Script / Documentation
Welcome to Just Facts Academy. In this series, we focus on our Standards of Credibility—7 standards that help you research like a genius.
In today’s lesson, we’ll focus on Clarity.
Now, the definition of clarity should be … clear, but let’s define it, look at an example of why it’s so important, and discuss how to use it in your own research.
Clarity simply means easy to perceive or understand. This is important when conducting good research because it lessens the chance of misinterpretation.
Now, vague language can be unintentional—the result of lazy writing—but it can also be, as George Orwell puts it, “consciously dishonest.”[1]
You’ve probably heard of Orwell. He’s best known for writing the books Animal Farm and 1984.[2] He also wrote a famous essay titled “Politics and the English Language.” In it, he argues that “the present political chaos is connected with the decay of language.” And this was back in 1946![3]
Much of this essay directly addresses this issue of clarity. For instance, he says certain words are “used in a consciously dishonest way. That is, the person who uses them has his own private definition but allows his hearer to think he means something quite different.”[4] No one would ever do that today, right?
Unfortunately, this is all-too-familiar. Politicians make ambiguous statements while avoiding precise language that could be used to hold them accountable. News sites publish bold headlines with bold implications; but in context, the full article is much less sensational. Let’s just say, there’s no shortage of click bait.
Whether intentional or not, a lack of clarity has caused much confusion during the COVID-19 pandemic.
The words “COVID-19” and “the coronavirus” are often used interchangeably,[5] when in fact, there is an important difference between them. Let me explain.
COVID-19 is in fact caused by a coronavirus, but just one type among many different coronaviruses that exist.[6] [7]
Coronaviruses, which includes some that cause the common cold,[8] are a family of viruses that tend to mutate rapidly. This means vaccines are often ineffective against them because the virus constantly changes.[9]
However—and this is key—the coronavirus that causes COVID-19 does not share that trait. Genetic research shows that it “does not mutate rapidly,” it’s very “vulnerable to antibody neutralization,” and it shows “no unexpected … signs of adaptation.”[10] [11] [12] [13]
Simply put, even though COVID-19 is caused by a coronavirus, this new type is very different. Hence, vaccines that provide decent protection have been developed in record time,[14] [15] [16] [17] and future vaccines that do a better job of replicating naturally acquired immunity will possibly work forever.[18] [19] [20] [21] [22] [23]
As a result of not understanding the difference between coronaviruses in general and the specific one that causes COVID-19, some journalists spread excess confusion and fear around this issue,[24] [25] which is also hazardous to our health.[26]
Now that we’ve seen how a lack of clarity can be dangerous, let’s discuss how to avoid these errors in your own research.
It’s actually quite simple, but it requires hard work. Whether you’re researching or writing, always ask yourself, “Can this be interpreted another way?” If so, you have more work to do.
If a word or concept is unfamiliar or seems vague to you, look up the definition in a highly credible source—not just the first news article you read.
And don’t forget to read the context. I’m not just talking about the surrounding sentence or two—but actually read the whole article. Yes, that’s more work, but it’s worth the effort. It’s more than just a grade.
If there’s any uncertainty or a disconnect in logic, write to the author and ask them to explain. This is much easier than it sounds because most scholars and serious authors have webpages with their email or a simple contact form. You’ll be shocked at how accessible and helpful they can be, especially when you show genuine interest in their work.
If they don’t reply, don’t settle. Find another source that’s crystal clear.
None of this requires a high IQ. It just takes effort, which is something we all can give.
And please, don’t make the same mistake in your own writing. Remember the golden rule: Don’t confuse others as you don’t like being confused. That means don’t use vague language and be vigilant to ask yourself, “Can this be interpreted another way?”
So, make sure you apply this Clarity principle—along with the rest of Just Facts’ Standards of Credibility—so you can research like a genius.
Footnotes
[1] Essay: “Politics and the English Language.” By George Orwell. Horizon, April 1946. <www.orwell.ru>
“Words of this kind are often used in a consciously dishonest way.”
