October 27, 2022 • 25 mins
Why do some people get Covid—but show no symptoms? That’s one of the mysteries being unraveled by Dr. Jill Hollenbach, immunogeneticist at the University of California, San Francisco, and head of The Hollenbach Lab. Hear how she went from a childhood as a self-described “science nerd” to leading important research at the intersection of immunology and genetics.
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Speaker 1 (00:04):
I will say that I was a science nerd from
a very young age. I actually have sitting in my
office at work, tiny little child's microscope that I was
given as a gift when I was, you know, very
very young. And I was that kid. You know, if
I cut myself, I would run into my room and
(00:27):
put some of the blood on the slide and see.
I didn't know what I was looking at. I don't
think the microscope was even strong enough to really see anything,
but the interest was there. That was Dr Jill Holland Back,
an immuno geneticist at the University of California, San Francisco. Today,
that former self described science nerd leads research into one
(00:51):
of the mysteries of COVID, specifically why some people get
the disease but show no symptoms, and what that can
tell is about treating and preventing it. I'm a land
ververe In. This is Seneca's one Women to Hear. We
are bringing you one hundred of the world's most inspiring
(01:11):
and history making women you need to hear. For years,
Dr Hollandbach and her team at the Hollandbach Lab have
focused on a set of genes called h L A
and h l a's relationship to autoimmune diseases like multiple sclerosis.
But since the pandemic, the Hollandbach lab has turned its
(01:34):
attention to COVID as well. Their answer to the question
of symptomless COVID may lie in the genetic mutation of
h l A. Listen and learn why. Dr Jill Hollandbach
is one of Seneca's One Women to Hear. I'm speaking
(01:56):
today with immuno geneticist Dr Jill Holland and we're going
to discuss her research on COVID. Welcome, Dr Holland Beck.
It's really wonderful to have you with us. I know
our listeners are going to be very interested in this topic.
Thanks so much for having me. Now I understand your
leading research into who does and who does not get
(02:18):
COVID well, I first of all, I want to say
that we're really focused on people who have tested positive
for the virus that causes COVID but never had symptoms.
So for those who actually have had the COVID virus
but don't show any symptoms, why is that? Is it
(02:39):
a genetic mutation? We think so, not probably not everybody,
but in a proportion of the individuals that we've studied,
it seems that a specific version of an immune system
gene that we're interested in generally in my lab seems
to make them much more likely to be symptomatic. So
(03:02):
perhaps you can tell us more about precisely what you're
looking at in your research or their implications in terms
of genetic mutation. What can you tell us about what
you've learned? Sure, so my lab is generally interested in
a set of genes called h L A, human leukocide
(03:22):
anergen and I think a good way to think about
it is to think about the transplant settings. So when
we talk about matching for a transplant, these are the
genes that we match on. And in fact two UM
one major component of our study involved going back to
individuals who are registered as potential bone marrow downors and
(03:45):
asking them about their COVID experience, because we already have
data on the genes of interest for them. So h
L A or genes that encode important immune system molecules,
and the job of those molecules is to present or
show to UH your effect or cells, your T cells
(04:07):
in your immune system, pieces of foreign anigen or peptide,
pieces of protein. Is probably a better way to put
that better derived from things like viruses and bacteria, and
then the T cells come along and they inspect those
pieces of foreign protein and generate an immune response if
(04:29):
it's something that is not supposed to be there. So
the interesting thing about h l A is that they're
extremely variable between people, between populations. So most genes have
maybe one or a few different versions that we refer
(04:50):
to as a leal. H l A has literally thousands
and thousands of different versions that we see, you know,
across the globe, and that's why it can be so
hard to match somebody for a transplant, because one person's
h l A looks very different from another person's h
l A. So what we and and many others hypothesized,
(05:13):
you know, very early in the pandemic, was that different
versions of these genes, because they're so important in the
immune response to pathogens, might be important in differential response
to the virus that causes COVID nineteen and so we
went out to start looking for individuals who had tested positive.
(05:38):
Because the important thing in studies like this is that
it's very hard to control for exposure, so it's very
hard to ask the question does somebody who gets infected
and who doesn't. Because there's so many variables in whether
somebody is exposed to the virus, what kind of mitigation
you know, are they have, they've been masking, and things
(06:00):
like the humidity in the room at the time of exposure.
