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] [14]

Simply put, even though Covid-19 is caused by a coronavirus, this new type is very different. Hence, naturally acquired immunity against it tends to be potent and long-lasting.[15] [16] [17] [18] [19] [20]

Now, that doesn’t mean you can’t get Covid-19 more than once.[21] [22] [23] [24] It means that it is unlikely to harm you after the first time you get it,[25] [26] [27] [28] [29] as long as your immune system isn’t compromised by factors like poor general health,[30] [31] [32] drugs,[33] heavy alcohol consumption,[34] or sleep deprivation.[35]

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,[36] [37] [38] [39] which is also hazardous to our health.[40]

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.


[1] Essay: “Politics and the English Language.” By George Orwell. Horizon, April 1946. <>

“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 <>

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. <>

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. <>

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. <>

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. <>

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. <>

“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. <>

“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. <>

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. <>

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 polymerase3. “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.

3 Denison MR, Graham RL, Donaldson EF, Eckerle LD, Baric RS (2011) Coronaviruses: an RNA proofreading machine regulates replication fidelity and diversity. RNA Biol 8: 270–279

[11] Paper: “Coronaviruses: An RNA Proofreading Machine Regulates Replication Fidelity and Diversity.” By Mark R. Denison and others. RNA Biology, March 1, 2011. <>

The CoVs, including murine [mouse] hepatitis virus (MHV) and SARS-CoV, encode a 3’-to-5’ exoribonuclease activity (ExoN) in nsp14 [nonstructural protein 14]. Genetic inactivation of ExoN activity in engineered SARS-CoV and MHV genomes … results in viable mutants that demonstrate 15- to 20-fold increases in mutation rates, up to 18 times greater than those tolerated for fidelity mutants of other RNA viruses. Thus nsp14-ExoN is essential for replication fidelity, and likely serves either as a direct mediator or regulator of a more complex RNA proofreading machine, a process previously unprecedented in RNA virus biology. …

CoVs are enveloped viruses that have positive-sense, non-segmented RNA genomes 27–32 kb in length. The basic gene organization and replication is similar for all CoVs and is illustrated for SARS-CoV (Fig. 1). …

… . Interestingly, M-ExoN has an estimated mutation rate similar to other known wt [wild-type] RNA viruses, while wt MHV in fact had a mutation rate 15-fold less than other RNA viruses, suggesting that ExoN confers very high replication fidelity on CoV genome replication. …

The results from both M-ExoN [murine hepatitis virus ExoN] and S-ExoN [SARS-CoV ExoN] mutants, as well as the in vitro ssRNA [single-stranded RNA] exonuclease activity of SARS-CoV nsp14, all argue strongly that nsp14-ExoN directly mediates or participates in the prevention or repair of mutations, which would constitute RNA proofreading, an enzymatic activity not previously reported during the replication of RNA viruses.

[12] Editorial: “COVID-19: A Puzzle with Many Missing Pieces.” By Pauline Vetter, Isabella Eckerle, and Laurent Kaiser. British Medical Journal, February 19, 2020. <>

“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.”

[13] 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. <>

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.

[14] For a litany of other studies with analogous findings, see Just Facts’ research on immunity to COVID-19.

[15] Paper: “Adaptive Immunity to SARS-CoV-2 and COVID-19.” By Alessandro Sette and Shane Crotty. Cell, February 18, 2021. <>

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.

[16] Paper: “Naturally Enhanced Neutralizing Breadth Against SARS-Cov-2 One Year After Infection.” By Zijun Wang sand others. Nature, June 21, 2021. <>

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.

[17] 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. <>

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.

[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. <>

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] Paper: “Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Naturally Acquired Immunity versus Vaccine-induced Immunity, Reinfections versus Breakthrough Infections: A Retrospective Cohort Study.” By Sivan Gazi and others. Clinical Infectious Diseases, July 1, 2022. <>


Waning of protection against infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) conferred by 2 doses of the BNT162b2 vaccine begins shortly after inoculation and becomes substantial within 4 months. With that, the impact of prior infection on incident SARS-CoV-2 reinfection is unclear. Therefore, we examined the long-term protection of naturally acquired immunity (protection conferred by previous infection) compared to vaccine-induced immunity.


