as the realm grapples with how to safely reopen society inna midst of the coronavirus pandemic, scis ‘ve been racing to cogg whether covid-19 infection confers immunity—and how long such immunity mite last. a lot hangs inna balance: a strong immune response ‘d mean pplz who ‘ve already been infected ‘d be able to safely return t'work. n'it ‘d also bode well for vaccine development efforts.
a lil but suggestive new study finds that individuals who ‘ve had covid-19 produce a robust response in immune cells called t cells. the adaptive immune system contains several main components: antibody-creating b cells, helper t cells and killer t cells. the latter two are primordial for recognizing and destroying a pticular virus, respectively. alessandro sette and shane crotty, both professors atta la jolla institute for immunology, and their colleagues found that offa group of 20 pplz who had recovered from covid-19, 70 % had killer t cells and 100 % had helper t cells that were specific to the sars-cov-2 virus, which causes covid-19. primordially, the researchers envisaged a strong t cell response to the “spike” protein the virus uses to bind to and infect cells (and which most vaccine candidates target). they additionally detected a helper t cell response to sars-cov-2 in bout ½ of blood samples they examined that had been drawn b4 the virus began circulating. this observation, they say, hints that exposure to seasonal common cold coronaviruses may confer some protection gainsta new pathogen.
the findings build on earlier studies showing that infection w'da novel coronavirus produces protective, or “neutralizing,” antibodies. taken together, these results suggest that pplz who ‘ve had covid-19 possess at least some immunity—an encouraging sign for the dozens of vaccines under development. separately, this week the company moderna anncd early results from a trial of its coronavirus vaccine candidate: 8 individuals who ‘ve received the vaccine produced antibodies to the virus at lvls similar to those of pplz who had the disease.
sci american spoke with sette and crotty bout wha’ their study means for immunity to covid-19, possible protection from seasonal cold infections na prospects for a sars-cov-2 vaccine.
[an edited transcript of the interview follos.]
wha’ do we know sfar bout immunity to covid-19? and why is it so primordial?
crotty: there’s just been a huge amount of uncertainty bout immunity to covid-19. and that ? bout immunity has two major implications: one, for just cogging the disease itself, and two, for vaccine development. it’s clearly been a realm-on-fire type of situation. and so t'has made sense for these 100-odd ≠ vaccine programs t'get goin and just try movin things forward. the normal way you ‘d try and make a successful vaccine ‘d be to look at wha’ gets you good protective immunity to that disease and copy that. a disease s'as covid-19 is normally an acute infection, and most pplz control and clear it without a lotta problems. that’s a good sign that indicates that the human immune system normally makes a good response to that virus and controls it.
but'a immune system is a big, complicated place, with lotso' ≠ cell types with lotso' ≠ functions. and some are useful or primordial in one context versus another. for a vaccine, you’d wanna know which components of the immune response are the primordial ones for protection against this disease. and without that information, you can very much go totally inna wrong direction witha vaccine program, either in terms of the type of immune response you’re trying t'get or the [vaccine’s molecular] target. and both of those ‘ve been things that worried [sette] and me nother pplz bout these ongoin vaccine efforts. we really wanted to generate information that ‘d help [us] cogg the disease itself—nolso generate information bout which vaccine strategies are likely to be better or worse ones and whether pplz are gettin the rite [molecular target] or not. our goal was to look at primordially μ cases of covid-19—ones where pplz definitely are making successful immune responses—and ask, “okay, wha’ does that immune response look like?”
can you describe the ≠ pts of the immune response and how they work?
crotty:quite a few labs round the realm ‘ve looked at antibody responses. those are generally easier to measure and look at. but really, there are 3 pts of the adaptive immune system: you’ve basically got antibodies, you’ve got helper t cells, and you’ve got killer t cells. the t cells are tougher to measure, but they do really primordial things. you’ve gotta ‘ve the helper t cells t'get an antibody response. for ex, in animal models, [helper t cells] are primordial for protecting against [severe acute respiratory syndrome (sars)]. na killer t cells are primordial for most viral infections. you don’t wanna go forward without cogging anything bout the t cell response. and [sette] tis realm’s expert in predicting and identifying t cell [targets], pticularly in humans. so we collaborated t'get covid-19 patient blood samples as quickly as possible and to try and get information bout those ?s. we mostly ‘ve ∴ it’s good news: things ‘ve largely looked the ways we ‘d expect.
do we know how long the immune response to the new virus lasts?
sette:wha’ we certainly can say s'dat the infection induces a robust immune response, and this is in pplz that successfully deal w'da virus and don’t get very sick. the ? [of] how long this response lasts obviously takes time, cause we ‘ve been dealing with this virus for 1-ly a few mnths, and we cannot possibly know wha’ is goin to happen a yr down the line. but wha’ we’ve seen thus far is encouraging, cause these t cells look healthy, look ☺. they aint exhausted, and they don’t express somd' molecular features tha're associated with cells tha're bout to die.