There's far too many variables for us to really say
for certain that somebody has or hasn't been exposed, or
that their lack of infection is due to something genetic.
But what the question that we can ask is, when
somebody has a confirmed infection, they've tested positive for the virus,
(06:26):
what does their disease course look like compared to the
person next to them? Because we know that there's a
huge range of disease course, everything from asymptomatic disease to
you know, extremely bad outcomes, people becoming hospitalized, ventilated, and
you know, we've had you know, tragic number of deaths,
and so what we want to know is what mediates that?
(06:51):
What you know, what is there something biological, Is there's
something genetic, No, is there's something about their h l
A that changes how somebody responds to the infection. And
a lot of the studies up to this point that
have been done thinking about not just h l A,
but genetics in general have really focused on the severe
outcome end of the spectrum. And there's really good reasons
(07:14):
to do that. You know, people have gotten really sick.
We want to understand why we want to prevent that.
Some of the reasons that those have been the patients
who have been focused on are practical because when people
are in the hospital, you're more you know, it's much
easier to get samples, biological samples like blood and DNA.
(07:39):
But really, you know, the vast majority of people who
experienced infection do not wind it in the hospital. They
have you know what we would term, you know, relatively
mild to moderate disease. And we were kind of interested
in those people, and specifically the subset of people who
just don't have symptoms at all, not a stuff, he knows,
(08:01):
not a scratchy throat, nothing, And so we asked that
question individuals who have in infected with the virus, did
you or did you not have symptoms? And what we
found was this extremely strong effect of a particular version
of one of the h l A genes called h
(08:22):
l A B that seems to really enhance somebody's chance
of not having symptoms when they're infected with the virus.
So fascinating, and can that be determined in advance for
somebody to know if they've got that makeup that they're
going to be symptomless. Well, first of all, I want
(08:43):
to be clear, just because you have this particular version
of this gene, so the gene is called h L
A B and and the version that we're interested in
is called h L A B fIF one doesn't mean
that you absolutely will be asymptomatic. It just means that
you're probably too to three times more likely to be asymptomatic.
So I think that it doesn't necessarily ensure that you
(09:08):
would be. I don't know that it would be particularly
helpful for somebody to know that it's UM. It's not
a test that's done commonly, unless somebody happens, for example,
to be a volunteer bone marrow donor they might know
their type. But I don't know that that would be
a particularly useful thing for somebody to know. I think
(09:28):
that you know. For me, it's more about what this
finding tells us about the immunopathology of the disease and
what kind of directions it can point us to. In
terms of possible vaccine design and possibly treatments. So this
is ongoing research as you keep probing and coming to
(09:52):
various conclusions along the way. Absolutely, So you know, after
this initial finding we went back to the lab. We've
since um and we're in the in the middle of
writing this up right now, so I'm hoping that this
paper will be released fairly soon. But went back into
the lab to understand first of all, can we detect
this in in other patient cohorts UM? And also you know,
(10:17):
what is the the actual um functional activity of T
cells in these individuals. So that's that's something that we've
been looking at carefully. And UM have some really interesting
new data on senecas one hundred women to hear. We'll
be back after the short break. You had a research
(10:49):
team called the Holland Buck Lab. Are there other scientific
questions besides those you've just been describing that you're looking
at as well trying to answer? Sure? So, my lab
at UCSF is broadly focused on immuno genetics in human
health and disease, So that mostly takes the form of
(11:09):
us thinking about these h l A genes and UM. So,
for example, one of the reasons that I'm in the
Department of Therology at UCSF is that a particular version
of h l A is also the most important predisposing
gene in multiple sclerosis. And we've examined a number of
(11:30):
neurological diseases from the point of view of this gene
system Parkinson's disease, my skinia gravis for example. So that's
ongoing work that we're focused on. We're very focused in
on multiple sclerosis in my lab, and we're also interested
in other common elements and and how different versions of
(11:53):
h l A predispose somebody or or protect them from
common illnesses as well as ubiquitous viruses like megalovirus. So
we're asking those questions all the time in the lab,
and that's really the main focus. And we were doing
that long before COVID, but you know, once the pandemic
(12:16):
came around, we absolutely refocused a lot of our energies,
as did so many others, to ask these questions well.
