Twiv 815 15

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00:00 this week in virology the podcast about
00:03 viruses the kind that make you sick
00:07 [Music]
00:10 from microbetv
00:12 this is twiv this week in virology
00:15 episode 815
00:18 recorded on october 8th 2021
00:21 i'm vincent dracaniello and you're
00:23 listening to the podcast all about
00:25 viruses
00:27 joining me today from fort lee new
00:29 jersey dixon de pommier
00:32 hello vincent and everybody else um
00:35 you know i always looked out the window
00:37 to tell you what i think the weather is
00:38 like but actually it's it almost feels
00:40 summer-like outside um a little bit high
00:43 humidity for this time of the year
00:45 there's a gray overcast uh patchy clouds
00:49 trees are starting to turn
00:51 um starting to think about thanksgiving
00:54 already
00:55 crazy
00:56 it's very nice to see very nice day
00:57 today yes yeah it is yes also joining us
01:00 from austin texas rich condit
01:03 hi everybody hey richard uh 86 degrees
01:06 is sunny headed for 92.
01:09 they keep promising us
01:11 that this is going to let up but i'm
01:14 so i'm having difficulty managing my
01:16 expectations but it looks like maybe a
01:18 week or so out they're talking about 70s
01:20 but they lie you know they do yeah
01:22 there's a profession that they get paid
01:24 to lie
01:26 monkey
01:27 except you know i don't think it's
01:29 really lying with intent no no they're
01:31 just wrong they're just wrong
01:33 the weather man can never lie they're
01:34 just never right
01:36 also joining us from ann arbor michigan
01:38 kathy spindler hi everybody here it's 71
01:42 degrees light drizzle may clear up
01:45 that's the same as 20 celsius we have
01:48 two guests for you today who are going
01:49 to tell you
01:50 a really cool story about covid so stay
01:54 tuned
01:55 uh from cedars sinai medical center in
01:58 los angeles moshe arditi welcome to twiv
02:03 thank you
02:04 vincent
02:05 um
02:06 uncharacteristically cloudy in la and 66
02:10 degrees here
02:12 and from the university of pittsburgh
02:15 school of medicine medicine yvette bahar
02:18 welcome to twiv
02:20 thank you very much it's a pleasure
02:23 uh so it is here also
02:25 uncharacteristically
02:27 nice
02:29 76 degrees beautiful day
02:32 in pittsburgh
02:34 boy we span the coast in in in between
02:36 as well today yeah we got everything
02:38 today east west north south how about
02:40 that
02:41 no complaints folks we got it all right
02:44 actually i want to i want to i want to
02:45 issue a correction before we get too
02:47 much mail or anybody gets too offended
02:50 the weathermen are
02:51 uh incredibly accurate most of the time
02:54 okay and i appreciate that we just
02:56 notice when they're not right right
02:58 exactly
02:59 because if you know scientists are wrong
03:01 a lot right but most people don't notice
03:04 except us
03:06 um so our guest today let me tell you
03:08 how
03:08 they came to be uh
03:10 moshe and i have been emailing for quite
03:13 a while
03:14 um
03:15 we've been complaining to each other
03:17 about uh how the variants have been
03:19 described in various ways uh and
03:22 so then um
03:24 they he and yvette have have uh
03:27 published this wonderful story that you
03:29 hear about today so i said come on and
03:31 talk about it so that's what we're going
03:33 to do today but i'd love to first hear
03:36 your histories because in the pre-show
03:38 we were
03:39 talking about it and it's
03:41 it's just uh so cool
03:44 tell us you know where you're from and
03:46 uh where you were trained and
03:48 how you
03:50 got to work with each other perhaps
03:51 moshe maybe you could start
03:54 uh okay so um i uh i'm originally from
03:59 istanbul turkey you know and i went to
04:02 a french high school there all boy
04:04 catholic high school uh and then um
04:07 uh um i went to medical school after
04:10 that in istanbul
04:12 finished and left
04:14 in 81
04:16 i worked at yale university for two
04:18 years on
04:20 surfactant you know used in
04:22 premature uh rabbits
04:24 for two years and then went to
04:26 university of chicago to do my
04:28 internship and residency training in
04:30 pediatrics
04:32 then to chicago my favorite
04:35 town where i did my well
04:38 stayed in chicago
04:40 at northwestern to do an infectious
04:42 disease fellowship in pediatrics
04:47 and then
04:49 moved to l.a
04:52 i worked at
04:53 la children's hospital and then i moved
04:55 to cedar sinai which is affiliated with
04:58 ucla
04:59 as as faculty affiliation and i've been
05:02 here 23 years so i've been working on
05:06 lps signaling and toll-like receptor
05:09 signaling
05:10 um role of these innate
05:13 immune molecules in atherosclerosis and
05:16 vasculitis and since a lot of people
05:19 tease me
05:20 that i
05:21 as a pediatrician i work in adult
05:23 inflammatory diseases i've been also
05:26 working on kawasaki disease vasculitis
05:28 for the last 20 years so
05:30 so that's in a nutshell that's how it is
05:33 and and and we can tell you how we met
05:35 with yvette which which you know maybe
05:38 i'll let her tell the story yvette tell
