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60:02 and then we found that one of them
60:04 actually
60:05 uh
60:07 is very you know highly conserved and
60:10 quite long actually you know it's not a
60:12 short segment it's quite a
60:14 significant portion
60:16 uh of uh between residues 299 300 and
60:20 299
60:22 and tyrosine 351 of the spike
60:25 and
60:26 the end of it one end of it here uh the
60:30 c terminal end is very exposed like the
60:33 you know the receptor binding domain or
60:36 the internal domain of the
60:39 s2 subunit or entire spike so we were
60:43 very intrigued by this neurotoxin motif
60:46 as well
60:47 which might
60:48 be
60:51 relevant to these effects you know we
60:54 observe in uh in the in the central
60:57 nervous system especially in the long
60:59 covet case
61:01 and then we wanted to see
61:03 whether
61:04 the the tcr's that have been identified
61:08 to be overexpressed expanded
61:11 in patients with a severe covet
61:15 and in this case we are talking about
61:16 adults
61:18 whether those tcrs could also bind this
61:21 neurotoxin motif and it turns out that
61:24 they bind this region
61:26 even stronger than the superantigenic
61:29 region so that is not another
61:31 you know motif neurotoxin-like motif
61:34 shown in green here
61:35 where the tcr's will be binding as well
61:39 and this is uh certainly
61:43 you know undergo in progress
61:46 but i just you know mentioned the
61:48 science paper of matias at all
61:51 where they have identified in people who
61:54 had not uh been exposed to sarsapoto
61:59 some cross-reactive epitopes from the
62:02 spike
62:04 and it turns out that that particular
62:06 neurotoxin like motif
62:09 uh
62:10 shown here
62:12 turns out to be one of the most highly
62:14 reactive
62:16 uh
62:17 segments
62:18 on the glycoprotein
62:21 so we
62:23 we are
62:24 right now pursuing this line of research
62:27 to better understand
62:29 the role of this particular segment
62:31 which is actually
62:33 partly concerned between the two stars
62:36 and has been uh
62:39 you know verified here to be
62:41 cross-reactive
62:43 uh even in uh you know in patients who
62:46 have not been exposed that
62:49 so i think uh maybe uh
62:51 moshe if you would like to add anything
62:53 else but
62:54 i think i think
62:55 what we're doing is that we are very
62:57 excited about this milky way we
63:00 have these uh uh uh neurotoxin motif
63:03 that yvette just showed
63:06 and we made a recombinant protein
63:09 and and uh doing uh uh uh
63:12 you know doing experiments with the
63:15 blood-brain barrier opening and and
63:17 going through i mean people have shown
63:20 um that uh s1 uh
63:23 spike protein opens up the blood-brain
63:25 barrier and so it's not inconceivable
63:28 that these uh shed or or neurotoxins can
63:33 pass through
63:34 the blood-brain barrier and may may
63:37 lead to some of the neurologic findings
63:40 that we see in uh
63:42 in acute covet neurologic findings i
63:45 think i think that's really interesting
63:47 i just want to finish with one
63:50 thing that you know when i started to
63:52 look into this and the role of
63:54 uh
63:56 super antigen
63:58 i i came across a paper in 1982 i love
64:02 these old papers you know so so so so so
64:06 so david uh aschenbah from seattle who
64:09 was an obstetrician who wrote this
64:11 incredible paper and you could take out
64:14 toxic shock syndrome in the title and
64:16 you can put long covet in there you know
64:19 and then the title of the paper is
64:21 persistent neuropsychological sequela of
64:25 toxic shock syndrome
64:27 1980 to 82. and he describes you know
64:32 16
64:33 or 10 or 12 women who go into toxic
64:37 shock
64:38 syndrome and then a year later they are
64:42 describing a syndromes of like uh
64:45 neuropsychiatric uh
64:47 uh
64:49 of headaches not a concentration enough
64:52 or or you know cannot really
64:54 uh ability to concentrate it's almost
64:57 like you're reading the long covet you
64:59 know from today and i thought it was
65:01 very interesting you know for to me i
