Spike Protein Goes to Nucleus and Impairs DNA Repair (In-Vitro Study)

Spike Protein Goes to Nucleus and Impairs DNA Repair (In-Vitro Study)

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00:01
all this is dr morgan sayeth welcome to one more show the study today is an in vitro study but still it almost looked like a halloween study for me because the important part of the study of the study in this study is that the researchers from sweden found the spike protein to be going into the nucleus and not only going there but but also impairing reducing stalling the dna repair this
00:32
can have drastic side effects balance this out during this whole discussion because when i was reading and going through this it made me very nervous so i'm sure that it would make you nervous as well but please balance that out with this that we have a lot of infections and we have a lot of vaccines which have spikes as well and we are not seeing this scale of damage so what is the actual truth we do not know yet it is not an in vivo study it is an in vitro study still concerning study so
01:05
let's look at this so i am still working on this new studio so my apologies for the sound system yet not being hundred percent and the background and those things so my please forgive me all right so here is the study itself the study is sascof2 spike impairs dna damage repair and inhibits vdj recombination in vitro so i'm gonna talk about both of those mechanism and more today the study is done in sweden uh
01:47
stockholm university jan is my best friend who is from sweden he pronounced it in the most beautiful way i cannot pronounce it that way and the umi university i hope i'm pronouncing it correctly as well uh i have been going back and forth in this studies since the morning trying to make sure that the mechanisms that they're observing make sense and um and the the data that they have makes and so to to an accident which i could see you can see that i have been just going through this the whole day
02:18
and my apologies today sean is not able to join us sean had to actually end up in the he had to go to emergency department for some health issues he's been going through the health issues for some time now and we he will be with us tomorrow praying for his complete recovery he's back home but he's not well enough and i requested him to take rest and he would join us tomorrow so my apologies for that okay so back here the here is the study here's what they found this study is an in vitro study
02:50
so it is not in vivo it's not observed in animals yet humans yet what they found was that spike protein causes reduces the repair of the dna now where do we get the dna repairs number one right now i'm sitting in the studio there is light shining on me so my cells where the light is shining it is possible that the end is breaking when you go to a beach and you sit under the sun dna is breaking when the cells are repairing and when the cells are fighting an infection for example subscribe to new cells are being formed
03:22
the cells gene expressions are opening up and they're functioning dna could be breaking during during that time as well new cells are formed dna could be breaking and repairing and then the most important thing this is the one thing i would request you to hold on to for the whole studies discussion that is the b cells when they are making antibodies when new baby b cells are being made in the bone marrow or the t cells are made in the thymus they their
03:52
binding region the region with which they bind with the antigen those regions are variable they are different for each b cell we'll discuss that that variability is produced by intentionally damaging the dna and then repairing it so every time you damage the dna repair it it would form a different shape and that would give rise to a different variation of the binding region now imagine if you try to repair damage and repair and create variations
04:22
to fight in the immune system and we could not repair correctly because there is task of two present which is stalling and impairing the repair imagine the immune system's deficiency the authors think that maybe that is the reason that some people cannot actually handle sasko2 very well and then we end up dying okay so what is their suggestion what is this the end result of the study they focused on the vaccines and they said that it is important to
04:53
think about maybe not create full spy protein vaccine instead in this research they found out that if you have partial pieces of the spike protein then this whole thing does not happen so they said maybe look at spike protein based vaccines but maybe smaller pieces i would extrapolate that to maybe not even have the whole spike routine just the rpd or maybe other parts of the virus but there the researchers suggestion is in light of
05:24
the study maybe full spike protein based vaccines are not the best so that is their suggestion that is their suggestion um what kind of issues can be observed we just went through some of those people who may be recovering from cancers maybe recovery from cancer means what there are cancer cells which are now being told not to to survive or they are learning to repair or they're becoming better or we are killing the cancer cells and the remaining cells are becoming better and
05:57
