A dangerous new trend has emerged on social media, which involves a new COVID ‘cure’ by gargling the widely used antiseptic, povidone-iodine (PVP).
This trend has been sparked by an online video in Thai which has been widely shared on social media, featuring someone who claims to be a doctor. However this has been debunked. The trend is also cause for concern as the PVP may accidentally be swallowed.
PVP, also sold under the name Betadine, is used for disinfection in surgical procedures and wound treatment. Gargling with 0.5% PVP has been shown to reduce the symptoms of sore throat associated with COVID, but has not been adequately shown to relieve any other symptoms. The immediate side effects of ingesting any PVP antiseptic include nausea, vomiting, general weakness, and diarrhoea. In severe cases, PVP ingestion can result in acute renal failure, cardiovascular collapse, liver function impairment, shortness of breath, low blood pressure, and even death.
In one study, researchers assessed the usage of 0.5% povidone-iodine mouthwash in patients as a way of reducing viral load during dental procedures, reducing possible exposure of healthcare workers. However, there is no evidence beyond in vitro testing that it actually reduces viral load in the throat.
An official statement on the Betadine website reads as follows: “Betadine® Antiseptic First Aid products have not been approved to treat coronavirus. Products should only be used to help prevent infection in minor cuts, scrapes and burns. Betadine Antiseptic products have not been demonstrated to be effective for the treatment or prevention of COVID-19 or any other viruses.”
A new study found that people infected with SARS-CoV-2 shed significant numbers of virus particles in their breath – and those infected with the Alpha variant put 43 to 100 times more virus into the air than people infected with the original strains.
The researchers also found that loose-fitting cloth and surgical masks reduced the amount of virus that gets into the air around infected people by about half. The study was published in Clinical Infectious Diseases.
“Our latest study provides further evidence of the importance of airborne transmission,” said Dr Don Milton, Professor, Environmental Health, University of Maryland School of Public Health. “We know that the Delta variant circulating now is even more contagious than the Alpha variant. Our research indicates that the variants just keep getting better at traveling through the air, so we must provide better ventilation and wear tight-fitting masks, in addition to vaccination, to help stop spread of the virus.”
The numbers of airborne virus particles coming from infections with the Alpha variant (the dominant strain circulating at the time this study was conducted) was much more (18 times more) than could be explained by the increased amounts of virus picked up in nasal swabs and saliva. Doctoral student Jianyu Lai, a lead author of the study, explained: “We already knew that virus in saliva and nasal swabs was increased in Alpha variant infections. Virus from the nose and mouth might be transmitted by sprays of large droplets up close to an infected person. But, our study shows that the virus in exhaled aerosols is increasing even more.” These major increases in airborne virus from Alpha infections occurred before the arrival of the Delta variant, suggesting that the virus is evolving to have improved airborne transmission.
To test the efficacy of masks in reducing transmission, the researchers measured how much SARS-CoV-2 is exhaled into the air with and without wearing a cloth or surgical mask. They found that face coverings significantly reduced virus-laden particles in the air around the person with COVID by about 50%.
Co-author Dr Jennifer German said, “The take-home messages from this paper are that the coronavirus can be in your exhaled breath, is getting better at being in your exhaled breath, and using a mask reduces the chance of you breathing it on others.” This means that a layered approach to control measures (including improved ventilation, increased filtration, UV air sanitation, and tight-fitting masks, in addition to vaccination) is critical to protect people in public-facing jobs and indoor spaces.
In an article in the BMJ, authors argue that menstrual changes after COVID vaccination are plausible and should be investigated.
Listed common side effects of COVID vaccination include a sore arm, fever, fatigue, and myalgia. However, changes to periods and unexpected vaginal bleeding are not listed, and primary care clinicians and those in the reproductive health field are seeing more and more people who have experienced these events shortly after vaccination.
More than 30 000 reports of these events had been made to the UK;s surveillance scheme for adverse drug reactions by 2 September 2021, across all COVID vaccines currently offered.
Most post-vaccination changes to periods return to normal, and there is no evidence that COVID vaccination adversely affects fertility. In clinical trials, there were similar rates for unintended pregnancies in vaccinated and unvaccinated groups. In fertility clinics, fertility measures and pregnancy rates are similar in vaccinated and unvaccinated patients. The UK’s Medicines and Healthcare Products Regulatory Agency (MHRA) says that there are few reported that
Menstrual changes have been reported after both mRNA and adenovirus vectored COVID vaccines, suggesting that, if there is a connection, it is likely to be a result of the immune response to vaccination rather than a specific vaccine component. Human papillomavirus (HPV) vaccinations have also been associated with menstrual changes. Indeed, the menstrual cycle can be affected by immune activation from various stimuli, including viral infection: one study found about a quarter of menstruating women with COVID experienced menstrual disruption.