[2] Article: “George Orwell.” By George Woodcock. Encyclopedia Britannica. Accessed September 2, 2020 at <www.britannica.com>
In 1944 Orwell finished Animal Farm, a political fable based on the story of the Russian Revolution and its betrayal by Joseph Stalin. … At first Orwell had difficulty finding a publisher for the small masterpiece, but when it appeared in 1945, Animal Farm made him famous and, for the first time, prosperous. …
Animal Farm was one of Orwell’s finest works, full of wit and fantasy and admirably written. It has, however, been overshadowed by his last book, Nineteen Eighty-four (1949), a novel he wrote as a warning after years of brooding on the twin menaces of Nazism and Stalinism.
[3] Essay: “Politics and the English Language.” By George Orwell. Horizon, April 1946. <www.orwell.ru>
I have not here been considering the literary use of language, but merely language as an instrument for expressing and not for concealing or preventing thought. Stuart Chase and others have come near to claiming that all abstract words are meaningless, and have used this as a pretext for advocating a kind of political quietism. Since you don’t know what Fascism is, how can you struggle against Fascism? One need not swallow such absurdities as this, but one ought to recognise that the present political chaos is connected with the decay of language, and that one can probably bring about some improvement by starting at the verbal end. If you simplify your English, you are freed from the worst follies of orthodoxy. You cannot speak any of the necessary dialects, and when you make a stupid remark its stupidity will be obvious, even to yourself.
[4] Essay: “Politics and the English Language.” By George Orwell. Horizon, April 1946. <www.orwell.ru>
It is almost universally felt that when we call a country democratic we are praising it: consequently the defenders of every kind of regime claim that it is a democracy, and fear that they might have to stop using that word if it were tied down to any one meaning. Words of this kind are often used in a consciously dishonest way. That is, the person who uses them has his own private definition, but allows his hearer to think he means something quite different.
[5] Search: “the coronavirus” “COVID-19”. Google, June 16, 2021. <www.google.com>
NOTE: This search produced about 177,000,000 results.
[6] Paper: “Bibliometric and Visualization Analysis of Human Coronaviruses: Prospects and Implications for COVID-19 Research.” By Ziqin Deng, Junsheng Chen, and Ting Wang. Frontiers in Cellular and Infection Microbiology, September, 23 2020. <www.frontiersin.org>
This is the seventh coronavirus identified so far to infect humans, with the others being HCoV-229E, HCoV-OC43, HCoV-NL63, HCoV-HKU1, SARS-CoV, and MERS-CoV (Geller et al., 2012). HCoV-229E, HCoV-OC43, HCoV-NL63, and HCoV-HKU1 are able to cause common cold in humans and majority of these infections only manifest mild symptoms in respiratory system (Mackay et al., 2012; Owusu et al., 2014; Annan et al., 2016). However, SARS-CoV and MERS-CoV are more serious and responsible for high case fatality rates, both of whom belong to genus Beta.
[7] Entry: “coronavirus.” Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health (7th edition). Saunders, 2003. <medical-dictionary.thefreedictionary.com>
“Any of a group of morphologically similar, ether-sensitive viruses, probably RNA, causing infectious bronchitis in birds, hepatitis in mice, gastroenteritis in swine, and respiratory infections in humans.”
[8] Entry: “coronavirus.” American Heritage Medical Dictionary. Houghton Mifflin Company, 2007. <medical-dictionary.thefreedictionary.com>
“Any of a family of single-stranded RNA viruses that infect mammals and birds, causing respiratory infections such as the common cold and SARS in humans, and that have spikes of glycoproteins projecting from the viral envelope.”
[9] Paper: “How the SARS Vaccine Effort Can Learn From HIV—Speeding Towards the Future, Learning From the Past.” By Anne S. De Groot. Vaccine, October 1, 2003. <www.ncbi.nlm.nih.gov>
There are worrisome similarities between SARS-CoV and HIV; both are RNA viruses and able to mutate under selection pressure in the host; and coronaviruses are especially prone to mutation and recombination. …
… More important, the HIV vaccine development effort initially focused on replicating the approach that had been used to develop Hepatitis B vaccine development, which was to clone and express the surface protein of the virus. This simplistic approach to a complex virus was recently proven to be a failure [3]. Will scientists once again pursue “quick and easy solutions” in the hopes of stimulating a protective antibody response despite existing evidence that coronavirus vaccines (for animals) based on the S or spike surface protein have largely been ineffective?