05:40 us your story
05:42 okay so it is uh amazingly similar
05:46 because i was born and raised in
05:48 istanbul too
05:50 and also went to a french catholic
05:52 school for all girls of course
05:55 that was very fashionable then in
05:57 istanbul these were really one of the
05:59 best high schools
06:01 and then uh
06:03 moved uh continued all my studies in
06:06 turkey actually
06:07 i got married i had two sons and i just
06:11 did everything
06:12 undergraduate masters and phd everything
06:14 in istanbul
06:16 and then became a professor there
06:18 right after my phd
06:20 uh for it uh
06:22 the university i graduated from which
06:24 was the most prestigious brazilian
06:26 university then
06:28 and in the chemical engineering
06:30 department so i started as an engineer
06:33 and i was a professor there for 15 years
06:36 until i moved in 2001 to the university
06:39 of pittsburgh
06:40 and so it's very simple 15 years in
06:43 istanbul 20 years here
06:46 and
06:47 in my career i of course started as a
06:49 chemical engineer i never liked the
06:51 engineering stuff i
06:53 uh quickly channeled to material science
06:56 first polymer physics
06:59 and chemistry
07:00 and polymers from polymers i switched to
07:03 biopolymers
07:04 and then gradually computational biology
07:07 because in turkey you know the best
07:09 thing you could do to be more
07:10 competitive worldwide was to do
07:12 simulations we had the best you know
07:16 simulation infrastructure
07:18 uh and then came the year and i i worked
07:22 every summer for nine years at nih just
07:24 doing research in the meantime
07:27 in the utah year
07:29 turn of the millennium
07:31 as you all know that was the real
07:33 breakthrough with the
07:35 human genome but at the same time
07:39 you know
07:40 first published by uh
07:42 francis collins and craig mentor
07:44 and that was the time where
07:46 bioinformatics computational biology
07:48 really
07:49 became very important
07:51 and lots of new opportunities
07:53 so i joined pittsburgh
07:55 to start a new center center for
07:58 computational biology which which soon
08:00 became a department
08:02 department of computational assistance
08:04 biology which i have been sharing
08:07 since then
08:09 and
08:10 i also started the joint program with
08:12 carnegie mellon in computational biology
08:14 you know how carnegie mellon is very
08:16 strong in computer science and
08:18 engineering
08:19 and physics so i found lots of
08:20 colleagues there
08:22 with whom i could collaborate and found
08:24 this very strong computational biology
08:26 phd program
08:28 now what i do is mostly
08:30 modeling and simulations as we're going
08:33 to talk about and i like to use
08:35 structure
08:36 so it is like engineering but at the
08:38 molecular levels trying to understand
08:40 how proteins function their machinery
08:43 and how we can modulate their function
08:46 you know by binding small molecules i do
08:48 lots of drug discovery
08:50 so and then of course with advances in
08:53 data
08:55 you know
08:56 lots of databases in biology we do lots
08:59 of data mining machine learning type of
09:01 computations
09:02 so
09:03 my lab is essentially
09:06 to we are tool developers you know we
09:08 simulate everything on the screen
09:10 and
09:12 we collaborate with uh people like moshe
09:15 who
09:16 give us stimulating questions and we try
09:19 to solve them so that's where uh
09:22 we that's how also this research on
09:24 stars go to spike started
09:28 okay moshe
09:30 so you guys were both you both educated
09:32 in istanbul and what happened in between
09:35 well we you know wait for i'm sorry
09:39 good good so we we didn't even know i
09:42 didn't even know that moshe was here in
09:44 the united states and
09:46 a few years ago all of a sudden he sent
09:48 me emails asking are you eventual zone
09:52 you know using my maiden name because
09:54 that's how
09:55 and i i say yes i am but who are you so
09:58 i couldn't remember
10:00 so that was really uh i don't know how
10:02 many is more than four years for sure
10:04 that we had we have completely lost
10:06 touch but we used to play together in
10:08 the streets i was the
10:11 uh
10:11 actually goalkeeper of the team we used
10:15 to play soccer
10:17 and then many other things
10:19 he was the only girl who was on the team
10:22 great great story it's lovely
10:25 so you you connected
10:27 before kovit i presume right
10:30 a few years before coffee drive okay
10:33 all right so
10:34 i'm not quite sure how to start this
10:36 story today there's so many pieces and
10:38 maybe you have a better way but i
10:40 thought maybe
10:42 we could start
10:43 with misc multi-inflammatory syndrome c
10:48 and telling us you know what it is and
10:50 then
10:52 taking your wonderful story from that
10:55 so so and it's exactly how it started
10:57 you know uh
10:58 uh yeah i mean this collaboration um
11:03 you know i mentioned that
11:05 i
11:06 also have been studying kawasaki disease
11:08 for over 20 years you know i i i go to
11:12 japan frequently i've met dr kawasaki
11:14 almost every year until he died last
11:17 year at age 90.