Biologically plausible mechanisms linking immune stimulation with menstrual changes include immunological influences on the hormones driving the menstrual cycle or effects mediated by immune cells in the lining of the uterus, which are involved in the cyclical build-up and breakdown of this tissue. Research may also help understand the mechanism.
Though the period changes are short lived, there is need for adequate research. Vaccine hesitancy among young women is largely driven by false claims that COVID vaccines could harm their chances of future pregnancy. Failing to thoroughly investigate reports of menstrual changes after vaccination is likely to fuel these fears. If a link between vaccination and menstrual changes is confirmed, this information will allow people to plan for potentially altered cycles. Clear and trusted information is particularly important for those who rely on being able to predict their menstrual cycles to either achieve or avoid pregnancy.
In terms of management, the Royal College of Obstetricians and Gynaecologists and the MHRA recommend that anyone reporting a change in periods persisting over several cycles, or new vaginal bleeding after the menopause, should be managed according to the usual clinical guidelines for these conditions.
The authors conclude by stating there is an important lesson in that the effects of medical interventions on menstruation should not be an afterthought in future research. In clinical trials, participants are unlikely to report changes to periods unless specifically asked, so in future trials, information about menstrual cycles and other vaginal bleeding should be actively solicited.
Though great progress has been made in developing intramuscular COVID vaccines, as yet nothing provides mucosal immunity in the nose, the first barrier against the virus encounters before it travels down to the lungs.
In terms of both immune cell deployment and immunoglobulin production, the mucosal immune system is by far the largest component of the entire immune system, having evolved to provide protection at the main sites of infectious threat: the mucosae.
In iScience, Navin Varadarajan, Professor of Chemical and Biomolecular Engineering, and colleagues, report the development of an intranasal subunit vaccine that provides durable local immunity against inhaled pathogens.
“Mucosal vaccination can stimulate both systemic and mucosal immunity and has the advantage of being a non-invasive procedure suitable for immunization of large populations,” explained Prof Varadarajan. “However, mucosal vaccination has been hampered by the lack of efficient delivery of the antigen and the need for appropriate adjuvants that can stimulate a robust immune response without toxicity.”
To get around this, Prof Varadarajan worked with Xinli Liu, associate professor of pharmaceutics, and an expert in nanoparticle delivery. Prof Liu’s team packaged the agonist of the stimulator of interferon genes (STING) inside liposomal particles to create an adjuvant called NanoSTING.
“NanoSTING has a small particle size around 100 nanometres, which exhibits significantly different physical and chemical properties to the conventional adjuvant,” said Prof Liu.
“We used NanoSTING as the adjuvant for intranasal vaccination and single-cell RNA-sequencing to confirm the nasal-associated lymphoid tissue as an inductive site upon vaccination. Our results show that the candidate vaccine formulation is safe, produces rapid immune responses—within seven days—and elicits comprehensive immunity against SARS-CoV-2,” said Prof Varadarajan.
Intramuscular vaccines have a fundamental limitation in that they are not designed to elicit mucosal immunity. As shown in previous work with respiratory pathogens like influenza, sterilising immunity to virus reinfection requires adaptive immune responses in the respiratory system.
The nasal vaccine will also help the equitable global distribution of vaccines, according to the researchers. Many smaller countries have only vaccinated a small percentage of their population, and outbreaks continue. These outbreaks and viral spread are known to facilitate viral evolution, ultimately leading to decreased efficacy of all vaccines.
“Equitable distribution requires vaccines that are stable and that can be shipped easily. As we have shown, each of our components, the protein (lyophilised) and the adjuvant (NanoSTING) are stable for over 11 months and can be stored and shipped without the need for freezing,” said Prof Varadarajan.
New research finds African countries, assessed as being least vulnerable to an epidemic were the worst affected by COVID, particularly South Africa.
A team of researchers from the NIHR Global Health Research Unit Tackling Infections to Benefit Africa (TIBA) worked with the World Health Organization (WHO) African Region to identify factors affecting mortality rates during Africa’s first two COVID waves and the timing of the first reported cases. The study, published in the journal Nature Medicine, found that countries with greater urban populations and strong international travel links were worst affected by the pandemic. Mortality rates and levels of restrictions, such as lockdowns and travel bans, were found to be lowest in countries previously thought to be at greatest risk from COVID.
