I've been thinking for this for a while. It seems there's no ethical experiment to perform to check if immunity is actually developed (the obvious experiment would be to expose someone that have recovered from the infection, but that's unethical).
My idea is that lack of immunity would eventually result in observation of reinfected subjects and one should be able to estimate the likelyhood of that. An experiment would for example be that if we study a set of subjects over time and at one time 1% are infected and later when these have recovered we at a later time find that 1% are infected then perhaps 1% of these would be expected to be among those that were infected the first time (unless immunity has developed).
How did we realize that we get immune to measles, chickenpox and mumps for example?
Protective immunity against SARS-CoV-2 could last eight months or more
New data suggest that nearly all COVID-19 survivors have the immune cells necessary to fight re-infection.
The findings, based on analyses of blood samples from 188 COVID-19 patients, suggest that responses to the novel coronavirus, SARS-CoV-2, from all major players in the "adaptive" immune system, which learns to fight specific pathogens, can last for at least eight months after the onset of symptoms from the initial infection.
"Our data suggest that the immune response is there -- and it stays," LJI Professor Alessandro Sette, Dr. Biol. Sci., who co-led the study with LJI Professor Shane Crotty, Ph.D., and LJI Research Assistant Professor Daniela Weiskopf, Ph.D.
"We measured antibodies, memory B cells, helper T cells and killer T cells all at the same time," says Crotty. "As far as we know, this is the largest study ever, for any acute infection, that has measured all four of those components of immune memory."
The findings, published in the January 6, 2021, online edition of Science, could mean that COVID-19 survivors have protective immunity against serious disease from the SARS-CoV-2 virus for months, perhaps years after infection.
The new study helps clarify some concerning COVID-19 data from other labs, which showed a dramatic drop-off of COVID-fighting antibodies in the months following infection. Some feared that this decline in antibodies meant that the body wouldn't be equipped to defend itself against reinfection.
Sette explains that a decline in antibodies is very normal. "Of course, the immune response decreases over time to a certain extent, but that's normal. That's what immune responses do. They have a first phase of ramping up, and after that fantastic expansion, eventually the immune response contracts somewhat and gets to a steady state," Sette says.
The researchers found that virus-specific antibodies do persist in the bloodstream months after infection. Importantly the body also has immune cells called memory B cells at the ready. If a person encounters SARS-CoV-2 again, these memory B cells could reactivate and produce SARS-CoV-2 antibodies to fight re-infection.
The SARS-CoV-2 virus uses its "spike" protein to initiate infection of human cells, so the researchers looked for memory B cells specific for the SARS-CoV-2 spike. They found that spike-specific memory B cells actually increased in the blood six months after infection.
COVID-19 survivors also had an army of T cells ready to fight reinfection. Memory CD4+ "helper" T cells lingered, ready to trigger an immune response if they saw SARS-CoV-2 again. Many memory CB8+ "killer" T cells also remained, ready to destroy infected cells and halt a reinfection.
The different parts of the adaptive immune system work together, so seeing COVID-fighting antibodies, memory B cells, memory CD4+ T cells and memory CD8+ T cells in the blood more than eight months following infection is a good sign.
"This implies that there's a good chance people would have protective immunity, at least against serious disease, for that period of time, and probably well beyond that," says Crotty.
The team cautions that protective immunity does vary dramatically from person to person. In fact, the researchers saw a 100-fold range in the magnitude of immune memory. People with a weak immune memory may be vulnerable to a case of recurrent COVID-19 in the future, or they may be more likely to infect others.
"There are some people that are way down at the bottom of how much immune memory they have, and maybe those people are a lot more susceptible to reinfection," says Crotty.
"It looks like people who have been infected are going to have some degree of protective immunity against re-infection," adds Weiskopf. "How much protection remains to be established."
The fact that immune memory against SARS-CoV-2 is possible is also a good sign for vaccine developers. Weiskopf emphasizes that the study tracked responses to natural SARS-CoV-2 infection, not immune memory after vaccination.
