@Sterling Mallory Archer The Spanish flu pandemic of 1918, the deadliest in history, infected an estimated 500 million people worldwide-about one-third of the planet's population-and killed an estimated 20 million to 50 million victims, including some 675,000 Americans.
@Sterling Mallory Archer I was laughing with you too.... Did I remember it wrongly? hmmmm.... anyway, It was a quote from history.com. It's worldwide Mate, so we are safe. :)
@Sterling Mallory Archer Hahaha. It's meant to be for "whole world" infected, NOT death toll. Anyway here's from WIKI: The Spanish flu, also known as the 1918 flu pandemic, was an unusually deadly influenza pandemic caused by the H1N1 influenza A virus. Lasting from February 1918 to April 1920, it infected 500 million people-about a third of the world's population at the time-in four successive waves. The death toll is typically estimated to have been somewhere between 17 million and 50 million, making it one of the deadliest pandemics in human history.
Great and clear explanation. What I don't understand is how neuraminidase is regulated at the surface of the virus. If it is constitutively present on mature viral particles then why it does not prevent the entry of the virus into cells as it would cleave the sialic acid to which HA attaches to?
How come when it comes to viruses, ironically we develop drugs that work after a cell has been infected. I am thinking specifically about how with HIV we have nucelocide inhibitors and even protesase inhibitors that work AFTER the fact. I am puzzled why we don't attack at the front line like creating fusion inhibitors or in the case of influenza why don't we attack the Hemagutanin protein?
I would guess hemagglutin can be found in our own cells and has other functions so a drug to inhibit the binding of hemagglutin to saliyic acid would harm our own cells?
As Carolyn said..."It's a very nice story." Amen.
Thank you for making a clearly explained video. I am infected.
Thanks for your emotional energy!!!
Neurominidases are responsible for Elution I have studied from book ...but u really clear the concept ..
Once again thank you so much very clear video
Do you know why Haemagglutination occurs in Influenza?
Thanks for clear explanation. It helped a lot understanding what viruses do to sialic acids
Great explanation
Thyanks
Spanish Flu I thought 500 million, but anyway, thank you for the splendid explanation of H and N mystery for lay man understanding. :)
@Sterling Mallory Archer The Spanish flu pandemic of 1918, the deadliest in history, infected an estimated 500 million people worldwide-about one-third of the planet's population-and killed an estimated 20 million to 50 million victims, including some 675,000 Americans.
@Sterling Mallory Archer I was laughing with you too.... Did I remember it wrongly? hmmmm.... anyway, It was a quote from history.com. It's worldwide Mate, so we are safe. :)
@Sterling Mallory Archer Hahaha. It's meant to be for "whole world" infected, NOT death toll.
Anyway here's from WIKI: The Spanish flu, also known as the 1918 flu pandemic, was an unusually deadly influenza pandemic caused by the H1N1 influenza A virus. Lasting from February 1918 to April 1920, it infected 500 million people-about a third of the world's population at the time-in four successive waves. The death toll is typically estimated to have been somewhere between 17 million and 50 million, making it one of the deadliest pandemics in human history.
thank you so much for this pub !
Great and clear explanation. What I don't understand is how neuraminidase is regulated at the surface of the virus. If it is constitutively present on mature viral particles then why it does not prevent the entry of the virus into cells as it would cleave the sialic acid to which HA attaches to?
How come when it comes to viruses, ironically we develop drugs that work after a cell has been infected. I am thinking specifically about how with HIV we have nucelocide inhibitors and even protesase inhibitors that work AFTER the fact. I am puzzled why we don't attack at the front line like creating fusion inhibitors or in the case of influenza why don't we attack the Hemagutanin protein?
I would guess hemagglutin can be found in our own cells and has other functions so a drug to inhibit the binding of hemagglutin to saliyic acid would harm our own cells?
Because HIV doesnt exist and the drugs cause the disease symptoms.
Follow the money.
Great Video
great video thank you
thanks alot 4 this informative video (Y)
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