[10] Paper: “The Spread of the COVID‐19 Coronavirus.” By Philip Hunter. EMBO Reports, March 17, 2020. <www.embopress.org>
There is though growing optimism over developing therapies against the COVID-19 virus. This applies particularly to vaccines and antibodies to neutralize the active sites of the virus surface that expedite the penetration of host cells, according to Michael Farzan, Co-chair of the Department of Immunology and Microbiology, Scripps Research, La Jolla, CA, USA. “This virus is a close cousin of SARS-CoV, and like SARS-CoV, it ‘chooses’, meaning has been selected, to move rapidly from host to host before an adaptive immune response emerges”, he explained. “Because of this, and unlike HIV-1 and Ebolavirus, it keeps its key epitopes exposed, probably so that it can be more efficient at binding the next cell. This makes it very vulnerable to antibody neutralization, and thus it is a relatively easy virus to protect against. I refer to it as ‘stupid’ on a spectrum where HIV, which lives in the face of an active immune system for years, is a ‘genius’.”
Furthermore, as Farzan added, it does not mutate rapidly for an RNA virus because, unusually for this category, it has a proof-reading function in its polymerase 3. “In short, a vaccine, and especially a vaccine targeted in part to the receptor-binding domain of the 2019-nCoV entry protein, the Spike or S protein, should be effective”, he said. As this protein is protected against mutation, a vaccine would not need regular updates, unlike seasonal influenza vaccines.
[11] Editorial: “COVID-19: A Puzzle with Many Missing Pieces.” By Pauline Vetter, Isabella Eckerle, and Laurent Kaiser. British Medical Journal, February 19, 2020. <www.bmj.com>
“The genome data available so far show no unexpected mutation rate or signs of adaptation, so viral factors are unlikely to be contributing to the differences observed between China and the rest of the world.”
[12] Paper: “A SARS-Cov-2 Vaccine Candidate Would Likely Match All Currently Circulating Variants.” By Bethany Dearlove and others. Proceedings of the National Academy of Sciences, September 22, 2020. <www.pnas.org>
Although we cannot predict whether adaptive selection will be seen in SARS-CoV-2 in the future, the key finding is that SARS-CoV-2 viruses that are currently circulating constitute a homogeneous viral population. Viral diversity has challenged vaccine development efforts for other viruses such as HIV-1, influenza, or Dengue, but these viruses each constitute a more diverse population than SARS-CoV-2 viruses (SI Appendix, Fig. S12). We can therefore be cautiously optimistic that viral diversity should not be an obstacle for the development of a broadly protective SARS-CoV-2 vaccine, and that vaccines in current development should elicit responses that are reactive against currently circulating variants of SARS-CoV-2.
[13] For a litany of other studies with analogous findings, see Just Facts’ research on immunity to COVID-19.
[14] Article: “COVID-19 Vaccine Safety Questions and Answers for Healthcare Providers.” By Sonali Kochhar and others. Vaccine, April 28, 2021. <www.ncbi.nlm.nih.gov>
To help stem the tide of the COVID-19 pandemic and its severe global repercussions, vaccines against SARS-CoV-2 have been developed and deployed in record time. …
The accelerated pace of vaccine development has raised concerns among some healthcare providers and the public regarding whether critical steps in vaccine development are being skipped, especially steps in assessment of vaccine safety, to compress the usual decades long vaccine development process into 12–15 months.
[15] Webpage: “Crotty Lab.” La Jolla Institute for Immunology. Accessed May 27, 2021 at <www.lji.org>
Shane Crotty, Ph.D.
Professor
Center for Infectious Disease and Vaccine Research …
Shane Crotty, Ph.D., and his team study immunity against infectious diseases. They investigate how the immune system remembers infections and vaccines. By remembering infections and vaccines, the body is protected from becoming infected in the future. Vaccines are one of the most cost-effective medical treatments in modern civilization and are responsible for saving millions of lives. Yet, good vaccines are very difficult to design, and very few new vaccines have been made in the past 10 years.
