmacophore Anchor Model and Drug Discovery

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Zika virus (ZIKV) of the flaviviridae family, is the cause of emerging infections characterized by fever, Guillain-Barré syndrome (GBS) in adults and microcephaly in newborns. There exists an urgent unmet clinical need for anti-ZIKV drugs for the treatment of infected individuals. In the current

Binding recognition of substrates in NS2B/NS3 serine protease of Zika virus revealed by molecular dynamics simulations.

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Zika virus (ZIKV) has become a global public health concern. The recent epidemiological data has revealed a possible association of ZIKV infection with more serious complications, particularly for Guillain-Barré syndrome in adults and microcephaly in newborn children. Till now, there is no vaccine

A mutation in the serine protease TMPRSS4 in a novel pediatric neurodegenerative disorder.

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BACKGROUND To elucidate the genetic basis of a novel neurodegenerative disorder in an Old Order Amish pedigree by combining homozygosity mapping with exome sequencing. RESULTS We identified four individuals with an autosomal recessive condition affecting the central nervous system (CNS).

Neurodevelopmental/neuroradiologic recovery of a child infected with HIV after treatment with combination antiretroviral therapy using the HIV-specific protease inhibitor ritonavir.

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BACKGROUND Neurodevelopmental impairment has been identified in children infected with human immunodeficiency virus (HIV). The frequency and spectrum of neurologic impairment are greater in children than those reported for adults. In children, HIV is known to enter the central nervous system early

Investigating into the molecular interactions of flavonoids targeting NS2B-NS3 protease from ZIKA virus through in-silico approaches.

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Zika virus (ZIKV), belongs to the flavivirus genus and Flaviviridae family that associated with serious diseased conditions like microcephaly and other neurological disorders (Guillan-Barré syndrome). As there is no vaccine or therapies available against ZIKV to date. Hence, it is an unmet need to

Recessive AFG3L2 Mutation Causes Progressive Microcephaly, Early Onset Seizures, Spasticity, and Basal Ganglia Involvement.

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BACKGROUND Mutations in AFG3L2, a gene encoding a subunit of the mitochondrion m-AAA protease, cause spinocerebellar ataxia type 28 and recessive spastic ataxia type 5. Neuroimaging shows cerebellar atrophy. METHODS Retrospective review of the patient charts including their clinical evaluation and

Extended substrate specificity and first potent irreversible inhibitor/activity-based probe design for Zika virus NS2B-NS3 protease.

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Zika virus is spread by Aedes mosquitoes and is linked to acute neurological disorders, especially to microcephaly in newborn children and Guillan-Barré Syndrome. The NS2B-NS3 protease of this virus is responsible for polyprotein processing and therefore considered an attractive drug target. In this

Quantum Mechanics/Molecular Mechanics (QM/MM) Calculations Support a Concerted Reaction Mechanism for the Zika Virus NS2B/NS3 Serine Protease with Its Substrate.

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Zika virus (ZIKV) is mainly transmitted to humans by Aedes species mosquitoes and is associated with serious pathological disorders including microcephaly in newborns and Guillain-Barré syndrome in adults. Currently, there is no vaccine or anti-ZIKV drug available for preventing or controlling ZIKV

The reaction mechanism of Zika virus NS2B/NS3 serine protease inhibition by dipeptidyl aldehyde: a QM/MM study.

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Zika virus (ZIKV) infection has become a global public health problem, associated with microcephaly in newborns and Guillain-Barré syndrome in adults. Currently, there are no commercially available anti-ZIKV drugs. The viral protease NS2B/NS3, which is involved in viral replication and maturation,

Substrate profiling of Zika virus NS2B-NS3 protease.

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Zika virus (ZIKV), isolated from macaques in Uganda in 1947, was not considered to be a dangerous human pathogen. However, this view has recently changed as ZIKV infections are now associated with serious pathological disorders including microcephaly and Guillain-Barré syndrome. Similar to other

Identification of potential Zika virus NS2B-NS3 protease inhibitors via docking, molecular dynamics and consensus scoring-based virtual screening.

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The Zika virus has recently become a subject of acute interest after the discovery of the link between viral infection and microcephaly in infants. Though a number of treatments are under active investigation, there are currently no approved treatments for the disease. To address this critical need,

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