65:04 wouldn't call that very old you know i'd
65:06 call 1939 in old paper
65:09 1982 was when i started at columbia you
65:12 know it depends on your perspective
65:15 so
65:16 what you're describing sounds like the
65:18 brain fog that is the term that people
65:21 are using now exactly for the for the
65:23 long coverage yeah yes do you have any
65:25 sense for what the
65:27 peptide might be hitting in the cns to
65:30 do this or is that something you're
65:31 interested in finding out
65:34 we are that's too early to
65:36 do that kind of stuff you know but uh
65:39 now i have one last question which is th
65:41 this uh
65:43 amino acid sequence must be an accident
65:45 that it has some other function it needs
65:46 to be cleaved by furan's right to
65:48 improve infectivity
65:51 so it's an accident that it causes
65:55 the t cell receptor amplification and so
65:57 forth right because that would be of no
65:59 benefit
66:00 evolutionarily speaking for
66:02 uh viral selection right well super
66:04 antigens are generally thought as
66:07 virulence factors to help uh the the
66:10 microbes to do the disease
66:14 well but
66:15 that is true yeah but ladies virus super
66:18 antigen is used apparently to bring the
66:21 virus from where the virus is in the
66:23 muscle all the way to the nerve endings
66:26 you know it plays a role by activating
66:28 specific t cell receptors so i have no
66:31 idea why why the origin of this might be
66:34 or what what the role of it is yeah i
66:36 just
66:37 you know it doesn't to me it is my
66:39 particular view it doesn't make sense
66:42 it doesn't seem like it would be
66:43 selected for
66:45 to cause this misc because it's late and
66:47 it has no impact on transmission
66:50 which is a you know a major selection
66:52 for so i would look at it as an accident
66:54 especially since sars1 doesn't have it
66:55 but who knows
66:58 anything else you wanted to mention that
67:00 was really it's a really cool thing oh
67:02 is there any implication for
67:05 treatment so should we look at
67:08 everyone's hla1 and say okay you are at
67:10 high risk for misc and be ready to treat
67:13 them would that be
67:14 one approach
67:16 well one thing i read was that covet 19
67:18 adults they were already an hla type
67:21 study you know like who would get sicker
67:24 but for kids
67:26 this needs to be you know
67:28 repeated and and in other cohorts i'm
67:31 aware of like two other cohorts that are
67:33 finding similar hla finding but once
67:37 once we confirm this
67:38 you know that that might be
67:41 that may give us
67:42 a clue you know which which patient may
67:45 develop more severe you know
67:49 hla i mean disease you know for uh yeah
67:52 it seems to me that the antibody would
67:54 be a good treatment
67:56 right
68:00 almost all of the antibodies right now
68:02 they target the rbd the receptor binding
68:05 domain yeah
68:06 and you know whenever there is a
68:08 mutation there you may have an effect uh
68:12 you know
68:13 evasion risk for multiple antibodies not
68:17 63 on the other hand and there is one
68:19 more antibody actually called 4a8 they
68:22 bind another region
68:24 and they have now shown a reduction in
68:27 effectivity
68:28 so i think uh using this antibody in
68:32 cocktails
68:34 my together with rbd binding antibodies
68:37 might be a good strategy
68:40 so of course to try this you need to
68:42 titrate in in appropriate animal models
68:45 i mean if you use an animal model where
68:48 you give lethal virus and then you give
68:51 this antibody you may not necessarily
68:54 see
68:54 a suddenly reversal of death but but to
68:59 look at the
69:00 pathology or level of pathology in the
69:03 lung might be might be the way to go
69:05 perhaps to try this and we're trying to
69:07 work
69:09 to have collaborators to help us that
69:12 those experiments
69:15 fascinating story um
69:18 really
69:19 nice example of how you can start to
69:20 figure out
69:22 pathogenesis right
69:24 uh what i like is this mechanisms it
69:26 starts with an idea
69:27 yeah that it's just an idea that i