[16] Paper: “Adaptive Immunity to SARS-CoV-2 and COVID-19.” By Alessandro Sette and Shane Crotty. Cell, February 18, 2021. <www.ncbi.nlm.nih.gov>
The adaptive immune system is important for control of most viral infections. The three fundamental components of the adaptive immune system are B cells (the source of antibodies), CD4+ T cells, and CD8+ T cells. …
… [A]lmost all COVID-19 vaccines target Spike [the SARS-CoV-2 spike protein] only.
[17] Paper: “SARS-CoV-2 mRNA Vaccines: Immunological Mechanism and Beyond.” By Emily Bettini and Michela Locci. Vaccines, February 12, 2021. <www.mdpi.com>
Of the multiple epitopes on SARS-CoV-2, the spike (S) glycoprotein is the target commonly selected for COVID-19 vaccine development [3], since it is the major SARS-CoV-2 surface protein and mediates viral entry by binding to the angiotensin-converting enzyme 2 (ACE2) receptor in host cells [17,18,19]. …
As discussed earlier, it appears desirable for a SARS-CoV-2 mRNA vaccine to elicit Th1 CD4 T cell responses. … In both the younger and the elderly study groups, these responses appeared to be higher in individuals receiving 100 μg of mRNA-1273 in comparison to the 25 μg dose group. On the other hand, SARS-CoV-2-specific CD8 T cell responses were almost undetectable in most vaccinated individuals for this vaccine formulation, even after the boost dose. This outcome is not surprising, given that no antigen-specific CD8 T cell responses were found after immunization with mRNA-1273 in rhesus macaques during preclinical trials, even with doses as high as 100 μg [7]. …
mRNA-based vaccines have become an increasingly attractive platform to fight the ongoing SARS-CoV-2 pandemic for a multitude of reasons. Firstly, the need for only a DNA template of the desired antigen to produce a vaccine candidate, resulting in an exceedingly fast manufacturing timeline [4]. Clinical testing of the first mRNA vaccine candidate (mRNA-1273) began on March 2020 [74], just 66 days after the SARS-CoV-2 sequence was publicly released on January 2020 [75], with the second candidates (BNT162b1 and BN162b2) entering into phase 1/2 clinical trials only a month later [76,77]. By contrast, the development of vaccine candidates utilizing traditional vaccine platforms has been lengthy because of the inherently slow nature of developing cell lines, generating virus, and/or producing clinical-grade protein subunits, as demonstrated by the fact that the only vaccines that have been granted emergency authorization by the FDA thus far are mRNA vaccines.
[18] Article: “Having SARS-Cov-2 Once Confers Much Greater Immunity Than a Vaccine—but Vaccination Remains Vital.” By Meredith Wadman. Science, August 26, 2021. <www.science.org>
The natural immune protection that develops after a SARS-CoV-2 infection offers considerably more of a shield against the Delta variant of the pandemic coronavirus than two doses of the Pfizer-BioNTech vaccine, according to a large Israeli study that some scientists wish came with a “Don’t try this at home” label. The newly released data show people who once had a SARS-CoV-2 infection were much less likely than never-infected, vaccinated people to get Delta, develop symptoms from it, or become hospitalized with serious COVID-19. …
The study, conducted in one of the most highly COVID-19–vaccinated countries in the world, examined medical records of tens of thousands of Israelis, charting their infections, symptoms, and hospitalizations between 1 June and 14 August, when the Delta variant predominated in Israel. It’s the largest real-world observational study so far to compare natural and vaccine-induced immunity to SARS-CoV-2, according to its leaders. …
The research impresses Nussenzweig and other scientists who have reviewed a preprint of the results, posted yesterday on medRxiv [see the next footnote for this research]. “It’s a textbook example of how natural immunity is really better than vaccination,” says Charlotte Thålin, a physician and immunology researcher at Danderyd Hospital and the Karolinska Institute who studies the immune responses to SARS-CoV-2. …
No one in the study who got a new SARS-CoV-2 infection died—which prevented a comparison of death rates but is a clear sign that vaccines still offer a formidable shield against serious disease, even if not as good as natural immunity. …
“We continue to underestimate the importance of natural infection immunity … especially when [infection] is recent,” says Eric Topol, a physician-scientist at Scripps Research. “And when you bolster that with one dose of vaccine, you take it to levels you can’t possibly match with any vaccine in the world right now.” …
As for the Israel medical records study, Topol and others point out several limitations, such as the inherent weakness of a retrospective analysis compared with a prospective study that regularly tests all participants as it tracks new infections, symptomatic infections, hospitalizations, and deaths going forward in time. “It will be important to see these findings replicated or refuted,” says Natalie Dean, a biostatistician at Emory University. …
For many infectious diseases, naturally acquired immunity is known to be more powerful than vaccine-induced immunity and it often lasts a lifetime.