"It is possible that immune memory will be similarly long lasting similar following vaccination, but we will have to wait until the data come in to be able to tell for sure," says Weiskopf. "Several months ago, our studies showed that natural infection induced a strong response, and this study now shows that the responses lasts. The vaccine studies are at the initial stages, and so far have been associated with strong protection. We are hopeful that a similar pattern of responses lasting over time will also emerge for the vaccine-induced responses."
The researchers will continue to analyze samples from COVID-19 patients in the coming months and hope to track their responses 12 to 18 months after the onset of symptoms.
"We are also doing very detailed analyses at a much, much higher granularity on what pieces of the virus are recognized," says Sette. "And we plan to evaluate the immune response not only following natural infection but following vaccination."
The team is also working to understand how immune memory differs across people of different ages and how that may influence COVID-19 case severity.
The study, "Immunological memory to SARS-CoV-2 assessed for up to eight months after infection," included first authors Jennifer M. Dan, Jose Mateus and Yu Kato, as well as Kathryn M. Hastie, Caterina E. Faliti, Sydney I. Ramirez, April Frazier, Esther Dawen Yu, Alba Grifoni, Stephen A. Rawlings, Bjoern Peters, Florian Krammer, Viviana Simon, Erica Ollmann Saphire and Davey M. Smith.
This research was supported by the National Institutes of Health's National Institute for Allergy and Infectious Disease (awards AI142742 and AI135078, contracts 75N9301900065 and HHSN272201400008C), the John and Mary Tu Foundation, UCSD T32s AI007036 and AI007384 Infectious Diseases Division, the Bill and Melinda Gates Foundation INV-006133 from the Therapeutics Accelerator, Mastercard, Wellcome, a FastGrant from Emergent Ventures in aid of COVID-19 research, the Collaborative Influenza Vaccine Innovation Centers (CIVIC) contract 75N93019C00051, the JPB foundation, the Cohen Foundation, the Open Philanthropy Project (#2020-215611), as well as private philanthropic contributions.
Types of Immunity
Immunity, in its simplest terms, is the body's ability to resist infections. This is mediated not only by white blood cells that are central to the innate immune response—the body's in-born defense—but also antibodies that make up the adaptive (aka acquired) immune response. The innate and adaptive immune responses are each made up of complicated networks of cells that work with each other to provide immune defenses.
The innate immune system recognizes many pathogens, but does not learn to adapt to new ones over a lifetime. On the other hand, the adaptive immune system, which is largely composed of B-cells and certain types of T-cells, learns from and responds to new challenges, and retains a memory of those challenges in later life.
Adaptive immunity can develop in one of two ways:
- When you are infected by an infectious agent like COVID-19, during which the immune system will respond in a way that is tailor-made to that attacker and usually that attacker alone. This can include antibodies (made by B-cells) or by T-cell mediated immune responses.
- When you are vaccinated, during which compounds are introduced into the body to stimulate a specific immune response to the disease specific to that vaccine. That immune response can last for months, years, or a lifetime long, depending on the vaccine type and a person's response to it.
With vaccines, the level of immune protection can vary as can the goals of vaccination. Some vaccines offer sterilizing immunity, in which a disease-causing pathogen is completely unable to replicate. Vaccines developed for the human papillomavirus (HPV) are one such example where viral replication is completely blocked in most vaccinated humans.
In other instances, a vaccine can offer effective (or practical) immunity, in which the vaccine can greatly reduce the risk of infection but may not prevent asymptomatic infection. So, while the risk of illness is greatly reduced, a person can still be a carrier and able to spread the virus.
The seasonal flu vaccine, which is 40% to 50% effective in preventing infection, is an example where people who get the vaccine get the flu less often, get fewer symptoms and are less likely to transmit it to others. The current COVID-19 vaccines may fall into the same category, albeit at a far higher level of effectiveness.
As effective as the Pfizer-BioNTech and Moderna vaccines are in preventing illness, we don't know yet if they will entirely erase the risk of infection or further transmission of the virus.
Researchers Identify Targets for Effective Immune Responses to SARS-CoV-2 Coronavirus
Scientists from La Jolla Institute for Immunology, the J. Craig Venter Institute and the University of California, San Diego used existing data from known coronaviruses to predict which parts of SARS-CoV-2, a novel coronavirus that causes the respiratory illness COVID-19, are capable of activating the human immune system.
