myelitis/protease

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Validating Enterovirus D68-2Apro as an Antiviral Drug Target and the Discovery of Telaprevir as a Potent D68-2Apro Inhibitor.

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Enterovirus D68 (EV-D68) is a viral pathogen that leads to severe respiratory illness and has been linked with the development of acute flaccid myelitis (AFM) in children. No vaccines or antivirals are currently available for EV-D68 infection, and treatment options for hospitalized patients are

[Secondary prophylaxis for herpes zoster wi oral acyclovir in HIV patients].

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We studied 39 AIDS patients from 1989 to 1996, with previous history of herpes zoster. Twelve of them received acyclovir (ACV) secondary prophylaxis. There were 31 males and 8 females, mean age 33.9 years (19-60) during first herpes zoster. Transmission was sexual in 71.8%. Among these 39 patients,

Molecular epidemiological study of enterovirus D68 in hospitalised children in Hong Kong in 2014-2015 and their complete coding sequences.

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Human enterovirus D68 (EV-D68) was first isolated in 1962 and has aroused public concern recently because of a nationwide outbreak among children in 2014-2015 in the USA. The symptoms include fever, runny nose, sneezing, cough and muscle pains. It might be associated with severe

Pharmacological characterization of the mechanism of action of R523062, a promising antiviral for enterovirus D68

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Enterovirus D68 (EV-D68) is a re-emerging virus that causes moderate to severe respiratory diseases in children. In severe cases, EV-D68 infection can lead to neurological complications called acute flaccid myelitis (AFM). There is currently no antiviral or vaccine available for EV-D68. The goal of

A virus-like particle vaccine confers protection against enterovirus D68 lethal challenge in mice.

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Enterovirus D68 (EV-D68) is increasingly associated with severe acute respiratory infection and acute flaccid myelitis (AFM) in children around the world. However, neither vaccines nor therapeutic drugs are available for EV-D68. Here we report the development of a virus-like particle (VLP) based

Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit.

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Enterovirus D68 (EV-D68) is a medically important respiratory plus-strand RNA virus of children that has been linked to acute flaccid myelitis. We have determined that EV-D68 induces autophagic signaling and membrane formation. Autophagy, a homeostatic degradative process that breaks down protein

Enterovirus pathogenesis requires the host methyltransferase SETD3.

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Enteroviruses (EVs) comprise a large genus of positive-sense, single-stranded RNA viruses whose members cause a number of important and widespread human diseases, including poliomyelitis, myocarditis, acute flaccid myelitis and the common cold. How EVs co-opt cellular functions to promote

Cleavage of cystatin C in the cerebrospinal fluid of patients with multiple sclerosis.

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OBJECTIVE The diagnosis of multiple sclerosis (MS) can be challenging because of the lack of a specific diagnostic test. Recent advances in proteomics, however, offer new opportunities for biomarker discovery and the study of disease pathogenesis. METHODS We analyzed cerebrospinal fluid (CSF)

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