11:20 and it became a passion to me uh through
11:23 my training
11:24 to treat karus occupations in children
11:27 and also work with a
11:29 there's a wonderful mouse model of
11:31 kawasaki vasculitis uh which you know my
11:34 my lab has been lucky to be funded by
11:37 nih for 20 something years for that so
11:41 so when
11:43 when
11:44 stars cove two came and and and in you
11:48 know march or april 2020 we started to
11:51 hear about these bizarre
11:53 cases in children first in uh france i
11:57 mean england uh and then uh bergamo
12:00 italy and and and other other
12:03 european countries
12:04 about this hyperinflammatory syndrome in
12:07 kids that that that that uh
12:10 follows
12:11 sarskoff too that had some
12:14 findings that are reminiscent of
12:16 kawasaki disease such as conjunctivitis
12:18 rash
12:19 you know and um
12:22 and mucosal oral mucosal changes which
12:25 also are present in toxic shock syndrome
12:28 uh and and they started to label this as
12:31 kawasaki disease-like and it went
12:34 further to even to be called that
12:37 this is it you know sarskoff too is
12:39 causing kawasaki you know and then this
12:41 is kawasaki disease you know
12:43 so it it really bothered me so much uh
12:47 that uh this was wrong because
12:49 you know since then we learned so much
12:51 more that these are two different
12:52 diseases demographics demographic
12:55 differences the older kids are you know
12:57 and then laboratory differences clinical
12:59 differences were so much
13:03 you know
13:04 you know clear that there were two
13:06 different diseases of course they may
13:08 use similar inflammatory pathways
13:11 that many diseases you know trigger um
13:14 so so i became very
13:18 uh
13:19 vocal you know in writing or or or
13:22 trying to tell that this is a different
13:24 disease
13:25 and if anything messy which is
13:28 characterized of kids having
13:31 multi-inflammatory organ system
13:32 involvement with hyperinflation that
13:35 follows the
13:36 infection
13:37 two three four six weeks later it's more
13:40 like a you know it's presenting more
13:42 like a toxic shock syndrome why because
13:45 you know it has the components of of of
13:48 multi-organ systems such as acute
13:51 gastrointestinal
13:52 acute gastrointestinal findings uh
13:55 abdominal pain
13:56 vomiting diarrhea myocardial in in you
14:00 know dysfunction
14:01 neurologic findings up to 38 percent
14:04 kidney uh
14:06 injury in addition to all those other
14:08 things which we don't see with kawasaki
14:10 disease but we do see with toxic shock
14:13 syndrome so and toxic shock syndrome is
14:15 caused by super antigens most people
14:17 think that only bacterias have super
14:20 antigens but then i realize there's a
14:22 remarkable literature on viral
14:25 superantigens and and and and the
14:27 diseases that they've been associated
14:29 with
14:30 so so i got in touch with yvette because
14:33 i knew she was doing computational
14:35 uh uh studies looking for
14:38 fda approve other drugs to to repurpose
14:40 those drugs for it for
14:42 sarskov too and i said to her that
14:47 do you think the virus or the spy
14:49 protein has a motif that may be like a
14:53 super antigen uh
14:55 and and the response was amazing to me
14:58 and that was what is a super antigen so
15:01 so when when yvette mentioned that then
15:03 i will leave it to her now and i sent
15:06 her uh papers about
15:08 staph enterotoxin b icb or tssd you know
15:12 the the typical staph and strep super
15:15 antigens and diseases that and the and
15:19 the
15:20 structure of those of those proteins and
15:23 a week later i get a phone call from her
15:25 and i'm going to leave her tell the rest
15:27 okay so
15:29 so at that time you know we were already
15:32 doing some research in starscope too
15:35 like a spike glycoprotein
15:38 and at that time i was very intrigued by
15:40 the fact that you know there is between
15:43 the s1 and s2 subunits of the
15:46 spike
15:47 there is this cleavage site
15:49 and there is this insertion that's very
15:51 unique to source code ii
15:53 and i was wondering why what is it so
15:56 special about it and i was you know at
