The Coronavirus Replication Cycle
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- Опубліковано 8 лип 2024
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thanks for explaining so clearly n making sense for details as well. this is really helpful! thanks a million
I am taking Virology, Bio 420, as a second-degree undergraduate at my college, the City College of New York, in New York, NY., and this was very, VERY helpful. Thank you SO much for this amazing video that explains the workings of the Coronavirus easily and in a simple way. Best wishes!
Thanks a lot. I was struggling so hard to understand this mechanism as I didn't understand it at all during lecture at school. Your explanations are very clear and easy to understand. Sincerely thanks.
So I was learning for my exam and I didn't quite get the discontinuous transcription part, but this video really helped so thanks!
Love this! Thank you for sharing your knowledge
Nice video - the receptor of the COVID-19 SARS-CoV-2 (which binds to the S1-CTD of spike) is ACE2. I think the video has likely been adapted from the replication of the related betacoronavirus MHV (mouse hepatitis coronavirus) which binds to CEACAM1 (via the S1-NTD of spike)
Thank you Emma I was sure the receptor was ace2 too. However I must compliment you on your movie work, I saw you in sense and sensibility this week and you were most agreeable.
@@deanmoncaster That's ace!
Material taken from *"Coronavirus infection of the central nervous system: host-virus stand-off"* (mouse central nervous system), *Nature 2006*
www.nature.com/articles/nrmicro1343 (this explains the mixup between CEACAM1 and ACE2)
question: so does the virus binding to ACE 2 decrease the production of ACE 2? and what stimulates the production of the amount of ACE2
Emma Thomson be smart
Lucid and easy to survey. Wonderful voice of the narrator.
Binding to the ACE2 receptor has been linked to NRP1 and TMPRSS2 as possible cofactors and even independent of ACE2 viral binding. Although the ACE2 receptor is commonly seen as the necessary component for viral infection, research is being published to suggest NRP-1 as a possible binding site for the cleaved portion of the Spike protein.
Very clear explanation and illustration... Thank you very much!!!
Thank you so much. Excellent explaination best video i've ever watched
Thank you so much for this brillant and cleary explanation. Awesome 👌
Thank you to posting such a knowledge able video.
This is the best explanation. Thank you!
thank you!this video used a really clear way to explain this.
Hello, what role does arginine have to do in the viral replication?
Thank you do much, it helped me a lot
Excellent demonstration !!
I want to ask about discotinious transcription at RNA (-) which create difirent Subgenomic mRNAs to translate viral structural proteins. How does transcription process regulate at difirent Body TRSs? Transscription ignores some parts (to create different mRNA+) of RNA(-) and pass to leader TRS. How? Thanks.
Very useful video , thank u very much 🌹
I've found this video useful.... I have Virology exams to write next week. Thank you
A very clear video, explaining simply and clearly the whole process. I was very wise from him
can I get the reference notes or book from this video ??? pleasee
I am currently working on my final year pharmacy project. This video helped me a lot in understanding the concepts of viral replication!!
I m also working on ORF1AB
@@hamzaali-ni8qg good luck akhi
Are the structural proteins translated directly into the Rough ER membrane? Do the viral envelopes form by a sort of reverse-budding into the ER lumen or are they created in some other way?
thanks - really helpul for me!
Great video! Very informative
Thank you for this explanation thank you
Thank you! Very helpful!
finally, some more in-depth explanation on the topic. Thank you. I thought the receptor was ACE2, though. I think CEACAM1 (also called CD66a) is an immunoglobulin which is also used for cell invasion by some coronal Hepatitis Viruses.
@@Thomaaasooo In what way?
it is ACE2 - not sure what happened in this video
Great video! Well explained. Thanks.
awesome video. was hoping you could follow it up with a video on how recombination of viral particles actually works - ie: how we actually got into this mess with COVID-19 in the first place. I'm also interested in the limits of recombination, whether or not recombination works only using RNA sequences whole hog, or if it is possible for recombination to mix and match sections of viral RNA at the nucleotide level.
*where did you get these **2:04** and **4:10** pictures? I checked the link on description but i didn't find it. Could you give me the articles link here? Thanks a loot btw 🙏✨*
Very clear explanation. Thank you so much 💓
Great video!
I was struggling to understand what on earth subgenomic mRNA was and how it was generated, this video has made it really clear.
Thank you! Finally understood sir!
thank u
but why we have a frame shift
please🙏🙏🙏 can you reply because i have this part in my project
Thank You so much for this
My question then is there a way to alter what has been omitted so that the original rna messaging may continue? Even if the part thats omitted is forced to cycle back to attain rhe original memory? If possible would this not double the omitted forgotten strands.... or?
Thank you very informative.
this was amazing
Great video, but do you know how long it takes in actual time between the receptor binding with the protein in the beginning to the end of the process there a new virus is released? And also how many copies get created from one virion? Thanks so much!
Would Interferon alpha 2B (recombinant) be useful ?
Amazing technique ,impress me so much 🧐
Thanks for this.
thanks for the clear explanation!!!!