[19] Working paper: “Comparing SARS-Cov-2 Natural Immunity to Vaccine-Induced Immunity: Reinfections Versus Breakthrough Infections.” By Sivan Gazit (Maccabitech Institute for Research and Innovation, Israel), Tal Patalon (Maccabitech Institute for Research and Innovation), and others. <www.medrxiv.org>
Methods We conducted a retrospective observational study comparing three groups: (1) SARS-CoV-2-naïve individuals who received a two-dose regimen of the BioNTech/Pfizer mRNA BNT162b2 vaccine, (2) previously infected individuals who have not been vaccinated, and (3) previously infected and single dose vaccinated individuals. Three multivariate logistic regression models were applied. In all models we evaluated four outcomes: SARS-CoV-2 infection, symptomatic disease, COVID-19-related hospitalization and death. The follow-up period of June 1 to August 14, 2021, when the Delta variant was dominant in Israel. …
Conclusions This study demonstrated that natural immunity confers longer lasting and stronger protection against infection, symptomatic disease and hospitalization caused by the Delta variant of SARS-CoV-2, compared to the BNT162b2 two-dose vaccine-induced immunity. Individuals who were both previously infected with SARS-CoV-2 and given a single dose of the vaccine gained additional protection against the Delta variant. …
The Delta (B.1.617.2) Variant of Concern (VOC), initially identified in India and today globally prevalent, has been the dominant strain in Israel since June 2021. The recent surge of cases in Israel15, one of the first countries to embark on a nationwide vaccination campaign (mostly with the BioNTech/Pfizer BNT162b2 vaccine), has raised concerns about vaccine effectiveness against the Delta variant, including official reports of decreased protection16. Concomitantly, studies have demonstrated only mild differences in short-term vaccine effectiveness17 against the Delta variant, as well as substantial antibody response18. Apart from the variant, the new surge was also explained by the correlation found between time-from-vaccine and breakthrough infection rates, as early vaccinees were demonstrated to be significantly more at risk than late vaccinees8. Now, when sufficient time has passed since both the beginning of the pandemic and the deployment of the vaccine, we can examine the long-term protection of natural immunity compared to vaccine-induced immunity. …
Individual-level data of the study population included patient demographics, namely age, sex, socioeconomic status (SES) and a coded geographical statistical area (GSA, assigned by Israel’s National Bureau of Statistics, corresponds to neighborhoods and is the smallest geostatistical unit of the Israeli census). The SES is measured on a scale from 1 (lowest) to 10, and the index is based on several parameters, including household income, educational qualifications, household crowding and car ownership. Data were also collected on last documented body mass index (BMI) and information about chronic diseases from MHS’ automated registries, including cardiovascular diseases19, hypertension20, diabetes21, chronic kidney disease22, chronic obstructive pulmonary disease, immunocompromised conditions, and cancer from the National Cancer Registry23. …
This is the largest real-world observational study comparing natural immunity, gained through previous SARS-CoV-2 infection, to vaccine-induced immunity, afforded by the BNT162b2 mRNA vaccine. Our large cohort, enabled by Israel’s rapid rollout of the mass-vaccination campaign, allowed us to investigate the risk for additional infection – either a breakthrough infection in vaccinated individuals or reinfection in previously infected ones – over a longer period than thus far described. …
Broadening the research question to examine the extent of the phenomenon, we allowed the infection to occur at any time between March 2020 to February 2021 (when different variants were dominant in Israel), compared to vaccination only in January and February 2021. Although the results could suggest waning natural immunity against the Delta variant, those vaccinated are still at a 5.96-fold increased risk for breakthrough infection and at a 7.13-fold increased risk for symptomatic disease compared to those previously infected. SARS-CoV-2-naïve vaccinees were also at a greater risk for COVID-19-related-hospitalization compared to those who were previously infected.