Existing data from known coronaviruses can be used to predict which parts of SARS-CoV-2 are capable of activating the human immune system. Image credit: Grifoni et al.
When the immune system encounters a bacterium or a virus, it zeroes in on tiny molecular features, so called epitopes, which allow cells of the immune system to distinguish between closely related foreign invaders and focus their attack.
Having a complete map of viral epitopes and their immunogenicity is critical to researchers attempting to design new or improved vaccines to protect against COVID-19.
“Right now, we have limited information about which pieces of the virus elicit a solid human response,” said La Jolla Institute for Immunology’s Professor Alessandro Sette, lead author of the study.
“Knowing the immunogenicity of certain viral regions, or in other words, which parts of the virus the immune system reacts to and how strongly, is of immediate relevance for the design of promising vaccine candidates and their evaluation.”
While scientists currently know very little about how the human immune system responds to SARS-CoV-2, the immune response to other coronaviruses has been studied and a significant amount of epitope data is available.
Four other coronaviruses are currently circulating in the human population. They cause generally mild symptoms and together they are responsible for an estimated one quarter of all seasonal colds.
But every few years, a new coronavirus emerges that causes severe disease as was the case with SARS-CoV in 2003 and MERS-CoV in 2008, and now SARS-CoV-2.
“SARS-CoV-2 is most closely related to SARS-CoV, which also happens to be the best characterized coronavirus in terms of epitopes,” said first author Dr. Alba Grifoni, also from La Jolla Institute for Immunology.
For the study, the researchers used available data from the Immune Epitope Database (IEDB), which contains over 600,000 known epitopes from some 3,600 different species, and the Virus Pathogen Resource (ViPR), a complementary repository of information about pathogenic viruses.
They compiled known epitopes from SARS-CoV and mapped the corresponding regions to SARS-CoV-2.
“We were able to map back 10 B cell epitopes to the new coronavirus and because of the overall high sequence similarity between SARS-CoV and SARS-CoV-2, there is a high likelihood that the same regions that are immunodominant in SARS-CoV are also dominant in SARS-CoV-2 is,” Dr. Grifoni said.
Five of these regions were found in the spike glycoprotein, which forms the ‘crown’ on the surface of the virus that gave coronaviruses their name two in the membrane protein, which is embedded in the membrane that envelopes the protective protein shell around the viral genome and three in the nucleoprotein, which forms the shell.
In a similar analysis, T cell epitopes were also mostly associated with the spike glycoprotein and nucleoprotein.
In a completely different approach, the team used the epitope prediction algorithm hosted by the IEDB to predict linear B cell epitopes.
In a recent study, University of Texas at Austin’s Dr. Jason McLellan and colleagues determined the 3D structure of the spike proteins, which allowed the authors of the new study to take the protein’s spatial architecture into account when predicting epitopes. This approach confirmed two of the likely epitope regions they had predicted earlier.
To substantiate the SARS-CoV-2 T cell epitopes identified based on their homology to SARS-CoV, the scientists compared them with epitopes pinpointed by the Tepitool resource in the IEDB.
Using this approach, they were able verify 12 out of 17 SARS-CoV-2 T cell epitopes identified based on sequence similarities to SARS-CoV.
“The fact that we found that many B and T cell epitopes are highly conserved between SARS-CoV and SARS-CoV-2 provides a great starting point for vaccine development,” Professor Sette said.
“Vaccine strategies that specifically target these regions could generate immunity that’s not only cross-protective but also relatively resistant to ongoing virus evolution.”
Grifoni, A. et al. Cell 181, 1489–1501.e15 (2020).
Sekine, T. et al. Cell 183, 158–168.e14 (2020).
Rydyznski Moderbacher, C. et al. Cell 183, 996–1012.e19 (2020).
Braun, J. et al. Nature 587, 270–274 (2020).
Dan, J. M. et al. Science 371, eabf4063 (2021).
Sattler, A. et al. J. Clin. Invest. 130, 6477–6489 (2020).