And they're so important obviously because they affect just so
many people who still don't have the answers they'd love
to have, right right I you know, I mean, on
the one hand, it feels like it's been a long time,
(12:37):
and and how are we still here? And why are
we still worrying about this? Nobody I don't think anticipated
this was going to go on for so long. But
you know, another way to look at it is there's
just been incredible, remarkable progress made in a very short
period of time. I'm completely blown away by, you know,
(12:59):
the amazing work that's been done all over the planet
trying to understand this disease. And it's really just been
an incredibly impressive scientific feat But I think that, you know,
people like me and and my colleagues are just incredibly
motivated because we're the same as everybody else. We've experienced
(13:19):
the pandemic the same as everybody else, right, And you know,
I first started putting together the project to look at
this like so many other people, sitting you know, in
my home office on lockdown. So I think there's you know,
a lot of motivation across biomedical science to answer these questions. Well.
(13:40):
And I think that's that's true about your mentioning MS
as well. So many people are afflicted with that absolutely, yeah,
And it's an extremely debilitating disease and impact you know,
people in the prime of their lives. So you know,
in general, this is just extreme, really gratifying work to do.
(14:02):
And you know, I feel like I've been really fortunate
to have been able to focus my my work life
on on solving these problems. It definitely helps me to
feel a little bit less helpless in the face of
what we've all experienced. Well, it's certainly critically important. Can
we talk about you a little bit you personally? I
(14:26):
know you're an you know, geneticist. What does that mean.
I mean, it's a big word, and I'm sure our
listeners are wondering what does she do or what does
that field represent? Sure, so it's really a sub field
of genetics. I trained as an immunologist. Um I did
my PhD in immunology at Berkeley, but I did my
(14:47):
training during that time in a genetics lab, and so
it's a sub field of genetics where we're focused specifically
on these very variable immune response genes. And it really
acquires an entirely different way of approaching genetics and thinking
about genetics because of the high levels of variation, but
(15:07):
also because it's so important to consider the structure and
the function of the immune molecules while we're thinking about
the genetic aspect. So it's a sub field that's generally
um focused on things like transplant and autoimmune diseases, but
it really has um kind of far reaching applications that
(15:32):
is certainly wonderfully rewarding. It sounds like to be able
to explore these areas. How did you get interested in
this field? Was it your upbringing? Was there a moment
when you really set to yourself, I want to be
a scientist. Yeah. I will say that I was a
science nerd from a very young age. I was interested
(15:55):
in scientific things as far back as I can remember.
I actually how of sitting in my office at work,
tiny little child's microscope that I was given as a
gift when I was, you know, very very young, and
I was that kid. You know, if I cut myself,
I would run into my room and put some of
(16:17):
the blood on the slide and see. I didn't know
what I was looking at. I don't think the microscope
was even strong enough to really see anything, But you know,
I was the interest was there. I used to you know,
graph the details from my doctor's appointments and things like that.
But you know, actually, when I was growing up, I
didn't really understand that being a scientist was a job.
(16:42):
I grew up in a you know, in a Jewish family,
where if you were interested in science, you became a doctor.
If you're interested letters, you became a lawyer. And those
were the only two options that were presented to me.
But you know, during the course of my education, I
really kind of fell in love with immunology. That was
(17:03):
during a period of time when I was working on
my master's degree in public health. At the time, I
had actually been interested in going into women's health and
health policy. I had gone to work for Planned Parenthood
straight out of college. UM, but I got a little
bit sidetracked and fell in love with immunology. And then
during the course of my PhD, I was particularly interested
(17:26):
in h l A because my mother had rheumatoid arthritis
and h l A is very important in autoimmune disease
and including room toid arthritis, and that kind of sparked
my interest and had an opportunity to work in a
lab that was focused on these genes. And it's um,
it's been quite a long time. The rest is history.