so there is cell division happening and there is damage happening and if that damage cannot be repaired correctly we have a problem similarly newer cells formation for example in the younger ones new cells are forming all the time and that means there could be the dna repair issues which are which are taken here we all have dna repair happening all the time even now right now all of us are getting some dna repairs at various parts so i want to put this in front of us how do we prevent this
06:27
we prevent it according to the researchers by not creating vaccines which are full spike protein that also means don't get infected because infection is also full spike protein and maybe use smaller subunits of the spike protein for example rbd or other parts of the virus now what are their findings i'm going to go through this now we are actually going into the studies details if you just wanted to understand that what this study says we're done now let's see what are the findings we're going to go in the details so for
06:58
the findings couple of things that we need to be on the same page with and that is we know that when a virus arrives the source of two we are talking that is the context when i say a virus that is susceptible we know that when suspect ii arrives in our cell its messenger rna starts becoming developed into proteins by the ribosome our ribosome our cell's ribosome correct then that ribosome makes
07:28
pieces of the sarcophagus including spike protein and then the non-structural proteins which are called nsps and then structural proteins like matrix protein and other so a bunch of things are made that are all for the virus then when all of those proteins are made they are sent into endoplasmic reticulum where they are kind of put together this is like making a car so you make the doors in one place and the tires in another place an engine in some other place and then you put them together in one place and then you give it to the golgi operators which would
08:00
package them up and that would then put a membrane on top of this structure and that would become an enveloped virus and then that virus would get out of the cell this is the normal behavior of the cell replication now this spy protein when it is produced either because of the infection or because of the vaccine when it is produced this is the first time they are showing it that the spike protein ends up inside the nucleus not only spike protein ends up inside the nucleus nsp non-structural proteins
08:33
ends up in the nucleus as well and not only they just end up there not only it's just contaminant that has entered this nucleus they actually go in there and interfere with the machinery of the dna with the repair system of the dna so that is the thing to keep in mind so back here there is spike protein that localizes in the nucleus goes to nucleus there are non-structural proteins these are the enzymes of the virus nsp non-structural protein there are various enzymes of the virus that help
09:08
virus replicate and make new viruses and so on so virus has some machinery this is that machinery these also the nsp 1 5 9 13 14 and 16 also end up in the nucleus my apologies this is luffy standing and scratching the door outside maybe i should just open up the door for him so give me one quick second my apologies so the door is open everyone is now a fair game to come in
09:54
so co-location occurs correct now what are the mechanisms to observe and the cat is here now so it is going to make its appearance in front of the camera anytime soon so here is something to keep in mind first concept to keep in mind is double stranded break double stranded break we know that our dna is kind of woven like two strands together correct so when both of those trends are broken down that is called a double strand break sometimes it is just
10:25
the one unit one strand breaks down not both so let's say this is one strand and let's say this is the other strand sometimes it is just one strand that breaks down and the repair would need to be repairing one strand and sometimes both strands break down that is called a double-stranded break so double-stranded break can occur it happens all the time especially in the immune system cells when they're making their binding regions double-standard breaks are intentionally created
10:58
secondly this is the cell cycles diagram itself cycle a cell that is dividing it goes through various phases of division so important thing to note just to keep in mind here g1 phase of the cell cycle if there are dna breaks that occur during this time and please remember this when our cells are dividing there are strict mechanisms to make sure that the dna is correctly repaired and correctly
11:29
copied and there is no damage otherwise the cell will become a cancer cell we have an elaborate mechanism to repair dnas and so through this cell cycle we stop the cell in various cycles this is like if you're making a building you stop the building at various milestones and you say we'll send inspectors in who are going to look at the building built so far and they're going to tell you give you a feedback and if there is anything that is not correct correct it before you
12:00