Hansen, C. H., Michlmayr, D., Gubbels, S. M., Mølbak, K. & Ethelberg, S. Lancet https://doi.org/10.1016/S0140-6736(21)00575-4 (2021).
Locci, M. et al. Immunity 39, 758–769 (2013).
Scientists uncover SARS-CoV-2-specific T cell immunity in recovered COVID-19 and SARS patients
The T cells, along with antibodies, are an integral part of the human immune response against viral infections due to their ability to directly target and kill infected cells. A Singapore study has uncovered the presence of virus-specific T cell immunity in people who recovered from COVID-19 and SARS, as well as some healthy study subjects who had never been infected by either virus.
The study by scientists from Duke-NUS Medical School, in close collaboration with the National University of Singapore's (NUS) Yong Loo Lin School of Medicine, (YLLSM), Singapore General Hospital (SGH) and National Centre for Infectious Diseases (NCID) was published in Nature. The findings suggest infection and exposure to coronaviruses induces long-lasting memory T cells, which could help in the management of the current pandemic and in vaccine development against COVID-19.
The team tested subjects who recovered from COVID-19 and found the presence of SARS-CoV-2-specific T cells in all of them, which suggests that T cells play an important role in this infection. Importantly, the team showed that patients who recovered from SARS 17 years ago after the 2003 outbreak, still possess virus-specific memory T cells and displayed cross-immunity to SARS-CoV-2.
"Our team also tested uninfected healthy individuals and found SARS-CoV-2-specific T cells in more than 50 percent of them. This could be due to cross-reactive immunity obtained from exposure to other coronaviruses, such as those causing the common cold, or presently unknown animal coronaviruses. It is important to understand if this could explain why some individuals are able to better control the infection," said Professor Antonio Bertoletti, from Duke-NUS' Emerging Infectious Diseases (EID) programme, who is the corresponding author of this study.
Associate Professor Tan Yee Joo from the Department of Microbiology and Immunology at NUS Yong Loo Lin School of Medicine and Joint Senior Principal Investigator, Institute of Molecular and Cell Biology, A*STAR added, "We have also initiated follow-up studies on the COVID-19 recovered patients, to determine if their immunity as shown in their T cells persists over an extended period of time. This is very important for vaccine development and to answer the question about reinfection."
"While there have been many studies about SARS-CoV-2, there is still a lot we don't understand about the virus yet. What we do know is that T cells play an important role in the immune response against viral infections and should be assessed for their role in combating SARS-CoV-2, which has affected many people worldwide. Hopefully, our discovery will bring us a step closer to creating an effective vaccine," said Associate Professor Jenny Low, Senior Consultant, Department of Infectious Diseases, SGH, and Duke-NUS' EID programme.
"NCID was heartened by the tremendous support we received from many previous SARS patients for this study. Their contributions, 17 years after they were originally infected, helped us understand mechanisms for lasting immunity to SARS-like viruses, and their implications for developing better vaccines against COVID-19 and related viruses," said Dr Mark Chen I-Cheng, Head of the NCID Research Office.
The team will be conducting a larger study of exposed, uninfected subjects to examine whether T cells can protect against COVID-19 infection or alter the course of infection. They will also be exploring the potential therapeutic use of SARS-CoV-2-specific T cells.
SARS-CoV-2 jumped from bats to humans without much change
Schematic of our proposed evolutionary history of the nCoV clade and putative events leading to the emergence of SARS-CoV-2. Credit: MacLean OA, et al. (2021), Natural selection in the evolution of SARS-CoV-2 in bats created a generalist virus and highly capable human pathogen. PLoS Biol 19(3): e3001115. CC-BY
How much did SARS-CoV-2 need to change in order to adapt to its new human host? In a research article published in the open access journal PLOS Biology Oscar MacLean, Spyros Lytras at the University of Glasgow, and colleagues, show that since December 2019 and for the first 11 months of the SARS-CoV-2 pandemic there has been very little 'important' genetic change observed in the hundreds of thousands of sequenced virus genomes.