(17:48):
Here I still am doing important work. Did your parents
nurture your interest as a child in science or were
there mentors along the way who inspired you. I think
you know, my parents, Um, my father was was a
c P A my you know, my mom had been
an English teacher. They were not really stem people, so um,
(18:12):
you know, they encouraged me, of course, but I think,
you know, to be honest, you know, to the day
my dad died, he used to variably describe me as
a microbiologist. You know what of this that he never
you know, he tried but didn't really understand what I
was doing. But I certainly, you know, I had some
(18:34):
great teachers along the way. I had a physiology teacher
when I was in high school who really sparked my
love for that topic, and I went on to become
a physiology major at Berkeley. And then some you know,
really key professors during during my time at Berkeley's so um, yeah,
some great mentors along the way, and um peers and
(18:57):
colleagues as well who have been extraored, early supportive through
the years. Well, here at Seneca women we often emphasize
how important it is to have women in science, and
we still have to do better in that respect. I
think you agree as a general proposition, but I wonder
what you think about why having a women's perspective is
(19:19):
important in your field if it is, well, I guess
what I would say is, I don't know that as
a woman, I necessarily have a different perspective, at least
not on the science necessarily. But you know what, as
a professor at a research and university, part of my
job is to train the next generation of scientists, and
(19:40):
I think that that's where, you know, having representation is
really just so important. I think that, um, you know,
we bring to the table a different set of life experiences, UM,
A different way of having experienced the world and moved
through the world, and that is really, um I think
(20:05):
an asset when we're training not just you know, the
next generation of women's scientists, but the entire next generation
of scientists. I think that having that different perspective on
you know, life and and life experiences is extremely important
and helpful, UM as as we train young scientists. Well,
(20:29):
I always hate this moment looking at the clock when
we're nearing the end of a fascinating conversation, but I
really would like to ask you before we have to
take leave. You know, given that we've all collectively gone
through a couple of years now of the epidemic. We've
been talking about COVID, We've been talking about other viruses.
(20:51):
Certainly there are more on the horizon we haven't named
or don't know anything about because there yet at the
development stage, probably, But given all that, what makes you optimistic?
What gives you hope? Because this is tough stuff, it is.
But you know, as I said earlier, I realized it
feels like it's it's been a long time, and that
(21:13):
it's been you know, one step forward, two steps back
through the pandemic. But you know, from where I sat,
I'm just absolutely marveling at the progress that we've made.
And it's really been an incredible experience to be in
(21:35):
the middle of these research efforts and to look around
me and see my colleagues at UCSF and across the
country and across the world who have really come together
in I think a unprecedented way. And I'll say that
the levels of collegiality and collaboration that I've experienced, you know,
(21:59):
particularly working on this topic, have just been so heartening.
Um I think that there's often a lot of um,
you know, competition and science and you know, trying to
be very protective and and get ahead because you know,
just like everybody else, we have careers that we're trying
(22:19):
to promote and move forward, and that's really a lot
of that has fallen by the wayside during the pandemic,
and the the level of collaboration has has been really
something to behold. And I think that the proof is
in the pudding the strides that we've made. I mean,
(22:42):
if if you just think about the vaccines alone, I mean,
it's it's really just an absolutely incredible scientific accomplishment. But
that's really just you know, the tip of the iceberg.
What we've learned in the last two and a half
years is absolutely mind blowing. And so when I think
about what comes next, I mean, there's there's always going
(23:06):
to be challenges. I really hope there's not going to
be another challenge of this magnitude in my lifetime, but
but who knows. But when I see how folks really
apply their expertise and come together to solve these problems,
and it makes me very hopeful that we'll be able
to deal with whatever comes next. Well, thank you so much,
(23:28):
Dr Jill Holland Beck for the important work that you
are doing and will continue to do. It makes such
a difference and I know you've made us a whole
lot smartyr today listening to you. Thank you so much,
Thank you so much for having me, and thanks for
your interest in this work. Appreciate it. It's amazing to
(23:50):
see how dedicated researchers like Dr Holland Beck are tackling
some of the world's most pressing challenges. Here are three
things things I took from that conversation. First, while COVID
has been a global plague, it's also brought about incredible
collaboration among scientists worldwide, and that has resulted in tremendous
(24:15):
progress against the disease in an incredibly short time. Second,
Dr Hollandback reminds us that good science requires a diversity
of viewpoints and backgrounds. As she says, different people bring
a different set of experiences to the table, and that
(24:36):
diversity is crucial as we train the next generation of scientists. Finally,
Dr Holland Back shows us how personally rewarding scientific research
can be. She says that working to solve problems like
COVID makes her feel a little bit less helpless in
(24:58):
the face of what we've all ex variant. Tune in
next time to hear about our next Featured Woman and
discover why she's one of Seneca's one hundred Women to Hear.