Individuals who were previously infected with SARS-CoV-2 seem to gain additional protection from a subsequent single-dose vaccine regimen. Though this finding corresponds to previous reports24,25, we could not demonstrate significance in our cohort. …
The advantageous protection afforded by natural immunity that this analysis demonstrates could be explained by the more extensive immune response to the SARS-CoV-2 proteins than that generated by the anti-spike protein immune activation conferred by the vaccine26,27. However, as a correlate of protection is yet to be proven1,28, including the role of B-Cell29 and T-cell immunity30,31, this remains a hypothesis.
Our study has several limitations. First, as the Delta variant was the dominant strain in Israel during the outcome period, the decreased long-term protection of the vaccine compared to that afforded by previous infection cannot be ascertained against other strains. Second, our analysis addressed protection afforded solely by the BioNTech/Pfizer mRNA BNT162b2 vaccine, and therefore does not address other vaccines or long-term protection following a third dose, of which the deployment is underway in Israel. Additionally, as this is an observational real-world study, where PCR screening was not performed by protocol, we might be underestimating asymptomatic infections, as these individuals often do not get tested.
Lastly, although we controlled for age, sex, and region of residence, our results might be affected by differences between the groups in terms of health behaviors (such as social distancing and mask wearing), a possible confounder that was not assessed. As individuals with chronic illness were primarily vaccinated between December and February, confounding by indication needs to be considered; however, adjusting for obesity, cardiovascular disease, diabetes, hypertension, chronic kidney disease, chronic obstructive pulmonary disease, cancer and immunosuppression had only a small impact on the estimate of effect as compared to the unadjusted OR. Therefore, residual confounding by unmeasured factors is unlikely.
[20] Paper: “Naturally Enhanced Neutralizing Breadth Against SARS-Cov-2 One Year After Infection.” By Zijun Wang sand others. Nature, June 21, 2021. <www.nature.com>
Here we report on a cohort of 63 individuals who have recovered from COVID-19 assessed at 1.3, 6.2 and 12 months after SARS-CoV-2 infection, 41% of whom also received mRNA vaccines3,4. In the absence of vaccination, antibody reactivity to the receptor binding domain (RBD) of SARS-CoV-2, neutralizing activity and the number of RBD-specific memory B cells remain relatively stable between 6 and 12 months after infection. … The data suggest that immunity in convalescent individuals will be very long lasting and that convalescent individuals who receive available mRNA vaccines will produce antibodies and memory B cells that should be protective against circulating SARS-CoV-2 variants.
[21] Paper: “The Spread of the COVID‐19 Coronavirus.” By Philip Hunter. EMBO Reports, March 17, 2020. <www.embopress.org>
There is though growing optimism over developing therapies against the COVID-19 virus. This applies particularly to vaccines and antibodies to neutralize the active sites of the virus surface that expedite the penetration of host cells, according to Michael Farzan, Co-chair of the Department of Immunology and Microbiology, Scripps Research, La Jolla, CA, USA. “This virus is a close cousin of SARS-CoV, and like SARS-CoV, it ‘chooses’, meaning has been selected, to move rapidly from host to host before an adaptive immune response emerges”, he explained. “Because of this, and unlike HIV-1 and Ebolavirus, it keeps its key epitopes exposed, probably so that it can be more efficient at binding the next cell. This makes it very vulnerable to antibody neutralization, and thus it is a relatively easy virus to protect against. I refer to it as ‘stupid’ on a spectrum where HIV, which lives in the face of an active immune system for years, is a ‘genius’.”
Furthermore, as Farzan added, it does not mutate rapidly for an RNA virus because, unusually for this category, it has a proof-reading function in its polymerase 3. “In short, a vaccine, and especially a vaccine targeted in part to the receptor-binding domain of the 2019-nCoV entry protein, the Spike or S protein, should be effective”, he said. As this protein is protected against mutation, a vaccine would not need regular updates, unlike seasonal influenza vaccines.