continue so at every cell cycle phase the cell is stopped then repair inspectors inspectors come in they inspect the cells dna then the repair workers come in and they repair it enzymes here and then they give a green light that okay you can go to the next like phase of the cycle and this is how the cell cycle occurs so if there is a break that occurs during g1 phase we can talk separately what are the cell cycle phases then nh non-homolog logos
12:30
and joining repair mechanism is used nh eg ej if the cell is in synthesis s or g2 phase growth two phase then hr or homologous repair mechanism is used so just keep in mind that there are multiple mechanisms for dna repair because there are multiple kinds of repair damages and so these two mechanisms are important to keep in mind because these two mechanisms are impaired by the spike proteins presence
13:01
okay continuing now one more mechanism to keep in mind so i'm just putting the contacts together so that then i can show you how the damage occurs the second mechanism is proliferation those of you who have been with me throughout this 20 months now you know that the when the infection occurs any infection occurs what happens is the cells b cells and t cells they proliferate proliferation means increasing in number increasing in number definitely means making copies of the dna which
13:33
definitely means there could be damage to the dm dna which definitely means there is going to be need for repair plus the proliferation in itself is an important immune system response this is why some people's lymph nodes would start swelling and paining or aching or tender why because there are cells that are increasing in number inside of them this increase in number is called proliferation so please keep this in mind as well this is one cell it gives rise to multiple daughter cells then those daughter cells
14:05
give rise to more daughter cells and so on and the proliferation occurs so please keep these so here this is a b cell and it has proliferated in the presence of infection let's say subscribe to and given rights to multiple b cells then here is a t cell in the presence of an infection or a stressor or a pathogen it has increased in number as well so proliferation has occurred all right continuing there's a lot to be discussed i'm still talking normal and we'll talk about it normally in a second now variable region this is the
14:37
important part look our b cells imagine if we have 1000 b cells standing in line and we ask them to show their hands all of their hands every b cell's hand will have a different pattern to grab their their hands are not like our hands that can be adapted they are given one fixed structure so some b cell would hand would be looking like this another b cell's hand would look like this somebody's hand look would look like this somebody's
15:07
hand would look like that so all of their variable regions are different so here in this diagram what am i showing look at this part this is an antibody an antibody we have been talking about it from ever has a heavy chain these are proteins so heavy cane is a big heavy protein this is another heavy chain and it has a light chain this is a structure this is another light chain
15:39
at the end of the heavy chain and light chain there is a variable region so imagine one antibody imagine me as an antibody every one antibody has two arms and that have two hands and they both have identical binding sites so these are the binding site this part which binds with the antigen which binds with the offender which captures a prisoner a
16:10
what is that criminal that part is called variable region formation of this variable region needs dna to be broken down and repaired and whenever it is repaired in weird ways there are weird variable regions that are formed on this side here this is a t cell receptor now just like b cell need to bind to an antigen to function with it b cell also needs to bind with the antigens to function with them so this is a t cell receptor that also has a similar binding
16:41
site and then it has a constant heart as well the structure is slightly different it has alpha chain and beta gene not here like heavy chain and the light chain and then further parts of them it has a alpha gene and a beta chain alpha chain insert in turn has a variable region and a constant region beta chain also has a variable region and a constant region the t cells variable region is made in the similar way by changing and modifying the dna
17:14
so what is the repeated pattern i'm explaining here dna repair break and repair can also be done in immune system cells intentionally for normal function of the immune system cell right now in all of us there are b cells being formed in our bone marrow and there are t cells probably getting trained in thymus or some other place in adults we don't exactly know but let's say thymus this is cat not me so these b and t cells when they're forming and then there is a binding region of theirs
17:44
which all of them have right now there are dnas that are being broken and then repaired and it's a normal thing so example of the variation so imagine these are various very variation or variable parts of various d or b cell receptors so this part here this variable region or binding region can bind to an antigen of this shape this part can bind to an antigen of this shape this part can bind to an antigen of this shape
18:15