Clear, concise and educational video for a non biologist to understand the replications of the virus. Hope can watch more videos such as virus mutation (delta), vaccination working mechanisms.
Great video sir , very crystal clear explanation 👍
Excelent Describing, The best video that I watched
And me 💯
Very good video! but in regards to the discontinuous transcription, at 7:56 you say that the different length segments result from the polymerase initiating transcription at different sites, later you explain that it always starts at the end (3´ I assume) and then it ¨decouples¨ at different points (reattaching near the other end) thus giving the different length of each segment. I suppose this is the correct explanation, did I misunderstood what you meant at 7:56? Again, aside from that (unless I am mistaken) it is a really good video. thanks
I have a question about the translation of the RNA-string. Does the process end with both 1ab and 1a polyproteins? Or is it only if the frameshift occurs , that the polyprotein 1ab is made?
Hello, I am taking up microbio, just tackled virology recently (but got kinda canceled due to this pandemic) and I am kinda confused. Can the proteins be derived from the original genome? Accdg to the Baltimore system, I thought (+) ssRNA viruses can readily translate their original genetic material to derive proteins? Why is it here, the viral proteins were needed to be derived from the antisense RNA after going through the discontinuous transcription?
Or can the proteins be derived both ways?
Thanks for the information. A question. How long does it take for this virus duplicate to complete?
A well made video, but it does have quite a few errors. First of all, as other people have noticed too, the receptor for SARS-CoV-2 is angiotensin converting enzyme 2 (ACE2). There's also evidence that SARS-CoV-2 can use neuropilin-1 (NRP1) as an entry receptor too.
The other error is in transcription of subgenomic RNA (sgRNA). In your illustration you state that -ssRNA is used as a template, and therefore transcription would happen in 5'-3' direction. Translation happes in 5'-3' direction, but transcription happens only in 3'-5' direction.
This is why Nidovirales (including CoV) use +ssRNA as a template to produce -sgRNA which is then used as a template for +sgRNA, and that is used as mRNA for translation of structrural proteins and accessory proteins. You got the principle right, but I guess you mixed a few things on the way. :)
Very useful video 🙋♀️
Right from infection or direct contact, how long does attachment and entry take? Days? Hours?
👍👍👍 fantastic. Thanks
On the last slide you show, it looks as if the virion is taking part of the host ER with it as it exits the cell. Is this correct? I seem to remember reading about this when I was an undergrad.
Wondering presentation, clear and catching points.
Very rich explanation. Subscribed.
what is the time duration of this replication cycle?
And is or does furan clipping different in other coronas?
How can a frameshift to a different reading frame occur? Great video by the way! Very informative.
Frame shift is usually a method in which most viruses including HIV make multiple proteins/ poly proteins from one transcript. There is a signal called the slippery sequence that slows down the ribosome during translation, followed by a pseudonot that pushes the Ribosome back one nucleotide, resulting in reading frame shift. Codons are read in 3s (bases) to give an amino acid, changing frame can result in different amino acid chain.
@@TheMagodana So, this would be the basis for mutations?
Thank you ... ✳️✳️❣️
Thanks!
Me encanto la explicacion :D , Thank YOU
Awsome explanation
Question is, what hereditary (genome of mixed race/not ideally compatible blood types.) and external factors (environmental/electrical/RF.) can affect the preliminaries in how they operate? Should we absolutely avoid certain amino acids, proteins, blood ph?
good molecular detail
Here in the pathogenesis discused about diffrent proteins that inhibiting normal inflamtory proteins lik IFN alpha n gamma which necessory to destroy virus....then what causes cytokine storm????
is there any specific viral proteins or lik bacterial superantigen that can bind with antigen-antibody complex in the T cell receptor site, cause excesive and non specific activation T cell and over production cytokine and lead to cytokine storm?
hi, very good video, thanks! could you provide a list of references to dive in, please?
Very clear explanation of the replication process in simple terms!
Would it not be possible to treat the virus by having a protein that binds to a specific TRS at the very least would it not be able to weaken the virus as each protein would seemingly have a role to play?
Great Video! But how does the RNA dependent RNA Polymerase know if to stop on the different TRSs (TRS2; TRS7 etc.)? Is there a specific RNA dependent RNA Polymerase for every TRS?
I'm note sure if it is known, but it is most likely a combination of secondary and tertiary structures that the RNA forms with associated proteins that facilitates the "jump".
@@CatalystUniversity thank you very much for your answer!
Catalyst University follow up question - what makes these structures functional sometimes but sometimes not? Where does the process become non-deterministic?
Loved your video by the way, thanks for making it!!
Is that pp1a, pp1b complex act as RdRp, as they both are engaged in replication @!!??
Ok I thought the SARS CoV 2 (COVID-19) initially binds to ACE2 receptors?
Scott Clark it does :(
Yes
Yeah that's true
How is this different than whats explained in this video? I'm being sincere and wish to learn. Rna is the Dna messenger, correct?
Yeah! In human it's initially binds to ACE2 receptors and gains the entry but in mice it is by CEACAM1 according to me for experimental purpose they introduced this virus
How does the RNA ‘know’ which sub genomes to translate?
How does it organize the proteins into a new virion?