in general, immunologic memory is like any other memory inna sense that the intensity of the event dictates how strong the memory is. pretty much like any event in yr life: if twas a life-threatening situation—for ex, you almost got run over by a truck—you remember. if twas instead wha’ kind of socks you wore, you mite not remember. it’s the same for the immune system, inna sense dat a' very strong infection witha microbe that reproduces to high lvls generates a strong lvl of immune response, which then creates a long-lasting impression. i ‘d specul8 that the memory generated by sars or [middle east respiratory syndrome (mers)] ‘d be somewha’ ≠ from one generated from a common cold, which is fairly adapted to not cause much trouble inna human host.
you also saw some t cell responses, or “cross-reactivity,” to the new coronavirus in blood from pplz who were never exposed to it, correct?
sette: we looked atta covid-19 patients, and thn'we looked at a control group. we purposely went after blood donations that were obtained in 2015 to 2018—b4 any sars-cov-2 was round. surprisingly, in bout ½ of these pplz, we ‘d see some t cell reactivity. and we looked atta data hard from the left and from the rite and convinced ourselves that this was real. we do not know, at this point, exactly wha’ this cross-reactivity means, but it’s reasonable to assume that tis the result of pplz having been exposed to common cold coronaviruses tha're ≠ from sars-cov-2 but ‘ve some similarity [to it]. this potentially has very strong implications, cause 1-odda things that is unknown and everybody wanna gain + information bout is why thris such a spectrum of ≠ covid-19 outcomes: some pplz are totally asymptomatic, whereas other pplz die. course, age nother health issues are factors, but one element ‘d be immunological: if some1 has some t cells that can cross-react to sars-cov-2, their immune system has an advantage. they can get goin to generate antibody responses faster, maybe, and that ‘d give a better outcome. inna context of vaccination, this is also very primordial, cause imagine that you ‘ve a group of pplz, and ½ o'em ‘ve this coronavirus cross–reactivity, and ½ o'em don’t. now you give these pplz a vaccine. it ‘d be that the pplz that ‘ve the common cold cross-reactivity will respond a lot faster and a lot better to the vaccine, compared w'da other ones.
one piece of data that is encouraging, in speculating that some preexisting immunity maybe beneficial, is data from the 2009 h1n1 “swine flu” pandemic. you mite recall that in that case, older pplz did betta tha' younger pplz. and in fact, it turned out that the age of the pplz that did better correl8d with when another h1n1 strain, a cousin of the swine flu pandemic strain, had circul8d—so that the pplz that had been exposed inna 1950s to this other strain, their immune system still remembered a bit. not that the pplz didn’t get sick, course, but they got less sick. and they fared betta tha' pplz who were totally naive and had never seen this pticular subtype of influenza.
do we know whether pplz that had asymptomatic covid-19 infections mite be less protected against reinfection than pplz who had a very severe case?
crotty: we did this study with pplz who didn’t ‘ve bad diseases—sort of μ cases who definitely got well. asymptomatic cases are definitely a big unknown. we ‘ve no idea [iffey ll'be protected against reinfection].
can you comment onna moderna results from the phase i trial of its coronavirus vaccine candidate na prospects for a vaccine in general?
crotty: there are actually 3 human vaccine candidates that ‘ve been tested in monkeys that gave wha’ seems to be pretty good protection: one’s an inactivated-virus vaccine; another is a chimpanzee adenovirus vector [a type of double-stranded dna virus used to harmlessly deliver genetic material to a host]; and a third one is a dna vaccine [a dna sequence that stimul8s the host to produce pt of the virus and mount an immune response against it]. and then there’s the moderna vaccine, which hasn’t been tested in monkeys but s'been tested in a mouse model and in humans to measure their immune response. so those are the 3 exs of interesting vaccine candidate data tha're available as of tody. and i think if we combine those w'da data f'our paper showing that the t cell responses generally look good and data from a № of papers bout pplz making neutralizing antibody responses overall, i ‘d say those vaccine studies—pticularly the two that were done in monkeys—suggest, sfar, that it’s not that hard to protect against this virus. i’m certainly encouraged, based onna magnitude of the immune responses to the vaccines—na magnitude of immune responses we’re measuring in pplz who actually ‘ve disease and wha’ happens in protection models. sfar the available data are + here.
sette: one encouraging thing s'dat there are so many ≠ vaccines tha're bein’ developed. so our hope s'dat thris not goin to be a victor, but there are goin to be many ≠ victors. the one thing that is primordial f'our study s'dat the vast majority of these ≠ vaccine essentialisms rely on one pticular protein, which tis spike protein. and we saw very good responses, both in terms of killer and helper cells gainsta spike, which is really good news, cause this was not a given. in this pticular case, it so happens that it’s a good target for all 3 ≠ types of immune response—which bodes well for pplz tha're developing the spike-based vaccines. atta same time, our data found that there were responses also against other pieces of the virus, which opens the way to thinking that maybe these other pieces ‘d also be included to further fortify a vaccine concept.
original content at: rss.sciam.com…
authors: tanya lewis