Professor Mark Woolhouse, TIBA Director, who co-led the study, said, “Our study shows very clearly that multiple factors influence the extent to which African countries are affected by COVID. These findings challenge our understanding of vulnerability to pandemics.
“Our results show that we should not equate high levels of preparedness and resilience with low vulnerability.
“That seemingly well-prepared, resilient countries have fared worst during the pandemic is not only true in Africa; the result is consistent with a global trend that more developed countries have often been particularly hard hit by COVID.”
Among 44 countries of the WHO African Region with available data, South Africa had the highest mortality rate during the first wave between May and August 2020, at 33.3 deaths recorded per 100k population. Cape Verde and Eswatini had the next highest rates at 17.5 and 8.6 deaths per 100k, respectively. At 0.26 deaths recorded per 100,000, the lowest mortality rate was in Uganda.
South Africa also recorded the highest mortality rate during the second wave between December 2020 and February 2021, at 55.4 deaths per 100,000. Eswatini and Botswana recorded rates of 39.8 and 17.7 deaths per 100,000, respectively. The lowest rate was in Mauritius, which recorded no deaths during the second wave.
“The early models which predicted how COVID would lead to a massive number of cases in Africa were largely the work of institutions not from our continent. This collaboration between researchers in Africa and Europe underlines the importance of anchoring analysis on Africa’s epidemics firmly here,” said Dr. Matshidiso Moeti, WHO Regional Director for Africa and co-author. “We can no longer focus our understanding of disease transmission purely on the characteristics of a virus—COVID operates within a social context which has a major impact on its spread.”
Countries with high rates of HIV were also more likely to have higher mortality rates. This may be because people with HIV often have other health conditions that put them at greater risk from COVID, the team suggests.
The weak association between mortality rate and the timing or severity of government-imposed social restrictions shows the varied impact and enforcement across the region, making a consistent impact pattern difficult to discern. Restrictions during peaks of infection are well documented to have interrupted transmission in the region.
The findings show that the earliest recorded cases of COVID were in countries where most people live in urban areas, with strong international travel links and greater testing capacity. Algeria was the first of 47 African countries to report a case, on 25 February 2020. Most countries had recorded cases by late March 2020, with Lesotho the last to report one, on 14 May 2020.
Higher death rates were observed during the second wave, compared with the first. The infection peak during the second wave was also higher, with 675 deaths across the continent on 18 January 2021 compared with 323 during the first wave peak on 5 August 2020. Potential under-reporting was accounted for in the analysis.
A new study found that the two-metre physical distance required to avoid the viral shedding from a person infected with COVID caused by speaking or breathing may be insufficient indoors.
Researchers from the Penn State Department of Architectural Engineering found that indoor distances of two metres may not be enough to sufficiently prevent transmission of airborne aerosols. Their results were published online in Sustainable Cities and Society.
“We set out to explore the airborne transport of virus-laden particles released from infected people in buildings,” said first author Gen Pei, a doctoral student in architectural engineering at Penn State. “We investigated the effects of building ventilation and physical distancing as control strategies for indoor exposure to airborne viruses.”
The researchers looked at three factors: the amount and rate of air ventilated through a space, the indoor airflow pattern associated with different ventilation strategies and the aerosol emission mode of breathing versus talking. They also compared transport of tracer gas, usually used to test leaks in air-tight systems, and human respiratory aerosols ranging in size from one to 10 micrometres, a size that can still carry SARS-CoV-2.
“Our study results reveal that virus-laden particles from an infected person’s talking — without a mask — can quickly travel to another person’s breathing zone within one minute, even with a distance of two meters,” said corresponding author Donghyun Rim, associate professor of architectural engineering. “This trend is pronounced in rooms without sufficient ventilation. The results suggest that physical distance alone is not enough to prevent human exposure to exhaled aerosols and should be implemented with other control strategies such as masking and adequate ventilation.”
Aerosols were found to travel farther and more quickly in rooms with displacement ventilation, where fresh air continuously flows from the floor and pushes old air to an exhaust vent near the ceiling. This is the type of ventilation system installed in most residential homes, and it can result in a human breathing zone concentration of viral aerosols seven times higher than mixed-mode ventilation systems. Many commercial buildings have mixed-mode systems, which bring in outside air to dilute the indoor air and result in better air integration as well as tempered aerosol concentrations, according to the researchers.