15:58 that time i was trying to see what is
16:01 unique about this uh sequence and i read
16:04 a paper by jean-pierre
16:06 on you know the significance of this
16:09 region that it resembles some uh
16:12 neurotoxins and could be targeted et
16:15 cetera things like that so when moshe
16:17 contacted me i said do you think it
16:20 might be similar a super antigenic
16:22 region there might be there and
16:25 and of course i asked what are super
16:27 antigens
16:28 and learned that for example bacterial
16:31 toxins are super antigens to those small
16:33 molecules that elicit this excessive
16:36 response
16:37 cytotoxic adaptive immunity
16:40 and i said okay there are some sequences
16:42 indeed that i've seen in the literature
16:44 short sequences similar to
16:46 bacterial toxins and other toxins
16:49 actually viral toxins as well
16:51 uh what viral and super antigens let's
16:54 see
16:55 and
16:56 then we started to do a more careful
16:59 analysis
17:01 and
17:02 maybe i can show you if you slice sure
17:04 sure
17:05 okay so for example uh one of the things
17:09 the ba yeah like background you know
17:11 super antigens now we know i learned
17:13 that they can bind tcr's
17:15 uh but also at the same time mhc2
17:18 molecules in contrast regular antigens
17:21 where you have a peptide super antigens
17:23 are themselves proteins
17:25 and there is here one of the super
17:27 antigens that have our attention sp
17:30 staphylococcus toxin b
17:32 which binds the beta chain variable
17:35 domain of c tcrs
17:38 so when we were modeling the structure
17:41 and this region
17:43 we noticed you know when you do a pdb
17:45 protein data bank blast and you find
17:48 similar sequences
17:50 uh
17:51 we what popped up was uh is actually
17:54 this staphylococcal antitoxin b let me
17:57 show you
17:58 uh here
18:01 so the the
18:03 this stuff eb
18:04 has indeed a super antigenic uh region
18:08 uh segment that is sequentially very
18:11 similar to that of source ii not starts
18:14 called the one 2003
18:17 but what was even more interesting is
18:19 that it has a what is called a
18:21 palindromic character so you can align
18:24 it you know parallel to each other but
18:26 also
18:27 in the anti-parallel way and then you
18:30 have even a longer segment that
18:32 apparently is similar to seb now not
18:35 only the sequence more strikingly we
18:38 also have the structure of that segment
18:40 you know in a cv
18:42 and it starts called the spike
18:45 and you see those these are positively
18:47 charged amino acids located at the same
18:49 position
18:51 or i'm sorry
18:52 you have you know lots of similarities
18:55 in the structure
18:56 and now we said this region this region
18:58 is definitely sequentially and
19:00 structurally very similar to
19:03 a bacterial
19:05 toxin seb
19:07 that was the starting point the
19:09 discovery of that sequence that
19:12 closely mimicked
19:14 a segment of the bacterial toxin acv
19:17 and then we said okay does it bind to
19:19 the tcr of course it does so that is
19:23 that is
19:24 located here and this is how it finds
19:26 the tcr
19:28 and we have lots of you know basic
19:30 residues on the uh spike and lots of
19:33 acidic residues on the tcrv beta chain
19:36 in particular so we were very pleased to
19:39 see that yes it does bind also
19:42 the uh tcr
19:44 should i continue i have a question i
19:46 have a question
19:48 so well
19:49 many but let's just have one
19:52 so the the super energetic is relatively
19:55 short right it's sort of like a
19:56 it is a peptide that would be presented
19:59 in uh mhc2 as you say right more or less
20:02 the peptide uh you know usually mhc2
20:05 presents the peptide alone
20:08 right it is not attached to a protein so
20:11 what happens is that in the case of a
20:13 super antigen
20:15 we have a peptide let's say again in
20:17 this case about 20 amino acids 24
20:20 but it is also surrounded by other parts
20:22 of the molecule that may assist also in
20:25 further binding so and that makes you
20:28 know the
20:29 affinity much higher
20:31 and
20:32 as a result you have a much larger
20:34 number of tissa receptors that are being