69:31 probably would have discarded and gone
69:32 to lunch you know
69:34 uh and then
69:36 experiment after experiment and paper
69:38 after paper using different approaches
69:41 turns out to support the idea okay so
69:43 it's a it's a great story it's a great
69:45 journey
69:46 right still in progress and we're still
69:48 uh continuing yeah that's right
69:51 all right moshe our dt from los angeles
69:54 thank you so much for joining us
69:57 you're welcome and yvette bahar
69:59 university of pittsburgh thank you both
70:00 for joining really appreciate it and
70:02 good luck
70:03 keep it up
70:04 bye-bye thank you for inviting us thanks
70:06 good talking to you pleasure all right
70:08 great good story i think it's cool
70:11 i mean i don't know of any other
70:12 pathogenesis where they're starting to
70:14 sort it out right misc looks like they
70:17 have a mechanism right
70:19 that's good i was
70:21 reminded of their story when they
70:23 started to refer back to the
70:26 streptococcus
70:28 and the
70:29 you know
70:30 the disease is an autoimmune disease
70:32 that uh has a lookalike molecule
70:35 someplace i was at rockefeller where
70:36 that data was first discovered by
70:38 zabriski
70:39 and framer
70:41 and i remember
70:43 everybody getting very excited about
70:44 that because rheumatic heart fever
70:46 could be now explained by
70:49 waiting to treat and then all of a
70:51 sudden you get another disease which is
70:52 even worse than the scarlet fever that
70:54 the strep throat that you have to begin
70:55 with so
70:57 so
70:58 nothing is unrelated staphylococcal
71:00 enterotoxin b seb that she said that it
71:03 fast a lot you might have missed it
71:05 scb seb and that's the super antigen
71:09 and um
71:10 which triggers tss right toxic shock
71:14 syndrome yeah exactly and the other
71:16 thing that maybe people got lost with
71:19 so the t cell receptor normally would
71:21 recognize a peptide
71:24 presented to it by mhc
71:26 right and so
71:28 this
71:29 super antigen is really good at
71:32 recognizing the t cell and somehow
71:35 amplifying certain ones so that they're
71:37 way higher basically yeah basically the
71:40 way i see it is is it it activates those
71:42 t cells
71:43 right okay which means that they
71:45 divide and proliferate and they also
71:48 send off all kinds of cytokines that's
71:50 right and that's what that's when they
71:52 talk about skewing that's what that
71:53 means is you've amplified a certain
71:55 population of t cells that the super
71:57 engine
71:58 reacts with which is another terrific
72:00 thing because they basically
72:02 predicted in their model that something
72:04 like that should happen and then they go
72:05 look at the kids and sure enough uh they
72:08 have a whopping fraction of their uh t
72:10 cells the kids with miss c whopping
72:13 fraction of their t cells are of a
72:14 certain type uh that react with this
72:17 super antigen amazing
72:20 i just i i don't know if it's actually
72:24 where's
72:25 s1 right
72:26 i guess it's being shed at entry so it's
72:29 got to be coming from virus particles
72:31 attaching to cells oh yeah
72:33 this one is shedding off right because
72:36 there's a lot of questions on the
72:37 biology that
72:38 need to be addressed but in one of their
72:40 papers they said you can't change the
72:42 sequence
72:43 because then you have no infect or less
72:46 infectivity if you change that if you're
72:47 in sight and then you can't dissect the
72:49 two
72:50 properties that's
72:52 i wonder if you put it into another
72:54 virus oh that's gain of function sorry
72:57 but you could put it into and if you had
72:59 an animal model
73:00 for another virus
73:02 say an animal virus that doesn't affect
73:04 people put it in and see if it triggers
73:07 mis or some inflammatory syndrome that
73:10 you wouldn't see
73:11 right
73:12 so vincent i noticed that they didn't
73:13 bring up the issue of blood type
73:15 i was going to even raise that but is
73:17 that an old story now that's not being