Seneca's one hundred Women to Hear is a collaboration between
the Seneca Women Podcast Network and I Heart Radio, with
(25:18):
support from founding partner PNG Have a Great Day,
I will say that I was a science nerd from
a very young age. I actually have sitting in my
office at work, tiny little child's microscope that I was
given as a gift when I was, you know, very
very young. And I was that kid. You know, if
I cut myself, I would run into my room and
(00:27):
put some of the blood on the slide and see.
I didn't know what I was looking at. I don't
think the microscope was even strong enough to really see anything,
but the interest was there. That was Dr Jill Holland Back,
an immuno geneticist at the University of California, San Francisco. Today,
that former self described science nerd leads research into one
(00:51):
of the mysteries of COVID, specifically why some people get
the disease but show no symptoms, and what that can
tell is about treating and preventing it. I'm a land
ververe In. This is Seneca's one Women to Hear. We
are bringing you one hundred of the world's most inspiring
(01:11):
and history making women you need to hear. For years,
Dr Hollandbach and her team at the Hollandbach Lab have
focused on a set of genes called h L A
and h l a's relationship to autoimmune diseases like multiple sclerosis.
But since the pandemic, the Hollandbach lab has turned its
(01:34):
attention to COVID as well. Their answer to the question
of symptomless COVID may lie in the genetic mutation of
h l A. Listen and learn why. Dr Jill Hollandbach
is one of Seneca's One Women to Hear. I'm speaking
(01:56):
today with immuno geneticist Dr Jill Holland and we're going
to discuss her research on COVID. Welcome, Dr Holland Beck.
It's really wonderful to have you with us. I know
our listeners are going to be very interested in this topic.
Thanks so much for having me. Now I understand your
leading research into who does and who does not get
(02:18):
COVID well, I first of all, I want to say
that we're really focused on people who have tested positive
for the virus that causes COVID but never had symptoms.
So for those who actually have had the COVID virus
but don't show any symptoms, why is that? Is it
(02:39):
a genetic mutation? We think so, not probably not everybody,
but in a proportion of the individuals that we've studied,
it seems that a specific version of an immune system
gene that we're interested in generally in my lab seems
to make them much more likely to be symptomatic. So
(03:02):
perhaps you can tell us more about precisely what you're
looking at in your research or their implications in terms
of genetic mutation. What can you tell us about what
you've learned? Sure, so my lab is generally interested in
a set of genes called h L A, human leukocide
(03:22):
anergen and I think a good way to think about
it is to think about the transplant settings. So when
we talk about matching for a transplant, these are the
genes that we match on. And in fact two UM
one major component of our study involved going back to
individuals who are registered as potential bone marrow downors and
(03:45):
asking them about their COVID experience, because we already have
data on the genes of interest for them. So h
L A or genes that encode important immune system molecules,
and the job of those molecules is to present or
show to UH your effect or cells, your T cells
(04:07):
in your immune system, pieces of foreign anigen or peptide,
pieces of protein. Is probably a better way to put
that better derived from things like viruses and bacteria, and
then the T cells come along and they inspect those
pieces of foreign protein and generate an immune response if
(04:29):
it's something that is not supposed to be there. So
the interesting thing about h l A is that they're
extremely variable between people, between populations. So most genes have
maybe one or a few different versions that we refer
(04:50):
to as a leal. H l A has literally thousands
and thousands of different versions that we see, you know,
across the globe, and that's why it can be so
hard to match somebody for a transplant, because one person's
h l A looks very different from another person's h
l A. So what we and and many others hypothesized,
(05:13):
you know, very early in the pandemic, was that different
versions of these genes, because they're so important in the
immune response to pathogens, might be important in differential response
to the virus that causes COVID nineteen and so we
went out to start looking for individuals who had tested positive.
(05:38):
Because the important thing in studies like this is that
it's very hard to control for exposure, so it's very
hard to ask the question does somebody who gets infected
and who doesn't. Because there's so many variables in whether
somebody is exposed to the virus, what kind of mitigation
you know, are they have, they've been masking, and things
(06:00):
like the humidity in the room at the time of exposure.
There's far too many variables for us to really say
for certain that somebody has or hasn't been exposed, or
that their lack of infection is due to something genetic.