20:37 expressed or t-cells themselves that are
20:40 expanded as you can see from skewed tcr
20:45 representations so here this is showing
20:48 as an example you know that is the
20:50 uh region you know superantigenic region
20:53 here
20:54 but there are extra interactions in the
20:56 vicinity including a
20:59 you know additional molecule intercellu
21:02 which serves for intercellular adhesion
21:06 which further stabilizes this
21:08 interaction so it is the fact that it's
21:10 part of a protein makes it uh
21:13 you know higher binding affinity so
21:15 would it be interacting as part of the
21:17 virus particle or on the cell surface if
21:20 it infected cell
21:23 it is on the spike
21:25 as
21:26 you know it's part of the spike
21:29 and it is
21:30 somewhere in the middle as i showed here
21:33 you see yeah
21:34 so it is uh we you know i had it is
21:37 sketched somewhere the way things
21:39 interacted
21:40 here
21:41 okay here is the host cell here is the
21:44 stars curve two
21:46 this is the spike this is the spark and
21:48 the way it interacts with acetone the
21:50 green eye is h2
21:52 and then there are i i didn't show here
21:55 but there are the proteases from the
21:57 host cell that cleave
21:58 the
22:00 spike
22:01 so the s2 timer remains here uh bound to
22:06 the virus and then
22:08 undergoes a structural change to become
22:11 primer you know right
22:13 and
22:14 trigger the fusion process and then the
22:17 s1 trimer after cleavage is just in this
22:20 extracellular region so it may bind
22:23 directly a kisa receptor or the t-cell
22:25 receptor itself may approach the virus
22:29 so there may be multiple ways
22:32 so you think it has to be released from
22:34 spike s1 has to be released in order to
22:36 be a super antigen right i don't think
22:38 it is a requirement uh because it's
22:40 still exposed okay but when it is really
22:43 you know shed into the s1 and s2 timer
22:46 it gets more exposed
22:49 so there might be a higher probability
22:51 of interaction
22:52 so i want to uh clarification does um
22:57 does the
22:58 t cell receptor
23:00 engage
23:02 this super antigen in a fashion similar
23:05 to
23:06 other ligands that it engages or is this
23:08 a special interaction yeah no it doesn't
23:10 have a slight event
23:12 yes it is very interesting because the
23:15 way the we you know we reported there
23:18 the interaction of
23:20 our super antigenic segment with the
23:22 tissa receptor was mostly with the beta
23:25 chain
23:26 and with a bunch of acidic craze on the
23:29 beta chain variable domain of the tcr
23:33 and this is exactly actually how a cd
23:35 itself also interacts with tcr's and
23:38 we're going to get there because that's
23:40 how we also came up with this idea of
23:42 designing an antibody
23:44 inspired by what was already known for
23:46 ecb
23:48 yvette maybe we can show the super
23:50 antigen slide okay so
23:53 that is also you know you have the
23:55 t-cell and you have the antigen
23:57 presenting cell
23:59 normally this is the antigen presented
24:01 by mhc class 2 but the super antigen
24:05 it doesn't even need uh oftentimes the
24:08 mhc class two but it may also uh you
24:12 know
24:12 serve as a glue between them it is it
24:15 has a much higher affinity binding
24:17 affinity to the t-cell receptor
24:20 variable beta chain variable domain of
24:23 the beta chain a lot of people listening
24:25 probably don't know what a super antigen
24:26 means right
24:28 yeah and what's the consequence so maybe
24:30 in the context of
24:32 the bacterial protein what does it mean
24:35 and what happens yeah super antigen is
24:37 like an antigen but it has super
24:39 activity
24:40 so antigen would be triggering this
24:43 adaptive immune response right tcars
24:47 detect what will be binding now what
24:49 happens is that in the case of a super
24:51 antigen
24:53 the response is excessive
24:56 so
24:57 for example the number of tcrs that are
24:59 being expressed or the t cells that are
25:02 that are expanded
25:03 are a few orders of magnitude larger
25:06 compared to an antigen and this
25:08 excessive response you know gives rise