73:19 adhered to anymore or are there certain
73:21 blood types that are more susceptible my
73:22 understanding is that that was no longer
73:25 held up on further examination the
73:27 connection with blood type and severity
73:30 yeah um
73:33 but uh what is the frequency of this i
73:35 wanted to ask them does anyone know the
73:37 misc kawasaki no no not kawasaki misc
73:41 like
73:41 well i don't know we should have asked
73:43 them that
73:44 it's not very common
73:48 but i just love that you may have a
73:49 mechanism to explain it right
73:51 immunological molecular and isn't it
73:54 great you look at this
73:56 and you see it looks like a super image
73:58 and wow that must have been cool that
73:59 day right
74:00 [Music]
74:01 anyway it's a great story that's why i
74:03 wanted them to tell it
74:05 right
74:05 let's do a couple of emails
74:07 oh you have a public service
74:09 announcement kathy yeah it's something
74:11 that i only just found out about but
74:14 we lost an important adenovirologist
74:16 bill wald
74:18 he died in june and i only just found
74:21 out about it last night
74:24 so bill wald has pretty much he spent
74:27 his entire scientific career at st louis
74:30 university uh having been trained in
74:32 manitoba so he was canadian
74:34 and uh
74:35 he was about to retire in august and uh
74:39 vancouver island in canada
74:43 but so uh
74:45 what i want to tell you about them uh we
74:47 have two links one is um the obituary
74:50 from the um
74:52 from the web and also a journal of
74:54 virology article that
74:56 a number of people who uh were with him
74:59 at st louis university
75:01 uh wrote together so it's it's just a
75:03 longer really nice tribute about his
75:06 life so he was an adenoverologist
75:08 um and he was e3 basically if you wanted
75:13 to know anything about e3 and human
75:15 adenoviruses bill wald was your guy and
75:18 um
75:19 one of the
75:20 things
75:22 said that
75:23 he was really
75:24 generous with uh
75:27 as a citizen he generated over 250 viral
75:30 mutants and all kinds of anacera and
75:32 monoclonal antibodies and was very happy
75:35 to provide them to anybody and
75:37 i was the recipient of that
75:40 back on um some of the kinds of things
75:42 that he did um
75:45 e3 is conserved among all the
75:47 adenoviruses i mean it's it's always
75:50 there and yet it can be quite different
75:52 from one adenovirus to the next and the
75:55 early things that the rap about it was
75:58 that it was dispensable well it was
76:00 dispensable for growth in cell culture
76:03 and bill
76:05 argued that no it must be important for
76:07 something in the virus in pathogenesis
76:10 in the natural host and so
76:12 he really worked to characterize that
76:15 um
76:16 there are a lot of nice tributes uh both
76:19 in this journal of virology article and
76:21 online um he was known not only for his
76:24 scientific achievements and leadership
76:26 at st louis university where he rose
76:29 through the ranks and became the chair
76:31 of the department he was a supportive
76:33 mentor caring person outstanding teacher
76:35 and a dear friend to many of us
76:37 um he was a favorite golf buddy a
76:40 passionate running coach he he ran
76:42 marathons and this is something i didn't
76:44 even know about him until now
76:46 um so he will be missed by a lot of
76:48 people and had a really positive impact
76:51 on the field
76:53 remember harry ginsberg used to say that
76:55 too
76:56 it's dispensable for herself but must be
76:58 doing something yeah yeah e3 really
77:01 important and and yeah so
77:05 uh
77:06 too bad
77:07 it's one of the genes to take out in
77:08 vectors right to give more space
77:11 right and and that you know and so
77:14 there were two ways that bill sort of
77:16 addressed that and one was let's figure
77:19 out what all these e3 genes are doing
77:23 and the other was if we can take it out
77:25 then maybe we can use it in as an
77:27 oncolytic vector and um so he had a lot
77:30 of connections with working on cancer
77:33 and things like that so yeah
