The beauty of the presentation is --- prof. updates the illustration every year. I watched his lecture in 2017. I came back this year and found a lot of changes in term of illustration. He added new animations which are nice and lively.
I wonder if any students dropped this class last spring. I think it would be wild, to sign up for Virology / BIO 4310 for the spring semester 2020, and then to watch this pandemic explode while you're learning about the viral world. I would have been on the edge of my seat every day in lecture.
Very very good. Very thought provoking. This is the fifth watched in 2 days. Going onto the rest over the next few days. Thank you for your work and letting us know what's going on. Thank you for introducing other researchers, and their work, and giving them praise for what they did. It was a team effort to get the (unadulterated and clean) knowledge you presented here to us. I'm not viewing your course as part of a formal study option. There is (currently) no need to take in much of the terminology. The insight from your lectures so far is huge and spans many facets of life. Thank you for connecting several dots.
This is incredible journey into the world of viruses. at times I got lost but all together I think I got it. I will have to review my organic chemistry and microbiology. Thank you
Very interesting and informative video. This information presented in this lecture represents almost unimaginable lab hours of research to determine these various mechanisms. Regarding the information presented at the conclusion of the lecture. My recollection is that much of the Neanderthal genome project was coordinated and completed (or nearly completed) at the Max Planck Institute. I hadn't realized that a sufficient genome had also been determined for Denisovans. Sounds very interesting and worth looking at the results, such as that presented at the conclusion of the lecture. Perhaps 529Y contributed to the extinction of Neanderthals and Denisovans.
That diagram is just incredible. As a non-biologist, I've always been confused how cells managed to move themselves about being just blobby sacks. Makes so much more sense now.
The entry into the cell by macropinocytosis was a new concept to me and the fact that Ebola enters the cell in such a way makes one think how such a lethal virus enters the cell in the most non-sofisticated way. There must be a lot of people with 529T in Australia, Sweden and Scotland in the UK, where they have 21.5 % , 20.2 % and 18.2 % highest prevalence of clinical asthma respectively. BMC Public Health. 2012; 12: 204. Great lecture again..Looking forward to my next one. Thanks
The numbers are not higher. On all death certificates they were told to put down Corona virus even if they died of something else. Happened to someone I know. This is fact! Other than that , this was a great video.
My interest in edible moulds, live cultures and friendly bacteria led me here.... only to realise that things that 'aren't alive nor dead' are much more dangerous! Fascinating stuff thank you.
I have a question about virus entry. How the virus ( SARS cov2) Cross the through the innate immunity specialty the mucus cell junction and other and still highly infectious? The virus (sars cov2) enter the cell through receptor ( ACE2 and TMPRSS2) which one of the leading to ER pathway ?
Vincent R is one of my favorites. But -- the initial CORVID-19 remarks in this lecture: over by July because SARS was over by July? SARS ended only because of rapid, stringent public health response. Looking forward to further comments as the semester preceeds. Who, on Feb 6, 2020, knew what, and when? -- there certainly were other forecasts at that time & preceding.
At 26:10, Prof. Racaniello said antibodies have to cross link the viral spike proteins in order to neutralize it. Why? If I have a mAb that can bind to the binding region of SU, won't that prevent the virus attaching to receptor of a host cell thus prevent infection?
So for Sars cov 2 to enter and replicate in a cell, it needs to be in a lung cell, with the ACE2 receptor. So you need to breathe in virus particle into your lung correct? I'm wondering the mechanism for if you were to touch your nose, eye, or mouth with a virus that has receptors in the lung tissue. How does the virus travel to the lungs at that point, or does it, must it need be breathed into the lungs via aerosolized particle?
There are many more tissues throughout the body that have ACE2 receptors, particularly the mucosa of oral cavity. Many organs also have ACE2 receptors which is why some people experience organ failure (I'm over simplifying here...). There's a lot of information on Google using "distribution of ace2 receptors in body."