25:10 to a cytokine storm moshe can explain
25:13 even better than me okay
25:15 yeah i mean
25:16 like yvette showed in the cartoon you
25:18 know if it's a traditional uh peptide uh
25:22 presented you know after a antigen
25:24 presenting cell presents the peptide in
25:26 the groove to the t cell receptor you
25:29 know those are the traditional antigen
25:31 presentation and you end up with 0.01
25:35 to
25:36 0.001 or percent of your t cells that
25:40 are specific to that antigen
25:41 superantigen bypasses that pathway
25:44 attaches from the side to the tcr and
25:47 mhc class 2
25:48 and now suddenly can activate 20 30 40
25:53 percent of your t cells suddenly and
25:54 with a major release of cytokine you
25:57 know this this super antigen term was
26:00 coined by pipameric in 1991 i believe
26:03 and initially from the memory uh memory
26:08 mouse uh
26:11 uh tumor virus yeah yeah right yeah um
26:14 so uh and of course
26:17 that's what causes flesh-eating bacteria
26:20 to uh toxic shock syndrome and
26:22 tampon tampon-induced
26:24 uh
26:25 uh
26:26 you know um
26:28 shock you know and additionally
26:30 traditionally has been associated with
26:32 bacterial uh but but we know we know now
26:36 that uh there are so many uh viruses
26:39 like
26:40 like i just said
26:42 mouse memory tumor virus and and
26:45 rabies virus uh
26:47 hiv gp120 is a is a as a super antigen
26:51 you know ebola has it shown to have a
26:54 super antigen and and of course ebv and
26:57 most interestingly
26:59 human endogenous retroviruses uh uh have
27:02 been associated with uh that been shown
27:05 to have super antigens and that's
27:06 important because we will get into this
27:09 maybe super antigens not only can cause
27:11 this massive release of cytokines that
27:14 may send you to shock with cytokine
27:17 storm but
27:18 repeated exposures to it can also cause
27:21 autoimmunity and and this is
27:24 what we think what's happening in missy
27:26 you know um is kawasaki's a super
27:29 antigen disease yeah so you know
27:31 vincent that has been this did
27:34 debunked you know like it's been like
27:36 when the 20 30 40 years ago 30 years ago
27:40 they found that maybe it's a staff super
27:42 antigen post event that those studies
27:44 have not been you know uh uh
27:46 you know replicated and although there's
27:49 a minority of people that think majority
27:52 of the people think it's a traditional
27:53 antigen of virus or viruses that have
27:57 not been discovered yet so yvette maybe
27:59 you can take it to do to do next uh
28:03 okay
28:03 so now you know think about it we found
28:07 a
28:09 segment
28:10 of the spike
28:11 which is sequentially and structurally
28:13 very similar to this staphylococcal
28:15 anti-toxin b
28:17 which is one of the typical toxins that
28:20 causes this toxic shock syndrome all
28:23 right
28:24 and for acv there is a huge literature
28:27 you know this has been a system that has
28:29 been widely studied and also studied by
28:32 bettina reese actually at stony brook
28:36 who has i'm sorry bettina fry latino
28:40 fries story
28:41 i i don't pronounce correctly
28:44 so she has identified and let me go back
28:48 to my presentation again to make things
28:50 easier for you so she she identified
28:53 three
28:54 antibodies
28:56 let's see where it is okay here it is
28:58 so this is from her work
29:01 and i can use full screen
29:04 so you see you can see here uh
29:07 a cb in the middle
29:09 gray
29:10 and she identified three antibodies fab
29:12 20 b1 63 and 14 g8
29:16 color coded here
29:18 that bind seb
29:20 that are known to you know neutralize
29:22 seb
29:23 and then we when we examined more
29:25 closely we found that one of them 63
29:30 binds exactly that segment which is
29:33 similar to our super antigenic segment
29:36 on the spike protein
29:38 so for the listeners who might not be
29:41 watching those three antibodies bound to
29:44 the seb in different regions exactly
29:48 exactly exactly
29:51 corresponding
29:52 one of them binds to that
29:56 segment which is similar to the spiked
29:59 glycoprotein superantigenic segment

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