“This is one of the surprising results: Airborne infection probability could be much higher for residential environments than office environments,” Prof Rim said. “However, in residential environments, operating mechanical fans and stand-alone air cleaners can help reduce infection probability.”
According to Rim, increasing the ventilation and air mixing rates can effectively reduce the transmission distance and potential accumulation of exhaled aerosols, but ventilation and distance are only two options in an arsenal of protective techniques.
“Airborne infection control strategies such as physical distancing, ventilation and mask wearing should be considered together for a layered control,” Prof Rim said.
The researchers are now applying this analysis technique to other kinds of occupied spaces, such as classrooms and transportation environments.
Interim results from a phase 1B/2A clinical trial conducted by the Wits Vaccines and Infectious Diseases Analytical (VIDA) research unit showed that the AstraZeneca vaccine conferred COVID protection in people living with HIV.
The findings, published in Lancet HIV, show that the AstraZeneca COIVD vaccine is likely to work as well in people living with HIV compared with people who are HIV negative.
These interim findings are vital for informing the clinical management of people with HIV during the COVID pandemic.
In general, clinical trials which evaluate the safety and immunogenicity of COVID vaccines in people living with HIV are limited, and in Africa they are virtually non-existent. This is despite the overwhelming prevalence of HIV infection in Africa, especially South Africa .
“We searched PubMed for peer-reviewed articles published between 1 January 2019 and 29 June 2021, using the terms ‘safety’ and ‘Covid-19’ and ‘vaccine’, but we did not find any reports that evaluated safety and immunogenicity of COVID vaccines in this population,” said Shabir Madhi, Professor of Vaccinology and Director of Wits VIDA, which led the first South African trial for a COVID vaccine in June 2020.
Compared to the general population, people living with HIV have an increased risk of infectious diseases and have a greater mortality risk when hospitalised with severe COVID.
In addition, compared with HIV-negative individuals, people with HIV are at greater risk for infectious diseases, such as influenza, including during antiretroviral therapy (ART).
Risk factors for severe COVID in people with HIV include more advanced stage of HIV/AIDS, the HIV-1 infection not being virally suppressed, and CD4 counts below 500 cells per microlitre.
The study was an interim analysis of a randomised, double-blind, placebo-controlled, phase 1B/2A trial. In 2020, the trial enrolled 104 people living with HIV were enrolled in the trial, HIV-negative people. Eligibility criteria for people with HIV included being on ART for at least three months, with a plasma HIV viral load of less than 1000 copies per microlitre.
The HIV study was a unique addition to the AstraZeneca COVID vaccine clinical trial, and aimed to assess safety and immunogenicity of this vaccine in people with HIV and HIV-negative people in South Africa. The primary endpoint in all participants regardless of HIV status was the safety, tolerability, and reactogenicity profile of the AstraZeneca COVID vaccine.
Reactogenicity refers to a subset of reactions that occur soon after vaccination, and are a physical manifestation of the inflammatory response to vaccination. Such symptoms include pain, redness, swelling or induration for injected vaccines, and systemic symptoms, such as fever, myalgia, headache, or rash. In clinical trials, information on expected signs and symptoms after vaccination is actively sought.
The interim findings show that the AstraZeneca COVID vaccine was well tolerated and showed favourable safety and immunogenicity in people with HIV, including heightened immunogenicity in SARS-CoV-2 baseline-seropositive participants.
New research finds that one cause of organ damage in COVID patients is abnormal crosstalk between blood platelets and cells lining blood vessels.
The study published in Science Advances, revealed the protein signals released by platelets cause inflammation, abnormal clotting, and damage to vessels when exposed to SARS-CoV-2.
The work identified two related genes, S1000A8 and S1000A9, which are turned up in the platelets of COVID patients, causing them to make more of myeloid-related proteins (MRP) 8 and 14. Higher levels of the dual proteins were linked in the study to higher levels of clotting and inflammation in vessels and worse outcomes.
In support of the theory that platelets are at the core of blood vessel damage in COVID, the research team also presented evidence that approved medications known to block platelet activation via the platelet surface protein P2Y12 (clopidogrel or ticagrelor) reduced COVID-related inflammation in vessels. The study also found that COVID-exposed platelets change cells lining blood vessels (endothelial cells) largely through a protein called p-selectin, which makes platelets stickier and more likely to form clots.