The RNA doesnt know, it's all driven by signals in proteins and RNA, through a series of RNA-protein, Protein-protein RNA-Rna interactions they assymble. This vedio is bit over simplified but the whole thing is much complex.
The RNA has the equivalent of full stops and comma's. Thats like that leader TRS bit. Certain base pairs repeat or create "on/off" switches.
The proteins are organized into new virons by eletrostatic and vaan der waals forces (weak force) interactions. In the case of Coronavirus - its actually quite weakly put together - hence huge sensitivity to detergents and 70% alcohol. (basically soap turns the virus into an emulsion completely destroying it)
In contrast - something like spores of anthrax are actually tough as hell and last 40+ years in savage & harsh environments (strong covalent bonds make the structure and shell - not the case for such a virus as Coronavirus.)
There is only ONE answer: matter ability to self-assemble. Self-organization.
Thank you for this excellent and detailed video. I wonder where the angiotensin converting enzyme 2 (ACE2) enter into the picture, as it looks to be involved in Covid-19 replication pathway somewhere.
Thanks
@@Thomaaasooo Video is not wrong - this paper explain mice infection / all of the mecanisms are some but ceacam is goning to be ACE2 at humans.
i think the CEACAM-1 is the receptor for nervous cell and ACE2 for lung cell
For entery spike protein attach ACE2 on type 2 pneumocyte and need cleavage proteas TMPRSS2.
😘
Great explanation, does this mean that this viruse does not enter the host cell nucleus???
I mean all the replication process takes place in the cytoplasm?
This replication cycle is occure in human or mice? Because in human it bind to ACE3 but here it bind to cemcam-1
Thank you
Hi, thanks for the video. In another video, it says that (-) strand subgenomic RNAs are transcribed from the (+) genomic RNA. These (-) strand subgenomic RNAs are then transcribed by RdRp into (+) strand subgenomic RNAs. Does this process happen as well?
Also, can you please give more detail on how the no.6, no.5, etc subgenomic RNAs get created if the RdRp just skips to the leader TRS after reaching the no.7 TRS?
I honestly think he made a mistake there as well. The subgenomic RNAs are (-), complementary to the original genomic strand. They then get capped and poly-A-tailed, therefore recognized as mRNA by the ribosomes.
Congratulations!
Its genome does not include U a base for RNA ..is it RNA viruse?
It was worth watching the complete video
Amazing video thanks I love biology
Various size of (-) subgenomic RNAs are generated first, and then they are used as templates for various sizes of (+) subgenomic RNAs. The fugure at 11:00 time point is confusing. However, Much thanks for this Video.
Superb
I was wondering how long process Replication Cycle will take???
Can you provide the link for the publication please?
www.nature.com/articles/nrmicro.2016.81
How does lysine effect this virus?
Does it attach only to this receptor(CEACAM-1) or other receptors?
ACE-2.
S2’ CD147 as well. Similar to malaria’s RBM
good information
What controls Discontinuous Transcription from making ALL of the different types of proteins?
There's got to be something that helps the transcription machinery decide which body TRS to stop at and which ones to run through.
If i were a lazy viral RdRp, I would only make protein 7 and then forget about making any of the other ones.
What roles does adenosine triphosphate play in the replication of SARS-CoV-2?
mic drop explanation... good job
I didn't find anything about SARS2 binding to CEACAM1. I thought that SARS-CoV, SARS-CoV2 (Covid-19), and HCoV-NL63 all bound to ACE2. BTW, I was reading about the angiotensin pathway and a little about coronavirus, and if you are taking high blood pressure meds, you might ask about aliskiren (which directly inhibits renin on its active site). ACE2, the cellular entry receptor for SARS2 (Covid) is downregulated from something I read in Nature (high impact journal). Angiotensin I and Angiotensin II are produced by and downstream of renin, respectively. While ACE coverts Agiotensin I to Angiotensin II, while ACE2, the target of Covid that gets internalized and degraded by cell entry of the virus, converts Angiotensin II to Ang1-7 (a vasodilator), owing to some of the pathophysiology of Covid (ACE and ACE2 have countering effects). However, since Aliskerin abrogates the synthesis of both Angiotensin I and Angiotensin II and downregulates ACE2 (presumably because of an otherwise positive feedback by the renin products), it may even have beneficial effects in slowing infection while still acting to lower blood pressure because there are fewer ACE2s on the cell membrane. Ask your doctor at least about your present BP medication at least.
See:
www.nature.com/articles/s41569-020-0368-x
Can someone tell me whats the point of the RNA+ being replicated in RNA(-). Cant the RNA+ process to other steps without being replicated to RNA - ?
@spatolatore viral proteins that produced is it from +ssRNA or -ssRNA
What is the genotype and phenotype of coronavirus???????
Excellent video, would know how long it might take from being exposed to being contagious. I work as a medic and if I was exposed at work how much time do I have before I am contagious and give it to my family???
probably 24-48 hours at least. err on the 24h side, if you're not sure. also, it could take a week or two until you feel symptoms.
@@meslud awesome, thank you.
Amazing video.
Thanks!