@@markh7765 when you get rhino virus or influenza common symptoms would be runny nose right? Because you're trying to shed the mucosa thats infected with virus. And yet runny nose is only observed in about 5 percent of people? So it it reasonable to say aerosol transmission is probably the main route of infection rather than droplet if no one is getting runny noses or mouth issues?
do not kno after this , but there is about 5 or 6 years of class lectures ,20 of them or so per year .. then .... the 760 TWIV s broadcasts , then , all you need aT MICROBETV. glad you got turned on !!!
There is a logical paradox involved in Vincent Racaniello's view that viruses, which are obligate parasites, as correctly defined by Vincent Racaniello,, are more ancient in the evolutionary ladder than ribosome containing living cells. According to Modern Evolutionary Theory, which I am sure Vincent Racaniello does not question, prokaryotes were the only form of life on Earth for millions of years until more complicated eukaryotic cells came into being through the process of evolution. Considering the prevailing view in the scientific community of the Darwinian evolutionary sequence stated above, viruses initially were parasitical exclusively of bacteria (i.e. prokaryotes). Vincent Racaniello's belief that viruses, always obligate parasites, "PRECEDED" bacteria, which have the complex machinery that the obligate parasite must access to reproduce, is a logical fallacy. It is putting the virus parasite "cart" before the bacterial host "horse". The more likely evolutionary scenario, one that most, if not all, virologists have unfortunately rejected, is that viruses devolved from prokaryotes that were subjected to several essentially simultaneous mutations that were both faulty and advantagious: 👉 The faulty mutation produced the obligate parasite, lacking the ribosome and other cell machinery that is sine qua non for perpetuation of the species through replication. 👉 The evolutionary advantage of the bacterial mutation to a virus (which had to have happened simultaneously with the loss of cell machinery for replication, or else there would be no viruses today), was an amazing toolbox of specific proteins beneficially mutated to facilitate attacking and hijacking a baterium in order to reproduce. There is no other logical way to view this. Any other way to view this is unscientific straw grasping. Viruses are an example of devolution, not evolution. No OBLIGATE parasite, be it a virus or any example of the highly complex species of parasites from the subphylum Chelicerata, has ever existed PRIOR to the existence of the host that said parasite requires, do not pass go, do not avoid extinction, for the survival of that species. There is no random "evolutionary pressure" that can be pseudo-scientifically speculated about, even with lots of hand waving and charts, that would constitute "evidence" of the PRIOR existance of a parasite to some, not yet evolved, life form. Furthermore, Vincent Racaniello's claim that viroids, that have a limited ability to self assemble, are the RNA spark that got the (added to his speculation that all those transposones in our genome are "evolutionary evidence" that we were "something else" before) evolution of life ball (i.e capsid) rolling is more unscientific straw grasping. WHY? While it is true that the T1 icosahedral capsid could certainly have come about randomly from this self assembling property of protein fragments, that does not even remotely begin to scientifically explain, steps by thousands of SIMULTANEOUSY REQUIRED random steps (SEE: Factorial math mind boggling numbers,) the amazingly specific viral machinery existing for the purpose of protecting some RNA (be it +RNA or whatever) inside that capsid and, within a limited amount of time from the moment the virus was formed and ejected into the intercellular environment, seek to gain entry into a specifically targeted host through a specifically targeted receptor site, at which point even more specifc, finely tuned tools to hijack the host machinery are used for replication. The point is that a capsid made of self assembling proteins is not the relevant evolutionary issue. The relevant evolutionary issue is that a virus, being an obligate parasite, that lacks even one of the tools I just listed above (in an overly simplistic fashion), goes extinct, period. NOTE: I recognize that Vincent Racaniello is, without a doubt, an expert in viruses, and explains their structure and function elegantly, clearly and beautifully. If he stayed away from the logically flawed speculation about the "evolutionary importance of viruses", he would be better off. Finally, there is the issue of proper protein folding, an indispensable part of successful protein synthesis. Read more: renewablerevolution.createaforum.com/general-discussion/darwin/msg16535/#msg16535
Dear Professor, thank you very much for your wonderful lectures: Greetings from Ireland. I have a question ( some what naive I suspect ) Would people taking ACE inhibitors have less chance of infection from the virus Covid 19 since the binding site is Angiotensin 2 converting enzyme is situated on lung tissue. Best wishes and stay safe.
thanks for the information. we know that ACE2 is also the receptor for SARS-CoV, it's kinda the first suspect for the new coronavirus, I'm curious that how do people identify the receptor if there is a virus first time seen?
what is the purpose for cells to have receptors? Unless there is a good purpose, would it not be worth researching how to disable ALL receptors? That way NO virus would ever be able to enter any cell. Can someone please enlighten me.