77:37 it's a day when you could focus on one
77:40 gene
77:42 well one
77:47 multiple genes oh yeah six or eight for
77:49 some of the human adenoids but still to
77:51 focus on one region your whole career
77:54 people did that all the time i don't
77:56 know if you could do it anymore yeah
77:58 and publish papers with two or three
78:01 four authors yeah yeah
78:02 yeah oh and his people were all very
78:05 loyal to him so the postdoc who left my
78:07 lab um was with him from 1996 till 2020
78:12 when i think he saw the writing on the
78:13 wall that bill was going to retire and
78:15 and he changed labs but
78:17 all those other co-authors on the jv
78:20 article i think
78:21 many were with him for
78:23 years and years
78:25 yeah yeah i met him a few times
78:29 all right rich can you take the first
78:31 email there
78:32 sure hal writes first of all thank you
78:34 for your excellence
78:36 i am a 64 year old relatively healthy
78:39 and fit internal medicine physician
78:43 practicing in southern maine my second
78:45 vaccination was on january 20th
78:48 recently just this week i contracted
78:50 sargo v2
78:53 uh
78:54 this is
78:56 day five and nothing more than an
78:58 annoying cough
79:00 mild fever and a runny nose for a few
79:03 days i'm almost back to
79:06 in quotes normal yay vaccines work
79:09 my question is
79:11 do i truly need a booster
79:14 fully vaccinated plus covet
79:17 more than likely with delta variant in
79:19 that order
79:20 i know there's no negative outcome in
79:22 getting the booster but is there truly a
79:24 benefit in this scenario
79:26 if so
79:27 what is it and when would be the best
79:30 time to get the booster shot
79:32 well
79:34 i'll give you my spin on this and others
79:36 can weigh in
79:38 i would say first of all and most
79:39 important
79:41 i don't know
79:42 okay
79:44 and i don't think anybody knows
79:47 we do know
79:49 that there are studies that say that if
79:52 you've had the disease and then get
79:54 vaccinated
79:56 you have a superpower
79:58 okay
79:58 that you are immunologically
80:01 cooler
80:02 than either infection or vaccination
80:05 alone okay
80:07 and i would presume
80:09 that the reverse is also true
80:11 that if you are vaccinated and then get
80:14 sick
80:15 that you have a superpower uh
80:19 but there are no data that i am aware of
80:22 so i don't know
80:23 uh your your thinking is all right
80:26 sounds to me
80:27 if i had to guess
80:29 i would say that at this point a booster
80:31 shot although no harm done is
80:34 superfluous
80:36 so a superpower that's different from a
80:38 super antigen right
80:40 yes
80:42 we got the super episode today
80:46 i yeah i would agree with that
80:48 but i like that hal has uh thought about
80:50 this and also you know he says i
80:52 contracted the sars cov2 virus good for
80:54 you
80:56 and yay vaccines work they do yeah
80:59 and this is what's gonna happen over
81:01 time
81:02 over the years
81:03 as we have said many times before
81:06 uh my
81:07 my belief my prediction
81:10 is that the virus is not going away
81:13 uh and you know depending on what
81:15 happens to the vaccination programs
81:17 um
81:18 i would
81:19 kind of expect
81:21 that all of us
81:22 if we live long enough
81:24 are gonna uh even having been vaccinated
81:28 going to get boosted by the virus itself
81:31 okay so
81:33 there you go
81:35 dixon can you take the next one
81:37 oh you gave me the long one sure no
81:40 it's a short
81:41 lamont writes
81:43 what i find interesting
81:46 there is a documented transmission
81:48 change of breakthrough infections in
81:51 fully pfizer vaccinated individuals
81:55 what i sort of expect
81:57 is this will be abused to continue to
82:00 argue that the vaccines don't work with
82:02 delta
82:04 and we that's a follow-up to the comment
82:07 that was just made
82:08 so this is
82:10 an emerging infectious disease very
82:11 short it's called the research letter
82:14 breakthrough infections of e484k
82:16 harboring saurus kov2 delta in lombardy
82:19 italy
82:21 um which um
82:23 was the legion really hammered in