A retrospective observational study of 124 500 persons, compared 2 groups: (1) SARS-CoV-2-naive individuals who received a 2-dose regimen of the BioNTech/Pfizer mRNA BNT162b2 vaccine, and (2) previously infected individuals who have not been vaccinated. Two multivariate logistic regression models were applied, evaluating four SARS-CoV-2-related outcomes—infection, symptomatic disease (coronavirus disease 2019 [COVID-19]), hospitalization, and death—between 1 June and 14 August 2021, when the Delta variant was dominant in Israel. …


SARS-CoV-2-naive vaccinees had a 13.06-fold (95% confidence interval [CI], 8.08–21.11) increased risk for breakthrough infection with the Delta variant compared to unvaccinated-previously-infected individuals, when the first event (infection or vaccination) occurred during January and February of 2021. The increased risk was significant for symptomatic disease as well. When allowing the infection to occur at any time between March 2020 and February 2021, evidence of waning naturally acquired immunity was demonstrated, although SARS-CoV-2 naive vaccinees still had a 5.96-fold (95% CI: 4.85–7.33) increased risk for breakthrough infection and a 7.13-fold (95% CI: 5.51–9.21) increased risk for symptomatic disease.


Naturally acquired immunity confers stronger protection against infection and symptomatic disease caused by the Delta variant of SARS-CoV-2, compared to the BNT162b2 2-dose vaccine-induced immunity.

[20] For a litany of other studies with analogous findings, see Just Facts’ research on immunity to COVID-19.

[21] Commentary: “COVID Reinfection: Bad News, or Good?” By Dr. David L. Katz. Edwardsville Intelligencer, August 31, 2020. <>

You have doubtless heard: there has indeed now been one confirmed case of reinfection with SARS-CoV-2, the viral agent of the COVID pandemic. This news has likely reached you via blaring headlines, wrapped in the standard measure of media drama. Chances are good the news as delivered, or perceived, skewed bad. Every way I look at it, however, I see good news. …

Immunity is not an all-or-nothing phenomenon, despite the media tendency to treat it as such. It is possible, after enough time or with changes in health, to get varicella (the chickenpox) twice; it is possible to get measles twice. However, these are uncommon occurrences, because they will only happen when there is a significant exposure that coincides with a nadir in immunity. There is every reason to expect some variant on this theme with SARS-CoV-2, so it should come as no surprise that re-infection after months is possible.

[22] Paper: “Loss of Population Levels of Immunity to Malaria as a Result of Exposure-Reducing Interventions: Consequences for Interpretation of Disease Trends.” By Azra C. Ghani and others. PLoS One, February 9, 2009. <>

“Clinical immunity develops over time dependent on the force of infection in the population and reduces the probability that an individual will develop clinical disease.”

[23] Paper: “Sterilizing Immunity to Influenza Virus Infection Requires Local Antigen-Specific T Cell Response in the Lungs.” By Avijit Dutta and others. Scientific Reports, September 6, 2016. <>

Sterilizing immunity is a unique immune status, which prevents effective virus infection into the host. It is different from the immunity that allows infection but with subsequent successful eradication of the virus. Pre-infection induces sterilizing immunity to homologous influenza virus challenge in ferret.

[24] Paper: “Does Malaria Suffer From Lack of Memory?” By Siske S. Struik and Eleanor M. Riley. Immunological Reviews, September 10, 2004. <>

It is widely perceived that immunity to malaria is, to an extent, defective and that one component of this defective immune response is the inability to induce or maintain long-term memory responses. If true, this is likely to pose problems for development of an effective vaccine against malaria. In this article, we critically review and challenge this interpretation of the epidemiological and experimental evidence. … Furthermore, protective immunity to severe pathology is achieved relatively rapidly and is maintained in the absence of boosting by re-infection. …

Clinically immune individuals have variable levels of immunity to gametocytes and gametes….

[25] Paper: “Severity of SARS-CoV-2 Reinfections as Compared with Primary Infections.” By Laith J. Abu-Raddad and Hiam Chemaitelly. New England Journal of Medicine, November 24, 2021. <>

Qatar had a first wave of infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from March through June 2020, after which approximately 40% of the population had detectable antibodies against SARS-CoV-2. The country subsequently had two back-to-back waves from January through May 2021, triggered by the introduction of the B.1.1.7 (or alpha) and B.1.351 (or beta) variants.1 This created an epidemiologic opportunity to assess reinfections. …

Using national, federated databases that have captured all SARS-CoV-2-related data since the onset of the pandemic … we investigated the risk of severe disease (leading to acute care hospitalization), critical disease (leading to hospitalization in an intensive care unit [ICU]), and fatal disease caused by reinfections as compared with primary infections in the national cohort of 353,326 persons with polymerase-chain-reaction (PCR)-confirmed infection between February 28, 2020, and April 28, 2021, after exclusion of 87,547 persons with a vaccination record. …

Reinfections had 90% lower odds of resulting in hospitalization or death than primary infections. Four reinfections were severe enough to lead to acute care hospitalization. None led to hospitalization in an ICU, and none ended in death. Reinfections were rare and were generally mild, perhaps because of the primed immune system after primary infection. …

