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== General Information==
The theme of SensUs 2021 is acute respiratory viruses. The current Covid-19 pandemic has made it apparent that large virus outbreaks can cause immense harm to human health and can disrupt society as a whole. The most common respiratory virus is influenza A. Therefore, the influenza virus serves as an interesting biomarker for this year’s Competition.
These two proteins are a target of interest for antiviral drugs. Furthermore, they are also the antigen proteins to which a host antibodies can bind and trigger an immune response. Influenza type A viruses are categorized into different subtypes, or strains, based on which type of these two proteins is present on the surface of the virion. Currently, there are 16 subtypes of HA and 9 subtypes of NA known to exist. The most prevalent form of the different subtypes is H1N1. Single hemagglutinin-neuraminidase proteins, in which both HA and NA are found in a single protein, also exist. However, these will not be used in SensUs 2021.
===Valproate Mode Mechanism of Action===The exact mode involvement of action the hemagglutinin and neuraminidase proteins in the infection of valproate on molecular level H1N1 is unknown, as there are many different substances that participate simultaneously in essential for the regulation of neuronal activity. <ref name=”[15]”> Sodium valproate (Epilim, Epivalvirus reproduction, Episenta). (2018, June 5) , at [https://www.netdoctor.co.uk/medicines/brain-nervous-system/a6665/epilim-sodium-valproate/ “https://www.netdoctor.co.uk/medicines/brain-nervous-system/a6665/epilim-sodium-valproate/”].</ref> VPA is connected to cortical inhibition in order to contribute to ‘neural synchrony’ and a more specific mechanism is known to provide protection from neural degradation and damage. <ref name=”[16]”> Williams, R. S. B., Cheng, L., Mudge, A. W., & Harwood, A. Jdiscussed below. The hemagglutinin protein (2002HA). A common mechanism has the role of action searching for three mood-stabilizing drugs , at [https://www.nature.com/articles/417292a “https://www.nature.com/articles/417292a”].</ref>VPA inhibits histone deacetylase, which causes hyperacetylation of histones. The drug is furthermore connected to inositol depletion by preventing the gene prolyl oligopeptidase to be expressed through indirect inhibition of myo-inositoalsialic acid receptors in respiratory-1-phophate-synthetase. <ref name=”[16]”> Williams, R. S. B., Cheng, L., Mudge, A. W., & Harwood, A. Jlining cell membranes. (2002figure _). A common mechanism Upon binding of action for three mood-stabilizing drugs , at [https://www.nature.com/articles/417292a “https://www.nature.com/articles/417292a”].</ref> In terms of epilepsythis protein and the receptor, it is believed that VPA is affecting the activity fusion of GABA. By increasing the activity of GABA, virus and the epileptic attacks are prevented. This cell membrane is established through inhibition facilitated with the help of succinic semialdehyde dehydrogenase which glycan proteins. The virus then increases enters the amount of succinic semialdehyde cell where it sheds its shell and subsequently increases GABA neurotransmission. <ref name=”[37]”> Flyyn, S., & Babi, M. A. (2017). Pathophysiology of Epilepsy , at [https://www.sciencedirect.com/topics/medicine-and-dentistry/pathophysiology-of-epilepsy “https://www.sciencedirect.com/topics/medicine-and-dentistry/pathophysiology-of-epilepsy”]approaches the cell’s nucleus.</ref> VPA affects Using the extracellular signal-regulated kinase pathway or ERK (Extracellular Receptor Kinase)host replication mechanisms, which results in phosphorylation of ERK 1/2 . This has an effect on the expression virus makes copies of proteins that contribute to the plasticity of neurons and neuronal growthitself. The downside of At this effect step of VPA is the additional increase in GABA activityinfection process, important viral proteins are synthesized. VPA has an influence on fatty acids production, leading These newly replicated viral elements subsequently attempt to lower leave through the cell membrane fluidity due to the presence of less sterols and glycerolipidsinfect other cells. Subsequently, this increases To inhibit the action potential threshold exit of the viral components, sialic acid receptors on the cell membrane and contributes attempt to bind the antiepileptic effects of valproate HA glycoproteins. <ref name=”[17]”> , . Drugbank, Valproic Acid Retrieved from November 25, 2019, at [https:This is where viral evolution//www.drugbank.ca/drugs/DB00313“https://www.drugbank.ca/drugs/DB00313”].</ref>===Pharmacokinetics of VPA===When introduced orally, VPA is found to be absorbed in a period of 4 hours. However, introducing it in other ways results in the same Cmax, AUC and Cmin in mutability can play a steady state, while all the differences role in absorption are neglected. When VPA is taken as extended release tablet and combined with meals, the absorption time increases from 4 to 8 hours. On the other hand, expansion of the increase in absorption time in the same situation increases from 3.3 to 4.8 hours when taken as a sprinkle tablet. There is 90% bioavailability capabilities of VPA in all oral forms. On the other hand, there is 100% bioavailability in enteric-coated formsvirus. <ref name=”[18]”> Gugler, R., & Unruh, G. E. von. The neuraminidase glycoprotein (2012, December 13N). Clinical Pharmacokinetics has the role of Valproic Acid cleaving the sialic acid receptors, at [https://link.springer.com/article/10.2165/00003088-198005010-00002 “https://link.springer.com/article/10.2165/00003088-198005010-00002”].</ref>The average half-life allowing the exit of VPA is 13-19 hours, the volume viral components which then go in search of distribution is 11 L/1a new host.73 m2 . The protein binding After infection is linear at low concentrationscomplete, but non-linear and decreased at high concentrationsthe H1N1 virus triggers cell apoptosis, which may be due leading to the different affinity binding sites of albumin. Parts death of the drug can be metabolized in different ways. The most relevant metabolism of VPA would be glucuronide conjugates cell and mitochodrial-ß oxidation. <ref name=”[17]”> , . Drugbank, Valproic Acid Retrieved from November 25, 2019, at [https://www.drugbank.ca/drugs/DB00313“https://www.drugbank.ca/drugs/DB00313”].</ref> Only 3% spread of the drug is eliminated through urine, about 30-50% is eliminated through hepatic metabolism, and about 40% being excreted through mitochondrial-beta oxidationvirions. <ref name=”[18]”> Gugler, R., & Unruh, G. E. von. (2012, December 13). Clinical Pharmacokinetics of Valproic Acid , at [https://link.springer.com/article/10.2165/00003088-198005010-00002 “https://link.springer.com/article/10.2165/00003088-198005010-00002”].</ref>
===Efficacy and influence on hepatic function===