“Our findings reveal a new role for platelets in COVID blood vessel damage, and may explain in large part what makes the COVID virus so much more deadly than its relatives that cause the common cold,” said corresponding author Tessa Barrett, PhD,.
Abnormal, body-wide inflammation and blood clotting were identified early in the pandemic as central features of severe COVID-19, with the two thought to be interrelated, say the study authors. As blood components that react to injuries in vessels by triggering inflammation, and by becoming sticky to clump together in clots, platelets are a possible culprit. Increasing evidence shows that interplay between platelets and endothelial cells may be important to these disease mechanisms.
For the current study, endothelial cells from small blood vessels were exposed to fluid released from the platelets of either COVID patients or healthy controls. RNA was then sequenced, In the presence of COVID-activated platelets, changes were observed in the activity of the exposed endothelial cells. Genes expressed differently in COVID-19 were linked to clotting, inflammation, and the weakening of junctions between endothelial cells, which lets blood serum seep into tissue to cause the pulmonary oedema seen in severe cases, where patients’ lungs fill with fluid.
The large list was narrowed down to S100A8 and S100A9, which coded for the building of MRP 8 and 14. COVID in patients was found to increase the amount of MRP8/14 produced by platelets and other cells by 166 percent compared to controls. Higher levels of these proteins were linked to abnormal thrombosis, inflammation, and critical illness among hospitalised COVID patients. Curiously S100A8/A9 were not upregulated after exposure of platelets to a coronavirus relative, CoV-OC43, which causes the common cold.
Additionally, damage and abnormal clotting could arise from p-selectin, which promotes platelet clumping and immune-boosting signals. The researchers also found that the anti-clotting P2Y12 inhibitors reduced the expression of S100A8 and S100A9 in platelets by 18 percent over four weeks, and in lab tests prevented COVID platelets from inducing blood vessel damage.
“The current study supports the theory that platelets are activating endothelial cells through P-selectin, and that both p-selectin and MRP8/14 contribute to vessel damage and an increased risk of dying,” said senior study author Jeffrey S. Berger, MD. “As our team also leads ACTIV4a, a large, ongoing NIH-funded, anti-clotting trial in COVID, we are currently testing in patients whether P2Y12 inhibitors can better prevent severe disease, with the results to be presented at the American Heart Association annual meeting in November.”
A study based on self-reported app data showed that people who eat a high quality, gut friendly diet are less likely to develop COVID-19 or become severely ill. Those eating poorer quality diets are more at risk, especially if they live in a more socioeconomically deprived area.
The study, presented in GUT, analysed data from almost 600 000 ZOE COVID Study app contributors. Participants completed a survey about the food they ate before the pandemic, in February 2020, making it the largest study in this space. 19% of these contributors contracted COVID-19.
People with the highest quality diet were around 10% less likely to develop COVID than those with the lowest quality diet, and 40% less likely to fall severely ill.
This is the first longitudinal study of diet and COVID and the first to show that a healthy diet cuts the chances of developing the disease in the first place.
Instead of looking at specific foods, the survey aimed to broadly capture people’s diets. A ‘diet quality score’ reflected the overall merit of each person’s diet. Diets with high quality scores were found to contain plant-based foods such as fruits, vegetables and whole grains, as well as oily fish, less processed foods and refined carbohydrates. A low diet quality score is associated with diets high in ultra processed foods and low amounts of plant based foods.
The researchers found that people who ate the highest quality diet were around 10% less likely to develop COVID-19 than those with the least nutritious diet and 40% less likely to become severely ill if they developed COVID.
The link between diet quality and COVID risk persisted after accounting for all potential confounding factors such as age and BMI. Mask-wearing habits and population density were also considered.
The effect of diet was amplified by individual life situations, with people living in low-income neighbourhoods with the lowest quality diet being around 25% more at risk from COVID than people in more affluent communities eating the same kind of diet.
Based on these results, the researchers estimate that nearly a quarter of COVID cases could have been prevented if these differences in diet quality and socioeconomic status had not existed. The study also showed that improved access to better food is an important public health consideration.
Dr Sarah Berry, study co-lead and Reader in nutritional sciences at the School of Life Course Sciences said: “For the first time we’ve been able to show that a healthier diet can cut the chances of developing COVID, especially for people living in the more deprived areas. Access to healthier food is important to everyone in society, but our findings tell us that helping those living in more deprived areas to eat more healthily could have the biggest public health benefits.”