But what the question that we can ask is, when
somebody has a confirmed infection, they've tested positive for the virus,
(06:26):
what does their disease course look like compared to the
person next to them? Because we know that there's a
huge range of disease course, everything from asymptomatic disease to
you know, extremely bad outcomes, people becoming hospitalized, ventilated, and
you know, we've had you know, tragic number of deaths,
and so what we want to know is what mediates that?
(06:51):
What you know, what is there something biological, Is there's
something genetic, No, is there's something about their h l
A that changes how somebody responds to the infection. And
a lot of the studies up to this point that
have been done thinking about not just h l A,
but genetics in general have really focused on the severe
outcome end of the spectrum. And there's really good reasons
(07:14):
to do that. You know, people have gotten really sick.
We want to understand why we want to prevent that.
Some of the reasons that those have been the patients
who have been focused on are practical because when people
are in the hospital, you're more you know, it's much
easier to get samples, biological samples like blood and DNA.
(07:39):
But really, you know, the vast majority of people who
experienced infection do not wind it in the hospital. They
have you know what we would term, you know, relatively
mild to moderate disease. And we were kind of interested
in those people, and specifically the subset of people who
just don't have symptoms at all, not a stuff, he knows,
(08:01):
not a scratchy throat, nothing, And so we asked that
question individuals who have in infected with the virus, did
you or did you not have symptoms? And what we
found was this extremely strong effect of a particular version
of one of the h l A genes called h
(08:22):
l A B that seems to really enhance somebody's chance
of not having symptoms when they're infected with the virus.
So fascinating, and can that be determined in advance for
somebody to know if they've got that makeup that they're
going to be symptomless. Well, first of all, I want
(08:43):
to be clear, just because you have this particular version
of this gene, so the gene is called h L
A B and and the version that we're interested in
is called h L A B fIF one doesn't mean
that you absolutely will be asymptomatic. It just means that
you're probably too to three times more likely to be asymptomatic.
So I think that it doesn't necessarily ensure that you
(09:08):
would be. I don't know that it would be particularly
helpful for somebody to know that it's UM. It's not
a test that's done commonly, unless somebody happens, for example,
to be a volunteer bone marrow donor they might know
their type. But I don't know that that would be
a particularly useful thing for somebody to know. I think
(09:28):
that you know. For me, it's more about what this
finding tells us about the immunopathology of the disease and
what kind of directions it can point us to. In
terms of possible vaccine design and possibly treatments. So this
is ongoing research as you keep probing and coming to
(09:52):
various conclusions along the way. Absolutely, So you know, after
this initial finding we went back to the lab. We've
since um and we're in the in the middle of
writing this up right now, so I'm hoping that this
paper will be released fairly soon. But went back into
the lab to understand first of all, can we detect
this in in other patient cohorts UM? And also you know,
(10:17):
what is the the actual um functional activity of T
cells in these individuals. So that's that's something that we've
been looking at carefully. And UM have some really interesting
new data on senecas one hundred women to hear. We'll
be back after the short break. You had a research
(10:49):
team called the Holland Buck Lab. Are there other scientific
questions besides those you've just been describing that you're looking
at as well trying to answer? Sure? So, my lab
at UCSF is broadly focused on immuno genetics in human
health and disease, So that mostly takes the form of
(11:09):
us thinking about these h l A genes and UM. So,
for example, one of the reasons that I'm in the
Department of Therology at UCSF is that a particular version
of h l A is also the most important predisposing
gene in multiple sclerosis. And we've examined a number of
(11:30):
neurological diseases from the point of view of this gene
system Parkinson's disease, my skinia gravis for example. So that's
ongoing work that we're focused on. We're very focused in
on multiple sclerosis in my lab, and we're also interested
in other common elements and and how different versions of
(11:53):
h l A predispose somebody or or protect them from
common illnesses as well as ubiquitous viruses like megalovirus. So
we're asking those questions all the time in the lab,
and that's really the main focus. And we were doing
that long before COVID, but you know, once the pandemic
(12:16):
came around, we absolutely refocused a lot of our energies,
as did so many others, to ask these questions well.