The receptors let a cell interact with things outside the cell. Get rid of the receptors and the cell can't take in nutrients, get rid of waste, signal other cells in the body, grow in the right place, divide at the right time, and on and on.
The beauty of the presentation is --- prof. updates the illustration every year. I watched his lecture in 2017. I came back this year and found a lot of changes in term of illustration. He added new animations which are nice and lively.
The MOST valuable videos on UA-cam today! Amazing stuff.
Fantastic!
Yeah agreed.
The virus has given me more time to stay home and watch lectures on the virus, silver lining.
I wonder if any students dropped this class last spring. I think it would be wild, to sign up for Virology / BIO 4310 for the spring semester 2020, and then to watch this pandemic explode while you're learning about the viral world. I would have been on the edge of my seat every day in lecture.
Very very good. Very thought provoking. This is the fifth watched in 2 days. Going onto the rest over the next few days. Thank you for
your work and letting us know what's going on. Thank you for introducing other researchers, and their work, and giving them praise for what they did. It was a team effort to get the (unadulterated and clean) knowledge you presented here to us. I'm not viewing your course as part of a formal study option. There is (currently) no need to take in much of the terminology. The insight from your lectures so far is huge and spans many facets of life. Thank you for connecting several dots.
same
@@julianw9857 I watched 2019 #18. You could skip ahead to that one without losing continuity. Its very very good.
These are quite intense but fascinating presentations. The mechanics of specific proteins are amazing
The universe of the smallest particles is amazing and I thank you for presenting your lectures in a most interesting format.
This is incredible journey into the world of viruses. at times I got lost but all together I think I got it. I will have to review my organic chemistry and microbiology. Thank you
May Allah bless you sir you put your valuable information free for us we appreciate your efforts I am from Iraq
Very interesting and informative video. This information presented in this lecture represents almost unimaginable lab hours of research to determine these various mechanisms. Regarding the information presented at the conclusion of the lecture. My recollection is that much of the Neanderthal genome project was coordinated and completed (or nearly completed) at the Max Planck Institute. I hadn't realized that a sufficient genome had also been determined for Denisovans. Sounds very interesting and worth looking at the results, such as that presented at the conclusion of the lecture. Perhaps 529Y contributed to the extinction of Neanderthals and Denisovans.
That diagram is just incredible. As a non-biologist, I've always been confused how cells managed to move themselves about being just blobby sacks. Makes so much more sense now.
The entry into the cell by macropinocytosis was a new concept to me and the fact that Ebola enters the cell in such a way makes one think how such a lethal virus enters the cell in the most non-sofisticated way. There must be a lot of people with 529T in Australia, Sweden and Scotland in the UK, where they have 21.5 % , 20.2 % and 18.2 % highest prevalence of clinical asthma respectively. BMC Public Health. 2012; 12: 204.
Great lecture again..Looking forward to my next one. Thanks
in depth education modules. the lectures came perfectly well at the time of the pandemic Covid-19
"By summer it will be over"
Meanwhile Ben Franklin is over in the corner, full of sass.
The numbers are not higher. On all death certificates they were told to put down Corona virus even if they died of something else. Happened to someone I know. This is fact! Other than that , this was a great video.
Thank you so much for making and sharing this!
My interest in edible moulds, live cultures and friendly bacteria led me here.... only to realise that things that 'aren't alive nor dead' are much more dangerous!
Fascinating stuff thank you.
I have a question about virus entry. How the virus ( SARS cov2) Cross the through the innate immunity specialty the mucus cell junction and other and still highly infectious?
The virus (sars cov2) enter the cell through receptor ( ACE2 and TMPRSS2) which one of the leading to ER pathway ?