[26] Paper: “Reinfection with New Variants of SARS-CoV-2 After Natural Infection: A Prospective Observational Cohort in 13 Care Homes in England.” By Anna Jeffery-Smith and others. Healthy Longevity, December 1, 2021. <>

We report on the duration, neutralising activity, and protection against the alpha variant of previous SARS-CoV-2 infection in care home residents and staff infected more than 6 months previously. …

SARS-CoV-2 reinfections were rare in older residents and younger staff. Protection from SARS-CoV-2 was sustained for longer than 9 months, including against the alpha variant. Reinfection was associated with no or low neutralising antibody before reinfection, but significant boosting occurred on reinfection. …

We found very low rates of reinfection among residents and staff, even in the high-risk, closed environment of care homes and after the emergence of the alpha variant, consistent with our previous observations and those of others.

[27] Paper: “ChAdOx1 nCoV-19 Effectiveness During an Unprecedented Surge in SARS COV-2 Infections.” By Ruma Satwik and others. European Journal of Internal Medicine, August 15, 2021. <>

An unprecedented surge in SARS-CoV-2 infections driven by the Delta variant was reported from India recently[[1]]. The total reported new cases from its capital, New Delhi, in April and May 2021 were more than those reported in a 13-month period since the onset of the pandemic….

The third key finding is that previous infections with SARS-CoV-2 were significantly protective against all studied outcomes, with an effectiveness of 93% (87 to 96%) seen against symptomatic infections, 89% (57 to 97%) against moderate to severe disease and 85% (-9 to 98%) against supplemental oxygen therapy. All deaths occurred in previously uninfected individuals. This was higher protection than that offered by single or double dose vaccine.

[28] Paper: “SARS-CoV-2 Antibody-Positivity Protects Against Reinfection for at Least Seven Months with 95% Efficacy.” By Laith J. Abu-Raddad and others. eClinicalMedicine (Published by the Lancet), May 1, 2021. <>

Among 43,044 antibody-positive persons who were followed for a median of 16.3 weeks (range: 0–34.6), 314 individuals (0.7%) had at least one PCR positive swab ≥14 days after the first-positive antibody test. …

Reinfection is rare in the young and international population of Qatar. Natural infection appears to elicit strong protection against reinfection with an efficacy ~95% for at least seven months. …

While one reinfection was severe, none were critical or fatal and a large proportion of reinfections were minimally symptomatic (if not asymptomatic) to the extent that they were discovered only incidentally, such as through contact tracing or random testing campaigns/surveys (Table 2). …

Incidence rate of reinfection versus month of follow-up did not show any evidence of waning of immunity for over seven months of follow-up.

[29] Paper: “Antibody Status and Incidence of SARS-CoV-2 Infection in Health Care Workers.” By Sheila F. Lumley and others. New England Journal of Medicine, December 23, 2020. <>

A total of 12,541 health care workers participated and had anti-spike IgG measured; 11,364 were followed up after negative antibody results and 1265 after positive results, including 88 in whom seroconversion occurred during follow-up. … There were no symptomatic infections in workers with anti-spike antibodies.

[30] Paper: “Immunosenescence: Implications for Vaccination Programmes in Adults.” By Pierre Olivier Lang and others. Maturitas, April 2011. <>

Because the efficacy of the vaccine mainly depends on the quality of the immune response, immunocompromised individuals are at greater risk of being insufficiently protected [1]. A multitude of changes in the immune system occur with aging (Table 1) and lead to limit the protective effects of vaccination in older adults. Collectively, these changes are known as immunosenescence [2], [3], [4], and their effects are evident in both the innate (consisting mainly of monocytes, natural killer cells and dendritic cells – DCs) and adaptive (represented by B and T-cell mediated immunity), branches of the immune system [2].

[31] Paper: “Obesity, Inflammation and the Immune System.” By Fatima Perez de Heredia, Sonia Gomez-Martinez, and Ascension Marcos. Proceedings of the Nutrition Society, March 20, 2012. <>

Obesity shares with most chronic diseases the presence of an inflammatory component, which accounts for the development of metabolic disease and other associated health alterations. This inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and it occurs not only in adults but also in adolescents and children. … Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity.

[32] Article: “Stress Damages Immune System and Health.” By Ronald Glaser. Discovery Medicine, July 18, 2009. <>

Because the immune system plays an important role in defending the body against a variety of infectious organisms, any abnormalities or changes in the ability of the immune system to perform normally can have implications for either more severe illness or a greater risk of mortality following infection.

