Talk:Neuraminidase
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Details on NA subtypes
[edit]Is there any more information on the different NA subtypes? (where they're found, what distinguishes one from another, how much variation there is for different strains within a subtype, etc.) -- 20:39, 27 August 2007 (UTC)
This article should probably be split up according to species. Currently the introduction/abstract refers only to mammalian NEU1, but other details refer to viral NEU. I would suggest this article discuss only the commonalities of neuraminidase catalysis and structure, followed by external references to the pages for viral NEU, NEU1, NEU2, NEU3, and NEU4. Since each of these enzymes has distinct functions (some clearly elucidated - and some not).--Glycoform (talk) 15:38, 3 January 2009 (UTC)
- Done. --Arcadian (talk) 18:16, 3 January 2009 (UTC)
Incorrect information
[edit]The article says: "Neuraminidase also plays a role in the helping influenza pathogenesis by cleaving sialic acid from the host glycoprotein and allowing the virus to enter the host (T-phages, macrophages, etc.)"
But my Open University sk185 "molecules, medicines, drugs: a chemical story" disagrees. It says: "The specific role...seems to be to help newly formed viruses to escape from the host cell and spread to other cells in the body. They are then able to move on and infect other cells. As part of this process, sialidase [also known as Neuraminidase] cleaves off sialic acid groups...from the membranes of the host cells".
Which is correct? Does nueraminidase/sialidase help influenza enter or leave the cell? 82.15.59.176 (talk) 17:06, 28 October 2008 (UTC)
The latter description is correct; or at least is the explanation generally used. This would be clearer with the addition of a scheme and references to reviews.--Glycoform (talk) 15:38, 3 January 2009 (UTC)
Pfam Box
[edit]As nueraminidase isn't a family of proteins, rather a grouping of protein with similar function, would any one mind if I remove the pfam box which can already found on the more relevant Viral neuraminidase page? I'm thinking the image should be left though as it's quite a nice illustration and not been used on many other pages =D Abergabe (talk) 12:21, 2 September 2010 (UTC)
Expression systems
[edit]I added this new article from PLoS One where suitable expression systems are described. It seems important to obtain enough pure neuraminidase for research purposes these days to find new anti-influenza drugs, diagnostics and vaccines. I added this paragraph under "structure" but if that seems inappropriate please add it to another section or delete it altogether.Osterluzei (talk) 06:06, 8 February 2011 (UTC)
Assessment comment
[edit]The comment(s) below were originally left at Talk:Neuraminidase/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.
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I have some issue with the statement below:
"Neuraminidase inhibitors are useful for combating influenza infection: zanamivir, administered by inhalation; oseltamivir, administered orally; and under research is peramivir administered parenterally, that is through intravenous or intramuscular injection." Neuramindase inhibitors are not particularly useful in combating influenza infection as that term implies that they are efficacious in diminishing an infection that is already in situ. This is not really the case as by the time a viral load has been reached that is detectable (symptomatically) a large number of cells are already infected and diminishing the number of influenza "escapes" does little to lessen the symptoms (they have something to the effect of .6 of day reduced illness). They have the most clinical utility in preventing outbreaks of the flu in at risk populations, by preventing the initial infection from spreading. I think some clarity could well be given to this statement. Pedantic, I know. Canuck79 (talk) 11:09, 20 September 2009 (UTC) |
Last edited at 11:09, 20 September 2009 (UTC). Substituted at 01:04, 30 April 2016 (UTC)
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