and here if this is a bacteria bacteria has some electrons on its surface and look at this t cell receptor i have removed the t cell just the receptors so the t cell receptor over here has bound to this antigen now through this antigen structure of course the other guys will not bind i hope this becomes clear that every b and t cell has needs a different
18:47
variable binding site and to create that variation we need dna to randomly restructure which needs dna break and repair then here is the actual dna break and repair which can happen for other reasons too as i said in the beginning radiation causes it chemicals cause that heat or cold can cause that physical injury can cause this so there are many many reasons that dna can
19:19
actually break dna new cell production cell cycle cell growth all of those things can cause it new sperm formation new over formation although over always present in the beginning so they're not newly formed sperms are formed every time so there are many such cases where new dnas are made and where dna repair may be now here is an example of a double stranded dna bridge where let's say this was the normal dna and this part got deleted and so now both strands of the
19:52
dna are broken this is called a double-stranded break this kneading is my cat it's kind of actually today it's not luffy if it was luffy luffy will do me out okay so here imagine this is the dna and this dna has a double-stranded break over here if this break occurred as i said earlier during the g1 phase then non-homologous and joining repair type will be used if it is synthesis or g2 or growth two
20:24
phase then homologous repair mechanism is used but for both of those mechanisms there are certain repair enzymes imagine there are repair workers in our body in our nucleus that would rush to the place of dns dna injury in dna break and go and fix it and there are different kinds of repairing enzymes so two important enzymes that this these research workers looked at one is called brca1
20:55
and the other one is 53bp1 and i have references in the description you can go and see the diagrams the point of these enzymes is that wherever there is the damage they would go and attach there they would create a focus there they would mark that place have you seen the road road construction workers they will go to the road and they'll mark various places where the next set of workers would come and work on similarly these enzymes brca or 53 bp1 they create foci
21:26
they create the focuses on the dna is damaged pieces they inspect the dna and say well it is damaged here i'm going to put a flag here then the repair guys would come in the enzymes and they would repair that part now imagine if these two enzymes cannot do their function imagine if they cannot even be produced who's going to repair who's going to mark the area for repair so this is like we have a pothole in a road road is damaged we want someone to come and put a flag
21:56
to say it needs repair here and then the repair people would see where the flag is and repair imagine the repair flagging enzyme cannot go and put the flag there's going to be no repair okay so these are the primary normal mechanism now let's see what researchers found what researchers did was the following and i'm going to go through the same mechanism again and show what was the problem they saw first cell proliferation
22:29
the researchers found look at my sneaky way of putting these things down here researchers found that the non-structural proteins number one 5 13 and 14 when they go in the nucleus i mean this is the first thing why are they going in the nucleus but when they go in the nucleus i mean just accept the fact that here they go to the nucleus when they go to the new nucleus and how did they do this in the research
23:00
they took this is an in vitro study so they took cells they injected in the cell the messenger rna and dna pieces to make these structures they did not infect the cells they just put these specific proteins and spike protein rnas in those cells they transfected them and then they observed the proteins being formed then they tracked those proteins where they are going why did they not just infect them with the sarcophagus because suscoff2 if infecting it is going to
23:31
destroy the cell they want to transfect a cell with more benign proteins and then they want to track the proteins inside the cell to see where are these things going and then they want to see what is the abnormality of the function of the cell so they cannot do that with by infecting the cell because the cyst is just going to destroy the cell so here they put the plasmid plasmids in the cell which had the genes to produce these proteins of the subscribe to when those proteins were created over
24:02
expression of those proteins was observed and this was intentional it's in vitro result was what reduced proliferation of the cells occur so how do we from in vitro to in vivo observe that what this means is if this is all correct and reproducible in vivo as well then what that will mean is that when the source of two is present inside a cell the sars of twos proteins are going to go to the nucleus and when this cell
24:33
let's say it is a b cell or a t cell and it is trying to divide the proliferation would not happen or will reduce now there is a lucky thing and they say it authors such of 2 is not known to infect b cells and t cells so that is the lucky part how did they observe it they actually transfected them or not b and t cells they took cells that they they made the the cells look like bmt cells