And they're so important obviously because they affect just so
many people who still don't have the answers they'd love
to have, right right I you know, I mean, on
the one hand, it feels like it's been a long time,
(12:37):
and and how are we still here? And why are
we still worrying about this? Nobody I don't think anticipated
this was going to go on for so long. But
you know, another way to look at it is there's
just been incredible, remarkable progress made in a very short
period of time. I'm completely blown away by, you know,
(12:59):
the amazing work that's been done all over the planet
trying to understand this disease. And it's really just been
an incredibly impressive scientific feat But I think that, you know,
people like me and and my colleagues are just incredibly
motivated because we're the same as everybody else. We've experienced
(13:19):
the pandemic the same as everybody else, right, And you know,
I first started putting together the project to look at
this like so many other people, sitting you know, in
my home office on lockdown. So I think there's you know,
a lot of motivation across biomedical science to answer these questions. Well.
(13:40):
And I think that's that's true about your mentioning MS
as well. So many people are afflicted with that absolutely, yeah,
And it's an extremely debilitating disease and impact you know,
people in the prime of their lives. So you know,
in general, this is just extreme, really gratifying work to do.
(14:02):
And you know, I feel like I've been really fortunate
to have been able to focus my my work life
on on solving these problems. It definitely helps me to
feel a little bit less helpless in the face of
what we've all experienced. Well, it's certainly critically important. Can
we talk about you a little bit you personally? I
(14:26):
know you're an you know, geneticist. What does that mean.
I mean, it's a big word, and I'm sure our
listeners are wondering what does she do or what does
that field represent? Sure, so it's really a sub field
of genetics. I trained as an immunologist. Um I did
my PhD in immunology at Berkeley, but I did my
(14:47):
training during that time in a genetics lab, and so
it's a sub field of genetics where we're focused specifically
on these very variable immune response genes. And it really
acquires an entirely different way of approaching genetics and thinking
about genetics because of the high levels of variation, but
(15:07):
also because it's so important to consider the structure and
the function of the immune molecules while we're thinking about
the genetic aspect. So it's a sub field that's generally
um focused on things like transplant and autoimmune diseases, but
it really has um kind of far reaching applications that
(15:32):
is certainly wonderfully rewarding. It sounds like to be able
to explore these areas. How did you get interested in
this field? Was it your upbringing? Was there a moment
when you really set to yourself, I want to be
a scientist. Yeah. I will say that I was a
science nerd from a very young age. I was interested
(15:55):
in scientific things as far back as I can remember.
I actually how of sitting in my office at work,
tiny little child's microscope that I was given as a
gift when I was, you know, very very young, and
I was that kid. You know, if I cut myself,
I would run into my room and put some of
(16:17):
the blood on the slide and see. I didn't know
what I was looking at. I don't think the microscope
was even strong enough to really see anything, But you know,
I was the interest was there. I used to you know,
graph the details from my doctor's appointments and things like that.
But you know, actually, when I was growing up, I
didn't really understand that being a scientist was a job.
(16:42):
I grew up in a you know, in a Jewish family,
where if you were interested in science, you became a doctor.
If you're interested letters, you became a lawyer. And those
were the only two options that were presented to me.
But you know, during the course of my education, I
really kind of fell in love with immunology. That was
(17:03):
during a period of time when I was working on
my master's degree in public health. At the time, I
had actually been interested in going into women's health and
health policy. I had gone to work for Planned Parenthood
straight out of college. UM, but I got a little
bit sidetracked and fell in love with immunology. And then
during the course of my PhD, I was particularly interested
(17:26):
in h l A because my mother had rheumatoid arthritis
and h l A is very important in autoimmune disease
and including room toid arthritis, and that kind of sparked
my interest and had an opportunity to work in a
lab that was focused on these genes. And it's um,
it's been quite a long time. The rest is history.