82:25 initially if you remember the beginning
82:27 that's right that's right um and
82:30 the last twist that i released
82:32 one of my guests uh
82:35 worked there and
82:36 studied it firsthand
82:38 so this is an interesting case it's
82:41 it is um
82:43 someone who got infected and then
82:46 his mother
82:48 they're all vaccinated and then the
82:49 mother who's vaccinated got infected and
82:52 then the
82:53 somebody else
82:55 close to them
82:57 and they all
82:58 the genome sequencing suggests that it's
83:01 all the same virus that they transmitted
83:03 to each other so they're thinking these
83:06 vaccinated people were transmitting it
83:07 to each other
83:09 yeah i i mean it's a couple of people i
83:11 agree and
83:12 i don't know what the bigger picture is
83:14 but of course yeah a small study like
83:16 that will be
83:17 used to say the vaccines don't work for
83:20 sure
83:22 but no one died
83:23 no one died nobody died that's right um
83:26 i think it worked
83:28 uh yeah the patio fatigue headache my
83:31 algae
83:32 dips near um fatigue none required
83:35 hospital admission
83:37 yes
83:38 a cold ran through the family it did
83:41 yeah yay vaccines work
83:43 that's it yeah to quote another proof
83:46 kathy can you take the next one
83:49 yes jeff writes hi i was trying to
83:51 explain the immune system to my 12 year
83:53 old son in simple terms i don't think
83:55 that there are really any simple terms
83:57 for the immune system which is what
83:59 makes it so fascinating but anyway i
84:01 came up with what i think is a pretty
84:03 interesting metaphor of musical
84:05 recordings and they're being played the
84:07 idea is that there is a memory the
84:10 stored music which has no specific
84:12 playing volume
84:14 but a spectral analysis would reveal
84:16 many combined frequencies each with a
84:18 relative amplitude
84:20 when played there's an overall
84:22 amplification that can be set regardless
84:25 of the recording's inscribed amplitude
84:28 this playing amplitude expresses all of
84:30 the memories at their relative
84:31 amplitudes
84:33 then we talk about immunomodulation it
84:36 is the external overall amplitude that
84:38 we're talking about
84:40 and the t and b memory is the spectral
84:42 decomposition the tnb memory inscription
84:45 process
84:46 is similar to our recording of music the
84:49 system records on the record
84:51 a response to what is going on in its
84:54 environment although we don't usually
84:56 represent music in terms of its spectral
84:58 decomposition
85:00 there's not reason
85:01 that we couldn't and if we did then the
85:04 tb immune memory system would actually
85:06 work similarly to that way of recording
85:09 music
85:10 anyway i'm not sure how far this
85:12 metaphor or analogy could go but i
85:14 thought it was fun at the time what i
85:16 wanted to ask you though after all this
85:18 is what is the best book on the immune
85:20 system for a 12 year old for under 150
85:24 so for instance janeway is out although
85:26 i could probably get a previous edition
85:28 cheap
85:29 cheers jeff
85:31 so um
85:33 if your 12 year old could understand
85:36 this analogy
85:38 with spectral analysis combined yeah
85:40 right
85:41 amplification
85:43 and so forth
85:45 um then
85:47 kudos to him and to you for knowing that
85:50 he could understand that because
85:52 um it i think it's a pretty complicated
85:55 analogy it is but um
85:57 anyway um
85:59 maybe it works and maybe it works for
86:01 some people who think more
86:02 about music in in physics terms which
86:05 reminds me i have the chance to go to
86:07 another saturday morning physics about
86:10 music in the near future um right to do
86:12 that
86:13 um
86:14 so uh
86:16 the book that we've suggested in the
86:18 past that i have and i refer to
86:21 is
86:22 about a quarter inch thick eight and a
86:24 half by 11 format paperback by lauren
86:27 samparak
86:29 called how the immune system works and
86:31 you want to get the sixth edition
86:33 because immunology is always changing