25:06
so good news is b and d cells actually do not get infected by sas co2 otherwise we'll have a problem more disastrous than hiv i mean imagine a respiratory virus which is also hiv-like attacker of the immune system cells will be will be done so it is not that however they say that it is known and they have cited the studies they say it is known that when sars goes to infect a cell let's say not a b cellularity cell some other cell
25:38
and it is making its proteins in that cell it's making more viruses in that cell parts parts of the genetic material of sarco of two can leak out of this under stress cell this is called exosome leakage exosomes are part of the dna rna material so some genetic structures some recipes can leak out of the cell
26:12
and these rna pieces can enter the other cells which could be b or t cell if they do enter there and if they go make spike proteins in them then we can have a problem with the bnd cell so it's a far-fetched idea but this is how they said can be possible and you could actually throw out this whole study on the basis of this one mechanism problem that sarso2 luckily does not is
26:42
not known to infect bnt cell so this theory over here this observation that they did in vitro by transfecting the cells is actually not possible in vivo but we also didn't think that this white protein will go in the dna so i'm going to keep myself open to understanding more of this part or this study of course there will be more studies that would try to replicate this and they would report further even maybe the same researchers would do more work okay so back here
27:14
as the nsps non-structural proteins are increased they go to the nucleus they affect the proliferation parts of the of the cells if that happens in the immune system then the immune system function will reduce because we cannot have enough b cells and t cells okay moving on first first observation from the study again in vitro transfected cell studies that cell division can be impacted now please keep in mind if the cell division is impacted for
27:48
bnt cell and that is not possible in vivo there are other cells whose division is needed maybe that is affected growth of the cell sperms many other cells are dividing red blood cells and so on stem cells in the bone marrows are dividing right so back here now the second part the variable region production which is also very important for immune system function now to produce this variable region as i
28:19
have been kind of saying it again and again that is what happens is look at this genetic material imagine this is the recipe to make an antibody or to make a t cell receptor what is important to keep an eye on at this time is that there is a constant part of an antibody or a t cell receptor we forget about that it is a variable part as well that variable part is this part this part
28:50
that variable part is the one that binds to various patterns here is how that variable part is produced by breaking and repairing dna here in the beginning is the dna recipes these are called v region b and g regions these are genes this is genetic material v d and j some pieces of this genetic material are taken from v
29:21
some from d come from j this is equal to if i ask you to cook some food and i give you a book and every page has some recipe on it and i say up to you do not just make one pages recipe instead take two instructions from any one page then take two instructions from another recipes page then take another five or seven instructions totally up to you from a different recipes page just open the
29:52
book wherever you like then combine those all statements that you read and just cook according to that whatever is formed is my luck this is how it happens so we take some statements from one recipe some more statements from another recipe some more from another we don't take a whole recipe just take some statements then what happens how do we take some statements we delete everything else so instead of you reading two lines from a recipe what you do is you you delete
30:24
everything else to leave two lines in there so that means you're tearing the book so here we intentionally are damaging the dna to leave parts of the dna then those parts are collected together and made into a variable regions genetic material but to put them together we need to repair this is an intentional dna damage and repair this is a somatic hypermutation this is the variable
30:55
region formation this is what protects us this is what protects us from from the infections so it isn't good thing we need it but this repair needs to repair men and we just saw that spike protein could cause the repair men not to function correctly that means the variable region generation for b and p cell will not occur very efficiently that means our
31:27
capability to respond to infections will not be good so now immune system cannot have more cells i'll keep reminding the audience that it is in vitro and immune system cells are not known to be infected by this ask of two so making this in vivo will have to be a far fetched idea if this happened then the variable regions will not work correctly and the authors say that why did they
32:00