(17:48):
Here I still am doing important work. Did your parents
nurture your interest as a child in science or were
there mentors along the way who inspired you. I think
you know, my parents, Um, my father was was a
c P A my you know, my mom had been
an English teacher. They were not really stem people, so um,
(18:12):
you know, they encouraged me, of course, but I think,
you know, to be honest, you know, to the day
my dad died, he used to variably describe me as
a microbiologist. You know what of this that he never
you know, he tried but didn't really understand what I
was doing. But I certainly, you know, I had some
(18:34):
great teachers along the way. I had a physiology teacher
when I was in high school who really sparked my
love for that topic, and I went on to become
a physiology major at Berkeley. And then some you know,
really key professors during during my time at Berkeley's so um, yeah,
some great mentors along the way, and um peers and
(18:57):
colleagues as well who have been extraored, early supportive through
the years. Well, here at Seneca women we often emphasize
how important it is to have women in science, and
we still have to do better in that respect. I
think you agree as a general proposition, but I wonder
what you think about why having a women's perspective is
(19:19):
important in your field if it is, well, I guess
what I would say is, I don't know that as
a woman, I necessarily have a different perspective, at least
not on the science necessarily. But you know what, as
a professor at a research and university, part of my
job is to train the next generation of scientists, and
(19:40):
I think that that's where, you know, having representation is
really just so important. I think that, um, you know,
we bring to the table a different set of life experiences, UM,
A different way of having experienced the world and moved
through the world, and that is really, um I think
(20:05):
an asset when we're training not just you know, the
next generation of women's scientists, but the entire next generation
of scientists. I think that having that different perspective on
you know, life and and life experiences is extremely important
and helpful, UM as as we train young scientists. Well,
(20:29):
I always hate this moment looking at the clock when
we're nearing the end of a fascinating conversation, but I
really would like to ask you before we have to
take leave. You know, given that we've all collectively gone
through a couple of years now of the epidemic. We've
been talking about COVID, We've been talking about other viruses.
(20:51):
Certainly there are more on the horizon we haven't named
or don't know anything about because there yet at the
development stage, probably, But given all that, what makes you optimistic?
What gives you hope? Because this is tough stuff, it is.
But you know, as I said earlier, I realized it
feels like it's it's been a long time, and that
(21:13):
it's been you know, one step forward, two steps back
through the pandemic. But you know, from where I sat,
I'm just absolutely marveling at the progress that we've made.
And it's really been an incredible experience to be in
(21:35):
the middle of these research efforts and to look around
me and see my colleagues at UCSF and across the
country and across the world who have really come together
in I think a unprecedented way. And I'll say that
the levels of collegiality and collaboration that I've experienced, you know,
(21:59):
particularly working on this topic, have just been so heartening.
Um I think that there's often a lot of um,
you know, competition and science and you know, trying to
be very protective and and get ahead because you know,
just like everybody else, we have careers that we're trying
(22:19):
to promote and move forward, and that's really a lot
of that has fallen by the wayside during the pandemic,
and the the level of collaboration has has been really
something to behold. And I think that the proof is
in the pudding the strides that we've made. I mean,
(22:42):
if if you just think about the vaccines alone, I mean,
it's it's really just an absolutely incredible scientific accomplishment. But
that's really just you know, the tip of the iceberg.
What we've learned in the last two and a half
years is absolutely mind blowing. And so when I think
about what comes next, I mean, there's there's always going
(23:06):
to be challenges. I really hope there's not going to
be another challenge of this magnitude in my lifetime, but
but who knows. But when I see how folks really
apply their expertise and come together to solve these problems,
and it makes me very hopeful that we'll be able
to deal with whatever comes next. Well, thank you so much,
(23:28):
Dr Jill Holland Beck for the important work that you
are doing and will continue to do. It makes such
a difference and I know you've made us a whole
lot smartyr today listening to you. Thank you so much,
Thank you so much for having me, and thanks for
your interest in this work. Appreciate it. It's amazing to
(23:50):
see how dedicated researchers like Dr Holland Beck are tackling
some of the world's most pressing challenges. Here are three
things things I took from that conversation. First, while COVID
has been a global plague, it's also brought about incredible
collaboration among scientists worldwide, and that has resulted in tremendous
(24:15):
progress against the disease in an incredibly short time. Second,
Dr Hollandback reminds us that good science requires a diversity
of viewpoints and backgrounds. As she says, different people bring
a different set of experiences to the table, and that
(24:36):
diversity is crucial as we train the next generation of scientists. Finally,
Dr Holland Back shows us how personally rewarding scientific research
can be. She says that working to solve problems like
COVID makes her feel a little bit less helpless in
(24:58):
the face of what we've all ex variant. Tune in
next time to hear about our next Featured Woman and
discover why she's one of Seneca's one hundred Women to Hear.
Seneca's one hundred Women to Hear is a collaboration between
the Seneca Women Podcast Network and I Heart Radio, with
(25:18):
support from founding partner PNG Have a Great Day,
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