Video series is amazing, so generous to share with us all. Thank you. I wish you’d have been right about COVID 19
Thank you for uploading these ❤️❤️❤️
Dear professor it is very useful and informative lecture. Could you explain receptors of SARS CoV-2.
Vincent R is one of my favorites. But -- the initial CORVID-19 remarks in this lecture: over by July because SARS was over by July? SARS ended only because of rapid, stringent public health response. Looking forward to further comments as the semester preceeds. Who, on Feb 6, 2020, knew what, and when? -- there certainly were other forecasts at that time & preceding.
Thank you for these videos!!
At 26:10, Prof. Racaniello said antibodies have to cross link the viral spike proteins in order to neutralize it. Why? If I have a mAb that can bind to the binding region of SU, won't that prevent the virus attaching to receptor of a host cell thus prevent infection?
10:51 - Didn't Shi Zhengli produce a mice model with human ACE2 to allow infection with the virus?
Yes.should be arrested
I've often questioned Blood pressure meds ACE 2 inhibitors, etc ( the usual prescribed coctail ) .
"my guess is, by the summer it will be over"... in fairness Vinny never said which summer.
“By summer it will be over”. In the USA Covid19 is out of control unfortunately.
Pulled a Rich Condit
This is beyond fantastic.
So for Sars cov 2 to enter and replicate in a cell, it needs to be in a lung cell, with the ACE2 receptor. So you need to breathe in virus particle into your lung correct? I'm wondering the mechanism for if you were to touch your nose, eye, or mouth with a virus that has receptors in the lung tissue. How does the virus travel to the lungs at that point, or does it, must it need be breathed into the lungs via aerosolized particle?
There are many more tissues throughout the body that have ACE2 receptors, particularly the mucosa of oral cavity. Many organs also have ACE2 receptors which is why some people experience organ failure (I'm over simplifying here...). There's a lot of information on Google using "distribution of ace2 receptors in body."
@@markh7765 when you get rhino virus or influenza common symptoms would be runny nose right? Because you're trying to shed the mucosa thats infected with virus. And yet runny nose is only observed in about 5 percent of people? So it it reasonable to say aerosol transmission is probably the main route of infection rather than droplet if no one is getting runny noses or mouth issues?
Excellent lecture!
Excellent and informative series. Can you tell us about the attachment and entry pathway for the novel coronavirus?
One particle???? ... & very keen minds to painstakingly dissect volumes of these materials!
this is fantastic. how many of these videos are available? I see random next numbers
do not kno after this , but there is about 5 or 6 years of class lectures ,20 of them or so per year ..
then .... the 760 TWIV s broadcasts , then , all you need aT MICROBETV.
glad you got turned on !!!
Weird question what's the pH level at the beginning of the process what's the deceleration great
There is a logical paradox involved in
Vincent Racaniello's view that viruses, which are obligate parasites, as correctly defined by Vincent Racaniello,, are more ancient in the evolutionary ladder than ribosome containing living cells. According to Modern Evolutionary Theory, which I am sure Vincent Racaniello does not question, prokaryotes were the only form of life on Earth for millions of years until more complicated eukaryotic cells came into being through the process of evolution.
Considering the prevailing view in the scientific community of the Darwinian evolutionary sequence stated above, viruses initially were parasitical exclusively of bacteria (i.e. prokaryotes). Vincent Racaniello's belief that viruses, always obligate parasites, "PRECEDED" bacteria, which have the complex machinery that the obligate parasite must access to reproduce, is a logical fallacy. It is putting the virus parasite "cart" before the bacterial host "horse".
The more likely evolutionary scenario, one that most, if not all, virologists have unfortunately rejected, is that viruses devolved from prokaryotes that were subjected to several essentially simultaneous mutations that were both faulty and advantagious:
👉 The faulty mutation produced the obligate parasite, lacking the ribosome and other cell machinery that is sine qua non for perpetuation of the species through replication.
👉 The evolutionary advantage of the bacterial mutation to a virus (which had to have happened simultaneously with the loss of cell machinery for replication, or else there would be no viruses today), was an amazing toolbox of specific proteins beneficially mutated to facilitate attacking and hijacking a baterium in order to reproduce. There is no other logical way to view this. Any other way to view this is unscientific straw grasping.