Professor Tim Spector, professor of genetic epidemiology at the School of Life Course Sciences, said: “These findings chime with recent results from our landmark PREDICT study, showing that people who eat higher quality diets (with low levels of ultra-processed foods) have a healthier collection of microbes in their guts, which is linked to better health. You don’t have to go vegan, but getting more diverse plants on your plate is a great way to boost the health of your gut microbiome, improve your immunity and overall health, and potentially reduce your risk from COVID.”
A series of studies in recent months has found that, thanks to the mRNA vaccine and previous infection, some people mount an extraordinarily powerful immune response against SARS-CoV-2 which some scientists have referred to as ‘superhuman’.
Called ‘hybrid immunity’, their bodies produce very high levels of antibodies, with great flexibility: likely capable of fighting off the SARS-CoV-2 variants currently circulating but also likely effective against future variants.
“Overall, hybrid immunity to SARS-CoV-2 appears to be impressively potent,” Crotty wrote in commentary in Science published in June.
“One could reasonably predict that these people will be quite well protected against most and perhaps all of — the SARS-CoV-2 variants that we are likely to see in the foreseeable future,” says Paul Bieniasz, a virologist at Rockefeller University who helped lead several of the studies.
Bieniasz and his colleagues found antibodies in these individuals capable of strongly neutralising the six variants of concern tested, including Delta and Beta, as well as several other viruses related to SARS-CoV-2, including SARS-CoV-1.
“This is being a bit more speculative, but I would also suspect that they would have some degree of protection against the SARS-like viruses that have yet to infect humans,” Bieniasz said.
People who have had a ‘hybrid’ exposure to the virus, were infected with it in 2020 and then immunised with mRNA vaccines this year. “Those people have amazing responses to the vaccine,” said virologist Theodora Hatziioannou at Rockefeller University, who also helped lead several of the studies. “I think they are in the best position to fight the virus. The antibodies in these people’s blood can even neutralize SARS-CoV-1, the first coronavirus, which emerged 20 years ago. That virus is very, very different from SARS-CoV-2.”
These antibodies were so effective they were even able to deactivate a virus purposefully engineered to be highly resistant to neutralisation, containing 20 mutations that are known to prevent SARS-CoV-2 antibodies from binding to it. Antibodies from those who were only vaccinated or who only had prior coronavirus infections were ineffecgtive against this engineered virus..
This shows how powerful the mRNA vaccine can be in those infected with SARS-CoV-2, she said. “There’s a lot of research now focused on finding a pan-coronavirus vaccine that would protect against all future variants. Our findings tell you that we already have it.
The catch is getting COVID. “After natural infections, the antibodies seem to evolve and become not only more potent but also broader. They become more resistant to mutations within the [virus].”
Hatziioannou and colleagues don’t know if this applies to all those mRNA-vaccinated and previously COVID-infected. “We’ve only studied the phenomena with a few patients because it’s extremely laborious and difficult research to do,” she said. “With every single one of the patients we studied, we saw the same thing.” The study reports data on 14 patients.
Several other studies lend credence to her hypothesis and reinforce the idea that exposure to both a coronavirus and an mRNA vaccine triggers an exceptionally powerful immune response. In one study in NEJM, scientists analysed antibodies generated by people who had been infected with SARS-CoV-1 back in 2002 or 2003 and who then received an mRNA vaccine this year.
Remarkably, these people also produced high levels of antibodies that could neutralise a whole range of variants and SARS-like viruses. Many questions remain, such as the effect of a third booster shot, or being infected again.
“I’m pretty certain that a third shot will help a person’s antibodies evolve even further, and perhaps they will acquire some breadth [or flexibility], but whether they will ever manage to get the breadth that you see following natural infection, that’s unclear.”
Immunologist John Wherry, at the University of Pennsylvania, is a bit more hopeful. “In our research, we already see some of this antibody evolution happening in people who are just vaccinated,” he said, “although it probably happens faster in people who have been infected.”
In a recent study, Wherry and colleagues showed that, over time, uninfected people with only two doses of the vaccine begin to produce more flexible antibodies, so a third dose would give even more of an evolutionary boost to the antibodies, Wherry said. So a person will be better equipped to fight off whatever variant the virus puts out there next.
“Based on all these findings, it looks like the immune system is eventually going to have the edge over this virus,” said Bieniasz, of Rockefeller University. “And if we’re lucky, SARS-CoV-2 will eventually fall into that category of viruses that gives us only a mild cold.”