[33] Paper: “Opioids and the Immune System.” By Paola Sacerdote. Palliative Medicine, January 2006. <>

Opioid compounds such as morphine produce powerful analgesia that is effective in treating various types of pain. In addition to their therapeutic efficacy, opioids can produce several well known adverse events, and, as has recently been recognized, can interfere with the immune response. The immunomodulatory activities of morphine have been characterized in animal and human studies. Morphine can decrease the effectiveness of several functions of both natural and adaptive immunity, and significantly reduces cellular immunity. Indeed, in animal studies morphine is consistently associated with increased morbidity and mortality due to infection and worsening of cancer.

NOTE: A wide variety of other drugs can also suppress the immune system. Numerous paper on this topic are available here.

[34] Article: “Alcohol and the Immune System.” By Dipak Sarkar and others. Alcohol Research: Current Reviews, 2015. <>

Clinicians have long observed an association between excessive alcohol consumption and adverse immune-related health effects such as susceptibility to pneumonia. In recent decades, this association has been expanded to a greater likelihood of acute respiratory stress syndromes (ARDS), sepsis, alcoholic liver disease (ALD), and certain cancers; a higher incidence of postoperative complications; and slower and less complete recovery from infection and physical trauma, including poor wound healing.

This issue of Alcohol Research: Current Reviews (ARCR) summarizes the evidence that alcohol disrupts immune pathways in complex and seemingly paradoxical ways. These disruptions can impair the body’s ability to defend against infection, contribute to organ damage associated with alcohol consumption, and impede recovery from tissue injury. …

In addition to pneumonia, alcohol consumption has been linked to pulmonary diseases, including tuberculosis, respiratory syncytial virus, and ARDS. Alcohol disrupts ciliary function in the upper airways, impairs the function of immune cells (i.e., alveolar macrophages and neutrophils), and weakens the barrier function of the epithelia in the lower airways (see the article by Simet and Sisson). Often, the alcohol-provoked lung damage goes undetected until a second insult, such as a respiratory infection, leads to more severe lung diseases than those seen in nondrinkers. …

Alcohol consumption does not have to be chronic to have negative health consequences. In fact, research shows that acute binge drinking also affects the immune system.

[35] Paper: “Sleep and the Immune System.” By Harvey Moldofsky. International Journal of Immunopharmacology, August 1995. <>

Disorganization or loss of the sleep-wake system is accompanied by alteration of the immunological, neuroendocrine and thermal functions of the body, and contributes to pathological processes such as infectious disease.

[36] 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. <>

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. …

Lipsitch is far from alone in his belief that this virus will continue to spread widely. The emerging consensus among epidemiologists is that the most likely outcome of this outbreak is a new seasonal disease—a fifth “endemic” coronavirus. With the other four, people are not known to develop long-lasting immunity. If this one follows suit, and if the disease continues to be as severe as it is now, “cold and flu season” could become “cold and flu and COVID-19 season.”

[37] Article: “ ‘No Evidence; Yet That Recovered COVID-19 Patients Are Immune, WHO Says.” By Colin Dwyer. NPR, April 25, 2020. <>

Coronavirus antibody test kits are key to plans for proposed “immunity passports,” but the World Health Organization is warning that such cards may simply encourage further transmission.

The World Health Organization has pushed back against the theory that individuals can only catch the coronavirus once, as well as proposals for reopening society that are based on this supposed immunity.

In a scientific brief dated Friday, the United Nations agency said the idea that one-time infection can lead to immunity remains unproven and is thus unreliable as a foundation for the next phase of the world’s response to the pandemic.

“Some governments have suggested that the detection of antibodies to the SARS-CoV-2, the virus that causes COVID-19, could serve as the basis for an ‘immunity passport’ or ‘risk-free certificate’ that would enable individuals to travel or to return to work assuming that they are protected against re-infection,” the WHO wrote. “There is currently no evidence that people who have recovered from COVID-19 and have antibodies are protected from a second infection.”

[38] Article: “Why the New Coronavirus Is So Hard to Cure.” By Umair Irfan. Vox, March 11, 2020. <>

“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.”

[39] Commentary: “Get Ready To Live With COVID-19.” By Todd Hixon. Forbes, March 12, 2020. <>

Corona viruses like influenza viruses are based on a single strand of RNA. This viral class has a propensity to mutate, requiring constant development of new vaccines, as with the flu. …

Seasonal flu is highly infectious, but its mortality rate is low: about 30,000 deaths in the U.S. in a bad flu season. …

How do we go forward with the burden of COVID-19, a disease that could recur annually like the seasonal flu but kill perhaps 100 times more people?

[40] 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.”