[22] Paper: “SARS-CoV-2 Variants of Concern Partially Escape Humoral but Not T-Cell Responses in COVID-19 Convalescent Donors and Vaccinees.” By Daryl Geers and others. Science Immunology, May 25, 2021. <immunology.sciencemag.org>
The emergence of SARS-CoV-2 variants harboring mutations in the spike (S) protein has raised concern about potential immune escape. Here, we studied humoral and cellular immune responses to wild type SARS-CoV-2 and the B.1.1.7 [UK/Alpha] and B.1.351 [South African/Beta] variants of concern in a cohort of 121 BNT162b2 mRNA-vaccinated health care workers (HCW). … Importantly, we observed no differences in CD4+ T-cell activation in response to variant antigens, indicating that the B.1.1.7 and B.1.351 S proteins do not escape T-cell-mediated immunity elicited by the wild type S protein. In conclusion, this study shows that some variants can partially escape humoral immunity induced by SARS-CoV-2 infection or BNT162b2 vaccination, but S-specific CD4+ T-cell activation is not affected by the mutations in the B.1.1.7 and B.1.351 variants.
[23] Paper: “Adaptive Immunity to SARS-CoV-2 and COVID-19.” By Alessandro Sette and Shane Crotty. Cell, February 18, 2021. <www.ncbi.nlm.nih.gov>
SARS-CoV-2 genetic variation has been a topic of intense interest. Whether SARS-CoV-2 will be able to exhibit sufficient genetic flexibility to escape humoral immune responses in the near term is unclear. Many RNA viruses, such as measles and polioviruses, exhibit antigenic stability and unchanging serotypes over periods of many years. As a result, the measles and polio vaccines remain highly effective now, 70 years after they were first introduced. Although the situation for any coronavirus is unclear, it is highly unlikely that SARS-CoV-2 mutations would escape T cell immunity, because a very broad array of SARS-CoV-2 epitopes are recognized in humans with COVID-19 … consisting of CD4+ and CD8+ T cell responses to >10 epitopes distributed throughout the SARS-CoV-2 genome, which vary from person to person…. For antibody responses, SARS-CoV-2 mutations exist that could affect individual neutralizing antibody epitopes. However, a key attribute of the neutralization epitopes on SARS-CoV-2 Spike is that the surface area on RBD [the receptor binding domain] that is targeted by neutralizing antibodies is large enough that no single viral mutation is expected to avoid neutralization by polyclonal human serum…. This is consistent with the broad range of SARS-CoV-2 neutralizing antibodies isolated from humans, indicating that SARS-CoV-2 is a relatively easy neutralization target that elicits a diverse array of antibodies in each person (see Antibodies and B cells section, above). The Spike D614G variant that is now globally common (that binds ACE2 more tightly and is more transmissible) … is neutralized by plasma from subjects infected with the original D614 virus…. The Spike N439 variant has enhanced binding to ACE2 but has been shown to still be robustly neutralized by serum from the vast majority of COVID-19 patients…. Thus, although it is important to track SARS-CoV-2 evolution, it is unlikely that the virus will be able to evolve escape variants that avoid the majority of humoral and cellular immune memory in COVID-19 cases or COVID-19 vaccine recipients soon.
[24] Article: “A Vaccine Won’t Stop the New Coronavirus.” By James Hamblin, M.D (Lecturer at Yale School of Public Health). The Atlantic, February 24, 2020, Updated February 25, 2020. <www.theatlantic.com>
And coronaviruses could present a particular challenge in that at their core they, like influenza viruses, contain single strands of RNA. This viral class is likely to mutate, and vaccines may need to be in constant development, as with the flu.
“If we’re putting all our hopes in a vaccine as being the answer, we’re in trouble,” Jason Schwartz, an assistant professor at Yale School of Public Health who studies vaccine policy, told me. The best-case scenario, as Schwartz sees it, is the one in which this vaccine development happens far too late to make a difference for the current outbreak.
[25] Article: “Why the New Coronavirus Is So Hard to Cure.” By Umair Irfan. Vox, March 11, 2020. <www.vox.com>
“There’s also a huge variety of viruses, and they mutate quickly, so tailored treatments and vaccines against a virus can lose effectiveness over time.”
[26] For a trove of studies documenting this, see Just Facts’ article “Anxiety From Reactions to Covid-19 Will Destroy At Least Seven Times More Years of Life Than Can Be Saved by Lockdowns.”