think of doing this that is because they observed people's immune system not to work correctly and that made them think that maybe there is something in this virus that is impacting their immune system so even when we do not know that this happens maybe it is exosome maybe we'll find out it actually does affect them anyways so this is i hope this point is clear we create variable regions by break and repair and if we cannot create variable regions successfully then immune system cannot function
32:32
successfully second part then it is kyrie which is just running around here third part third abnormality these enzymes please realize what happens is these enzymes are produced in the cytosol in the cells cytoplasm how let's say this is a cell and it needs the dna repair enzymes here is how it works from inside the dna
33:05
the recipe to make these enzymes will be copied in the form of messenger rna that messenger rna will be sent outside of the nucleus because inside the nucleus there is no mechanism to be able to translate messenger rna so even when nucleus needs its own machinery it still has to request the people outside of the nucleus to say can you please make me enzymes so they would say what do you want and he nucleus would write down i need
33:36
following machinery to be made how does it do that it sends messenger rna outside so please remember if the messenger are an event in the nucleus it doesn't do anything even nucleus is all the needs are written on a messenger rna and sent outside because insider doesn't do anything outside this messenger rna goes to a ribosome it would work with the ribosome and the enzymes will be produced those enzymes will then go back in the nucleus and go and function there and what did they find the researchers
34:07
they found that these repair enzymes when they were being produced outside and they wanted to go in the nucleus spike proteins presence in the nucleus reduce the production of messenger rna which would go and get the machinery made to come in wicked clever wicket that the spike and other proteins are actually blocking the nucleus from forming
34:38
the machinery to repair itself and so what they observed was in this study that only with the full length spike not with the pieces of the spike and they did this in the research they took pieces of the rna as well and kind of made pieces of the spike they created plasmids that could only have enough genetic material to make pieces of the spike and not the full length only in the full length spike the cells
35:10
those cells that were transfected with the genetic material to create a full length spy protein they had marked inhibition of production of brca and 53 bp1 and their function that means the repair focus was not present that means dna repair was not occurring this doesn't matter what kind of a cell it is
35:41
any cell that has spike protein in it if it needs repair its dna is repaired then spike protein can reduce the dna repair so now the question this is the end of it now the question is if you said all right dangerous and scary what will happen to the cell normally a cell that cannot repair its dna usually that cell dies it would commit suicide first it would
36:13
try to fix it if it cannot fix its dna usually it commits apoptosis and dies but we know there are cancer cells cancer cells are the cells where the the dna with the dna i still have to figure out where the mouse is where the dna has escaped the repair it has become damaged and it has just started building a weird
36:45
kind of a cell that is not responding to any controls and that becomes cancer so there is a even if we dismiss this research to say well b and t cells will not be infected in vivo so we should be okay there still are two risks one is exosomes can go into the bnt cell and the second one is that the dividing cells or repairing cells any cell in the presence of cysco of two proteins either with the infection or with the vaccine can end up in trouble
37:17
and so that is the discussion um i hope that it makes sense somebody made a comment this is the last thing and then i'll stop and we'll come back with a chit chat somebody made a comment that i only share studies that are a specific type and i feel bad that i have been for 20 months sharing all kinds of studies pro vaccine studies and vaccine side effect studies
37:49
and so i cannot stop people from labeling me but still when somebody wants to say i do not do something they should at least look at my list of lectures which is i think about 1000 now to see have i covered topics and if they cannot then it is just a very lazy thing to just put their comment out there anyways with this let's stop please do me a favor if you can like subscribe and share that would be awesome if you don't want to do anything
38:21
but you enjoyed this or you had use of this then at least like this and if you would like to support this work then there are three links in the description you can buy me a coffee or you can be a patron or you can use paypal and enemy is quite close to me tomorrow i have a big day because we have one of the auditors providing their feedback to us so they are trying to shut down everything i'm trying to stay afloat so anyways all your support is welcome and thank you very much i'm gonna hang up
38:53
now and come back

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