The study is a collaboration between researchers in the UK, US and Belgium. The lead authors Prof David L Robertson (at the MRC-University of Glasgow Centre for Virus Research, Scotland) and Prof Sergei Pond (at the Institute for Genomics and Evolutionary Medicine, Temple University, Philadelphia) were able to turn their experience of analysing data from HIV and other viruses to SARS-CoV-2. Pond's state-of-the-art analytical framework, HyPhy, was instrumental in teasing out the signatures of evolution embedded in the virus genomes and rests on decades of theoretical knowledge on molecular evolutionary processes.
First author Dr. Oscar MacLean explains, "This does not mean no changes have occurred, mutations of no evolutionary significance accumulate and 'surf' along the millions of transmission events, like they do in all viruses." Some changes can have an effect for example, the Spike replacement D614G which has been found to enhance transmissibility and certain other tweaks of virus biology scattered over its genome. On the whole, though, 'neutral' evolutionary processes have dominated. MacLean adds, "This stasis can be attributed to the highly susceptible nature of the human population to this new pathogen, with limited pressure from population immunity, and lack of containment, leading to exponential growth making almost every virus a winner."
Pond comments, "what's been so surprising is just how transmissible SARS-CoV-2 has been from the outset. Usually viruses that jump to a new host species take some time to acquire adaptations to be as capable as SARS-CoV-2 at spreading, and most never make it past that stage, resulting in dead-end spillovers or localised outbreaks."
Studying the mutational processes of SARS-CoV-2 and related sarbecoviruses (the group of viruses SARS-CoV-2 belongs to from bats and pangolins), the authors find evidence of fairly significant change, but all before the emergence of SARS-CoV-2 in humans. This means that the 'generalist' nature of many coronaviruses and their apparent facility to jump between hosts, imbued SARS-CoV-2 with ready-made ability to infect humans and other mammals, but those properties most have probably evolved in bats prior to spillover to humans.
Joint first author and Ph.D. student Spyros Lytras adds, "Interestingly, one of the closer bat viruses, RmYN02, has an intriguing genome structure made up of both SARS-CoV-2-like and bat-virus-like segments. Its genetic material carries both distinct composition signatures (associated with the action of host anti-viral immunity), supporting this change of evolutionary pace occurred in bats without the need for an intermediate animal species."
Robertson comments, "the reason for the 'shifting of gears' of SARS-CoV-2 in terms of its increased rate of evolution at the end of 2020, associated with more heavily mutated lineages, is because the immunological profile of the human population has changed." The virus towards the end of 2020 was increasingly coming into contact with existing host immunity as numbers of previously infected people are now high. This will select for variants that can dodge some of the host response. Coupled with the evasion of immunity in longer-term infections in chronic cases (e.g., in immunocompromised patients), these new selective pressures are increasing the number of important virus mutants.
It's important to appreciate SARS-CoV-2 still remains an acute virus, cleared by the immune response in the vast majority of infections. However, it's now moving away faster from the January 2020 variant used in all of the current vaccines to raise protective immunity. The current vaccines will continue to work against most of the circulating variants but the more time that passes, and the bigger the differential between vaccinated and not-vaccinated numbers of people, the more opportunity there will be for vaccine escape. Robertson adds, "The first race was to develop a vaccine. The race now is to get the global population vaccinated as quickly as possible."
The immune response to coronavirus
When a virus attacks its first cell in the body, that cell has two jobs to do before it dies, said Benjamin tenOever, a professor of biology at the Mount Sinai Icahn School of Medicine. The infected cell needs to issue a call for reinforcements, sending out a cascade of chemical signals that will activate an army of immune cells to come battle the invading virus. And it needs to issue a warning to other cells around it to fortify themselves, something it does by releasing proteins called interferons. When interferons land on neighboring cells, they trigger those cells to enter defensive mode. The cells slow down their metabolism, stop the transport of proteins and other molecules around their interiors, and slow down transcription, the process by which genetic instructions become proteins and other molecules. (Transcription is the process that viruses hijack to make more of themselves.)
In a study accepted to the journal Cell, tenOever and his colleagues found that SARS-CoV-2 appears to block this interferon signal, meaning it messes with the cell's second job. So the first job &mdash the call for immune system reinforcement &mdash works just fine, but the cells in the lungs don't enter defensive mode and so remain vulnerable to viral infection.