Viruses are an example of devolution, not evolution. No OBLIGATE parasite, be it a virus or any example of the highly complex species of parasites from the subphylum Chelicerata, has ever existed PRIOR to the existence of the host that said parasite requires, do not pass go, do not avoid extinction, for the survival of that species. There is no random "evolutionary pressure" that can be pseudo-scientifically speculated about, even with lots of hand waving and charts, that would constitute "evidence" of the PRIOR existance of a parasite to some, not yet evolved, life form.
Furthermore, Vincent Racaniello's claim that viroids, that have a limited ability to self assemble, are the RNA spark that got the (added to his speculation that all those transposones in our genome are "evolutionary evidence" that we were "something else" before) evolution of life ball (i.e capsid) rolling is more unscientific straw grasping. WHY? While it is true that the T1 icosahedral capsid could certainly have come about randomly from this self assembling property of protein fragments, that does not even remotely begin to scientifically explain, steps by thousands of SIMULTANEOUSY REQUIRED random steps (SEE: Factorial math mind boggling numbers,) the amazingly specific viral machinery existing for the purpose of protecting some RNA (be it +RNA or whatever) inside that capsid and, within a limited amount of time from the moment the virus was formed and ejected into the intercellular environment, seek to gain entry into a specifically targeted host through a specifically targeted receptor site, at which point even more specifc, finely tuned tools to hijack the host machinery are used for replication.
The point is that a capsid made of self assembling proteins is not the relevant evolutionary issue. The relevant evolutionary issue is that a virus, being an obligate parasite, that lacks even one of the tools I just listed above (in an overly simplistic fashion), goes extinct, period.
NOTE: I recognize that Vincent Racaniello is, without a doubt, an expert in viruses, and explains their structure and function elegantly, clearly and beautifully. If he stayed away from the logically flawed speculation about the "evolutionary importance of viruses", he would be better off.
Finally, there is the issue of proper protein folding, an indispensable part of successful protein synthesis.
Read more:
renewablerevolution.createaforum.com/general-discussion/darwin/msg16535/#msg16535
mechanical entry 4.56 ? how about chemical damage opening a route for the virus?
Dear Professor, thank you very much for your wonderful lectures: Greetings from Ireland.
I have a question ( some what naive I suspect )
Would people taking ACE inhibitors have less chance of infection from the virus Covid 19 since the binding site is Angiotensin 2 converting enzyme is situated on lung tissue. Best wishes and stay safe.
This has been explored. But as it drops blood pressure, and the infected people become hypotensive very easily, it is counterproductive.
Why are there not many viruses that replicate in myocytes? There are a few that can but they are rare.
Thankyou for fabulous contact
thanks for the information. we know that ACE2 is also the receptor for SARS-CoV, it's kinda the first suspect for the new coronavirus, I'm curious that how do people identify the receptor if there is a virus first time seen?
"My guess is by the summer it will be over" .... Right
Wouldn't it be the same for all retroviruses
I really want to skip to lecture 20 soo badly the vaccine and infections stuff seem so cool and interesting!
Amazing!
I wish we had essay questions
Virions in reverse transcription size of molecule importance go over
By summer, it's still escalating at a rate u didn't expect Prof. +_+ ~
08:32 bats
Yes. As often mentioned bats are reservoirs for many coronaviruses.
Who else thinks professor’s voice resembles the voice of Cypher from the Matrix?
Your guess that it would be over in summer.. How wrong was that.. But of course thats what most thought at the time anyway..
👍
It was spreading all through America about this time
what is the purpose for cells to have receptors? Unless there is a good purpose, would it not be worth researching how to disable ALL receptors? That way NO virus would ever be able to enter any cell. Can someone please enlighten me.
The receptors let a cell interact with things outside the cell. Get rid of the receptors and the cell can't take in nutrients, get rid of waste, signal other cells in the body, grow in the right place, divide at the right time, and on and on.
@@acr08807 thanks
It is that a spider man of the world.
those predictions did not age well
I'm taking lopinavir/ritonavir for Prep for coronavirus.