86:35 and you want to have the most current
86:36 one so how the immune system works
86:40 nice
86:41 so uh susanna lopez
86:44 she's not written anything that would do
86:47 the trick
86:48 has she yet she needs to tackle this one
86:51 i think
86:52 she might have said she's working on it
86:54 yeah she's she's written some things
86:57 that kind of get it at some aspects of
87:00 the immune system but
87:02 and then yeah i don't know it seems to
87:04 me that her books are targeted more
87:07 younger yeah the younger age group um
87:10 but that could also work
87:12 for understanding immunology it's true
87:16 yeah
87:17 the other answer is as soon as we
87:18 understand the immune system that book
87:20 will be written but that hasn't been
87:21 done yet
87:23 right
87:25 all right this next one is from johannes
87:27 twixtors i'm a little behind in
87:29 listening so i'm sure someone already
87:31 told you
87:32 but just in case and twiv
87:35 rats more coronaviruses from august 29th
87:38 you were talking about a ligation method
87:39 that leaves no traces and that you
87:41 didn't know of one
87:43 gibson assembly
87:45 would be my obvious example as i use
87:46 that in the lab all the time and all you
87:48 need is for that is fragments that have
87:50 overlapping sequences of 20 to 30 base
87:52 pairs and an enzyme mix
87:54 containing a five prime exonuclease that
87:57 generates long overhangs a polymerase
87:58 that fills in the gaps of the annealed
88:00 single strand regions and a dna ligase
88:03 that seals the nicks of the annealed and
88:05 filled in gaps and voila no traces of
88:07 ligation because you do not have to use
88:10 restriction sites if you synthesize or
88:12 pcr amplifier fragments and no
88:14 recombination scars like in gateway
88:16 cloning yeah i forgot about gibson yep
88:20 have a great day from perth australia
88:23 okay
88:25 let's do one more round
88:26 rich adam writes greetings vincent and
88:29 everyone i love twiv
88:31 but i gotta take a very slight exception
88:34 to your discussion of star trek red
88:37 shirts in twit 802 which was in every
88:41 other respect a terrific episode
88:44 god a star trek booboo
88:47 this is terrible
88:49 how many times has it been said on
88:51 twitter when discussing statistics check
88:53 the denominator
88:55 if we apply that principle to the star
88:57 trek red shirt phenomenon
88:59 we get a different story than the usual
89:02 narrative
89:04 by the way the usual narrative is that
89:06 if you show up in a star trek episode
89:09 wearing a red shirt you're doomed those
89:11 are the characters that wind up getting
89:13 killed
89:15 uh while there's actually a book written
89:17 about this a novel about red shirts
89:21 while it is true that more red shirts
89:23 engineering communications and security
89:25 personnel that's their uniform is read
89:28 died in the three seasons of star trek
89:31 then either gold shirts command
89:33 positions or blue shirts science and
89:35 medical staff if we look at the
89:37 population of the enterprise we see
89:39 something else
89:41 by the way i've heard rumors that there
89:44 were some sarge some star trek shows
89:46 after the original series but i suspect
89:49 that may be fake news anyway
89:51 by raw numbers the deaths break down as
89:54 red shirt
89:55 25 that is 58 of total deaths gold shirt
89:59 10
90:01 23 of total deaths blew eight 19 percent
90:05 of total test the star trek enterprise
90:08 technical manual
90:10 states that
90:12 there were 239 red shirts on the
90:15 enterprise 55 gold shirts and
90:18 136 blue shirts this means
90:22 that the death rate by shirt color
90:24 is red shirt
90:26 uh roughly 10
90:28 gold shirt roughly 18 percent and blue
90:31 shirt roughly 6 percent that means the
90:35 safest position statistically is to be a
90:37 blue shirt science officer next is to be
90:40 a red shirt engineer security person and
90:43 the riskiest position or highest death
90:45 rate is what the gold shirt command
90:47 officers
90:48 credit for this calculation is not mined
90:51 but goes to mathematician james grimes
90:54 some of you some
90:56 whom some of you may know from number
90:59 file or singing banana it's a new one to
91:02 me i gotta look that up keep up the
91:04 great work i love twiv and all the
91:06 microbetv offerings thanks for all the
91:09 knowledge and entertainment sincerely
91:11 adam
91:12 well we stand corrected
91:15 uh and i love
91:17 the data it's uh marvelous that's it
91:19 that's what does it
91:21 i
91:22 so i don't know anything about this but
91:24 i was on some kansas medical center show
91:27 and one of the doctors said this and so
91:30 i just passed it on here on twitter and
91:33 i think you guys may have agreed or
91:35 something well there was a there was a i
91:38 think one of the reasons this came up
91:40 was that there was a
91:42 a photographic meme going around for a
91:45 while that's right with four star trek
91:48 crew
91:49 three of whom were wearing masks and one
91:51 of whom wasn't and the one who wasn't
91:53 was was a red shirt right right
91:56 right okay all right dixon now you get a
91:58 longer one
92:00 now i get a longer one georgia writes
92:02 hi vincent and crew
92:05 listening to shane croney's responses to
92:07 your questions and impact of timing of
92:09 boosters i wondered if i might apply
92:11 that to my situation with the shingles
92:13 vaccine i got the first shingrit shot at
92:16 the end of august
92:17 timing for the second shot has
92:19 identified as two to six months
92:21 based on the discussion in the above
92:22 episode do you think it might be better
92:24 to get the second shing shingrich
92:27 uh sigrid uh injection towards the later
92:31 time frame
92:32 is it fair to extrapolate response to
92:34 covet 19 vaccinations to the shingrix
92:37 vaccine as far as timing of the booster
92:40 is concerned some background i developed
92:42 shingles
92:43 of the trigeminal ganglia on the
92:45 maxillary branch v2 early in july after
92:48 i finished a 10 day course of acyclovir
92:50 800 milligrams per 5 5 times a day
92:54 the shingles resurged and expanded to
92:56 include the ophthalmic branch v1 and i
93:00 took another course of acyclovir and my
93:03 eye doctor put me on a 90-day course of
93:05 1 000 milligrams of
93:07 valacyclovir as soon as i finish the
93:09 acyclovir
93:11 i need
93:12 i read up one
93:14 at the cdc on shingrich
93:16 how come i can't say that word
93:18 shingrik rix
93:20 and confirmed that the use of antivirals
93:22 wouldn't interfere with getting the
93:24 vaccination alas i was left with some
93:26 nerve damage but i haven't given up on
93:28 the hope that it might eventually
93:30 improve
93:31 love all the microbe tv shows and listen
93:33 faithfully
93:35 i'll practice that word over the week
93:39 sorry
93:42 if they say two to six months
93:44 then you can go anywhere in that range
93:46 that's a pretty broad range though isn't
93:47 it yeah and i doubt if there's any data
93:49 that says
93:50 that uh any
93:52 uh particular interval is better than
93:54 yeah any other i wouldn't necessarily uh
93:57 uh
93:58 um
94:00 translate experience with one vaccine to
94:04 another
94:05 okay so
94:06 whatever i would in your circumstance i
94:10 might want to get boosted as soon as
94:11 possible yeah that sounds it sounds like
94:14 i'm sorry about your
94:16 situation that sounds like a pretty
94:19 awful uh
94:20 experience that's right that's right
94:23 for a while the shingrix
94:25 uh there was a shortage of it and so i
94:28 was faced with i had gotten the first
94:30 dose and i was toward the end of the six
94:34 months or maybe just outside of that
94:36 before i was able to procure a second
94:38 dose
94:39 but now i think that's
94:41 long since eased up so yeah i think i
94:43 got my second dose at seven or eight
94:45 months just because i uh forgot
94:49 at any rate
94:51 behind a little behind the scenes here
94:53 there's a good
94:54 uh i love this sentence that um read up
94:57 on cdc on shingrix and confirmed that
94:59 the use of antivirals wouldn't interfere

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