"It just keeps replicating in your lungs, and replicating in your lungs and all the while you keep calling in for more reinforcements," tenOever told Live Science.
In many people, even this crippled immune response is enough to beat back the virus. But for reasons not yet fully understood, some people enter a vicious cycle. As the virus keeps replicating, the immune army that arrives to battle it starts doing its job: attacking infected cells, digesting debris and chemicals spewed out by dying cells, even killing nearby cells in an attempt to staunch the damage. Unfortunately, if the virus continues to penetrate lung cells, this army may do more damage than good. The lung tissue becomes hopelessly inflamed the blood vessels begin to leak fluids into the lung and the patient begins to drown on dry land. This seems to be the reason that some people become severely ill a couple of weeks after their initial infections, tenOever said.
"At that point, it's not about what the virus has done," he said. "At that point, it's about controlling the severe inflammation."
This cycle is very bad news. But there is a glimmer of hope in the findings. Because the system that calls in the army of immune cells works fine, it seems likely that survivors of COVID-19 will retain immunity to the virus. And indeed, studies have found high levels of antibodies to SARS-CoV-2 in recently recovered patients. Antibodies are proteins made by immune system cells called B cells. They stick around in the blood post-infection and can bind to the virus, either neutralizing it directly or marking it for destruction by other immune cells.
For example, a study led by researcher Chen Dong of the Institute for Immunology and the School of Medicine at Tsinghua University in Beijing analyzed the blood of 14 COVID-19 patients who had experienced relatively mild COVID-19 symptoms 14 days after discharge from the hospital. They found that 13 of them showed high levels of antibodies to SARS-CoV-2, indicating immune protection from immediate reinfection. The findings have been accepted for publication in the journal Immunity.
These findings coincide with results from other studies of recovered patients, and are the main reason that scientists aren't concerned by the occasional reports of people recovering from COVID-19, testing negative for the virus via a nasal swab PCR test that detects the viral genome, and then testing positive again within a few weeks. These people aren't reinfected, tenOever said. Their antibody levels are high and their immune system is armed against further attack. Instead, the PCR tests are simply picking up bits of inert viral genetic debris left over from the previous infection.
Neutralizing the foe: tracking the immune response to SARS-CoV-2 infection
In times of stress and danger such as come about as the result of an epidemic, many tragic and cruel phases of human nature are brought out, as well as many brave and unselfish ones. -William Crawford Gorgas
All crises bring out the best and worst of human nature. In its devastation, SARS-CoV-2 has birthed a new generation of heroes and villains: anti-maskers or, depending on one’s views, overly restrictive state and local governments. Selfless healthcare and essential workers, serving the public at great personal risk. And, at the forefront of the crisis, a community of scientists equipped with a modern arsenal of genetic and immunological expertise and intent on the rapid evisceration of this disease. Thus, as the world awaits the vaccines that could bring this pandemic to a halt, the public psyche has never been more focused on the topic of immunity. How effective is immunity to this virus? And how long does it last? A new paper published in the Journal of Infectious Diseases from the lab of Dr. Jesse Bloom, from the Basic Sciences Division at Fred Hutch, studied the immune response to SARS-CoV-2 infection over time to understand the durability of immunity, and what implications it may have for the future of the pandemic.
There are, fortunately, clear indications that exposure to SARS-CoV-2, by infection or vaccination, generates some degree of protection from the virus in the form of immunity. And studies of other viruses provide an understanding of how immunity usually works. “For most acute viral infections, neutralizing antibodies [which defend our cells from pathogens] rapidly rise after infection owing to a burst of short-lived antibody-secreting cells and then decline from this peak before reaching a stable plateau that can be maintained for years to decades by long-lived plasma and memory B cells,” write the authors. But even after decades of study the immune system is notoriously unpredictable, raising the question of whether SARS-CoV-2 infection has the same effect. Thus, the Bloom lab teamed up with the University of Washington’s Dr. Helen Chu, whose work tracking viral respiratory infections in Seattle residents led to the first discovery of COVID-19 community transmission in the United States. Together, they studied how immunity evolves for several months following SARS-CoV-2 infection.
Using blood samples from COVID-19 patients, “we investigated the dynamics of neutralizing antibodies against SARS-CoV-2 in the three to four months following infection,” said Kate Crawford, a graduate student in the University of Washington Medical Student Training Program and lead author on the study. And, as with all research on this rampaging disease, haste was of the essence. “Thanks to [Dr. Chu and her team], we were able to get samples from individuals who were infected early in the pandemic. Thus, by mid-summer, we were already able to investigate antibody dynamics several months post-infection. it was exciting (although somewhat stressful) to be on the leading edge of figuring out these antibody dynamics,” said Crawford. The authors found that the immune response to SARS-CoV-2 infection was similar to other viruses – for individuals across the disease severity spectrum, neutralizing antibody levels spiked in the first 30 days following infection, and then declined – but remained at substantial levels – over the next two to three months. The results offered no particular surprises, as Crawford reflected. “It’s fun and exciting to write papers about finding something you didn’t expect in science, but sometimes it’s just as important to publish the papers showing what you did expect and why you expected it.” In this tumultuous year, an unsurprising result has never been more welcome, especially when it suggests that the immune system is doing just what it is meant to do – generating a robust and, hopefully, durable response to protect from future infections by this virus.
While the results reported by the Bloom lab are promising, understanding how long this immune protection will last is a waiting game – we cannot know this until the immunity has worn off, and I think we can all agree that this is one scientific question for which we’ll all be happy to wait many years for an answer. In the meantime, Crawford has turned her attention to another means by which immunity may be lost, even in the continued presence of neutralizing antibodies. “My research is now focused on understanding the effects of mutations to the spike protein of SARS-CoV-2 [the protein that is recognized by neutralizing antibodies] and how mutations to spike might affect neutralization of the virus [by preventing antibodies from recognizing the mutated virus],” Crawford said.
An mRNA vaccine against SARS-CoV-2: Lyophilized, liposome-based vaccine candidate EG-COVID induces high levels of virus neutralizing antibodies
In addition to the traditional method of vaccine development, the mRNA coronavirus vaccine, which is attractive as a challenging vaccination, recently opened a new era in vaccinology. Here we describe the EG-COVID which is a novel liposome-based mRNA candidate vaccine that encodes the spike (S) protein of SARS-CoV-2 with 2P-3Q substitution in European variant. We developed the mRNA vaccine platform that can be lyophilized using liposome-based technology. Intramuscular injection of the EG-COVID elicited robust humoral and cellular immune response to SARS-CoV-2. Furthermore, sera obtained from mice successfully inhibited SARS-CoV-2 viral infection into Vero cells. We developed EG-COVID and found it to be effective based on in vitro data, and we plan to initiate a clinical trial soon. Since EG-COVID is a lyophilized mRNA vaccine that is convenient for transportation and storage, accessibility to vaccines will be significantly improved.
COVID-19 research is still in its early stages, and we need further research worldwide to better face this pandemic. We still need to learn about the biology of the disease and the variable response that patients display in their disease manifestation and recovery. We expect that the process of biomarker discovery and validation will largely guide an accelerated translational strategy to address this global health crisis. A standardized pathway approach toward the biomarker validation process is thus becoming increasingly important. Quality and reproducibility are essential for translating basic findings into concrete clinic interventions and only following this approach is an effective response to the pandemic guaranteed. Significant efforts and resources have been invested in the development of biomarkers for COVID-19 and AMRI urges that research must be of good quality, providing robust, ethical evidence that stands up to scrutiny and can be used to inform policy making. For COVID-19 management, structural use of the relevant research infrastructures is strongly advised, as they play an important role in centralized management of biomarkers Rɭ pipelines, biobanking, and clinical trials. The collective efforts of AMRI and collaborative actions of the scientific community will create high-quality knowledge that is openly available and will bring a better understanding of SARS-CoV-2, with benefits for all.
Potential conflicts of interest. The authors: No reported conflicts of interest. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest.