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Tens of millions of farm animals cross state lines every year, traveling in cramped, stressful conditions that can facilitate the spread of disease.The bird flu virus that is spreading through American dairy cows can probably be traced back to a single spillover event. Late last year, scientists believe, the virus jumped from wild birds into cattle in the Texas panhandle. By this spring, the virus, known as H5N1, had traveled hundreds of miles or more, appearing on farms in Idaho, North Carolina and Michigan.The virus did not traverse those distances on its own. Instead, it hitched a ride with its hosts, the cows, moving into new states as cattle were transported from the outbreak’s epicenter to farms across the country.Live animal transport is essential to industrial animal agriculture, which has become increasingly specialized. Many facilities focus on just one step in the production process — producing new young, for instance, or fattening adults for slaughter — and then send the animals on.The exact number of chickens, cows and pigs being transported on trucks, ships, planes and trains within the United States is difficult to pinpoint because there is no universal national system for tracking their movement.But estimates from official sources and animal advocates offer a sense of the scale: In 2022, some 21 million cattle and 62 million hogs were shipped into states for breeding, or feeding, according to the Agriculture Department; these figures do not include poultry, movement within the same state or journeys to slaughter. That same year, more than 500,000 young dairy calves, some only a few days old, were shipped from just six states, according to the Animal Welfare Institute, a nonprofit group. Some traveled more than 1,500 miles.“The movement can contribute to long-distance transport of pathogens and make outbreaks, and the management of outbreaks, challenging,” said Colleen Webb, an expert on livestock epidemiology at Colorado State University.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

The inquiry’s report is thought to be more than 2,000 pages long across multiple volumes.But most attention will focus on a number of key questions.Was there a cover-up? Greater Manchester Mayor and former health secretary Andy Burnham thinks so – in 2017 he told the House of Commons there has been one on an “industrial scale”.Among the inquiry’s terms of reference is a requirement to explore whether there were attempts to conceal what happened by the government or NHS.Attention will also be paid to what the report says about the timeliness of government action.Was it too slow to recognise the risks of infected blood? Should the UK have stopped using blood products imported from the US, where prisoners and drug-users were paid for blood, sooner?And was enough done to subsequently identify those who were infected?A BBC investigation suggests the UK government and the NHS failed to adequately trace those who were most at risk of having the virus.

Published1 hour agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Nick Triggle and Jim ReedBBC NewsThe public inquiry into the infected blood scandal, known as the biggest treatment disaster in NHS history, is due to publish its findings.More than 30,000 people were infected with HIV and hepatitis C between 1970 and 1991 by contaminated blood products and transfusions.Around 3,000 of them have since died – many haemophiliacs given infected blood products as part of their treatment.Chairman Sir Brian Langstaff will present his findings on Monday.The Infected Blood Inquiry took evidence between 2019 and 2023.What is the infected blood scandal and how many people died?The stories behind the infected blood scandal,

Published27 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, Charlotte DickensBy Hugh Pym and Aurelia FosterHealth editor and health reporterThere has been a surge in demand for hepatitis C tests since the BBC revealed that hundreds of people in the UK were unknowingly infected with the virus, the Hepatitis C Trust says.Up to 27,000 people caught it when they were given transfusions with infected blood from the 1970s until 1991. According to BBC analysis, a further 1,700 people who caught it in the same way have not yet been diagnosed.Left untreated, hepatitis can cause chronic liver disease and can be fatal.Known as the “silent killer”, hepatitis C may cause few symptoms initially, with early signs including night sweats, brain fog, itchy skin and fatigue. But for every year a person carries the virus, their chance of dying from liver cirrhosis and related cancers increases. The Hepatitis C Trust told the BBC 12,800 people in England have requested NHS home-testing kits in just over a week, compared with 2,300 in the entire month of April.The charity said it had been “inundated with callers across the UK seeking further advice and testing”. “It has been incredible seeing the response from the public as they have become more aware of the risks of hepatitis C,” said Rachel Halford, from the charity. “Most people who get tested will receive a negative result and have peace of mind, but it is important to find those individuals who are unaware of their status so that we can get them access to a simple and effective treatment.” Undiagnosed casesThe BBC recently exclusively revealed the true scale of undiagnosed cases of the disease, related to the infected blood scandal.The BBC’s calculation of 1,700 undiagnosed cases is based on statistics submitted to a public inquiry,

Published1 hour agoShareclose panelShare pageCopy linkAbout sharingImage source, Family photoBy Jim ReedHealth reporterIt was February 2017 when the message arrived on Facebook. “There’s a much bigger scandal that you need to look into,” it read. “Thousands have died and still nobody talks about it.”That was the first time I heard from Su Gorman and Steve Dymond. I’d been working on a story about hepatitis C treatments. But they wanted me to go to Ramsgate, in Kent, to meet them about something else.A few days later, a heavy bundle of A4 papers arrived: handwritten notes, photocopies of old documents, press clippings from the Kent Messenger newspaper. I quickly learnt that Su was not someone you could easily argue with – or put off with an excuse. Train to Kent coastShe had met Steve at Exeter university in the mid-1970s, where they both studied Russian. They married on 25 October 1980, which was, Su was fond of pointing out, the anniversary of the Bolshevik revolution.Steve had been born with a mild form of the bleeding disorder haemophilia. He didn’t really need a new type of treatment, called Factor VIII, but he was given it anyway. We now know that whole batches of the blood product, made from pooled or mixed donations, often from the US, were contaminated with deadly viruses. Much of the blood had been donated by high-risk donors, such as prison inmates and drug users. If just one was carrying a virus, the entire batch could be contaminated.I read the bundle of documents and later took a train down to the Kent coast where Su and Steve lived in a small bungalow, not far from the seafront. It was the first of perhaps half a dozen trips over the next few years as I – and other journalists – continued to report on what would become a national scandal. Image source, Family photoSteve had first been told something might be wrong in 1983. His local hospital called and warned he may have been exposed to HIV, or HTLV-3 as the virus was then known. At the time, there was no quick test. The couple had to wait 18 long months until they were given the all-clear. “It was an absolutely terrifying period,” Su said to me, a time when the “fear and panic” around Aids was only just starting to emerge. Su and Steve put off having children, something they both deeply regretted later in life. Around 1,250 haemophiliacs were infected with HIV as part of the infected blood scandal,

A lack of detailed record-keeping in clinics and emergency departments may be getting in the way of reducing the inappropriate use of antibiotics, a pair of new studies by a pair of University of Michigan physicians and their colleagues suggests.
In one of the studies, about 10% of children and 35% of adults who got an antibiotic prescription during an office visit had no specific reason for the antibiotic in their record.
The rate of this type of prescribing is especially high in adults treated seen in emergency departments and in adults seen in clinics who have Medicaid coverage or no insurance, the studies show. But the issue also occurs in children.
Without information about what drove these inappropriate prescriptions, it will be even harder for clinics, hospitals and health insurers to take steps to ensure that antibiotics are prescribed only when they’re really needed, the researchers say.
Overuse and misuse of antibiotics raise the risk that bacteria will evolve to resist the drugs and make them less useful for everyone. Inappropriately prescribed antibiotics may also end up doing more harm than good to patients.
“When clinicians don’t record why they are prescribing antibiotics, it makes it difficult to estimate how many of those prescriptions are truly inappropriate, and to focus on reducing inappropriate prescribing,” said Joseph Ladines-Lim, M.D., Ph.D., first author of both of the new studies and a combined internal medicine/pediatrics resident at Michigan Medicine, U-M’s academic medical center.
“Our studies help contextualize the estimates of inappropriate prescribing that have been published previously,” he added. “Those estimates don’t distinguish between antibiotic prescriptions that are considered inappropriate due to inadequate coding and antibiotic prescriptions truly prescribed for a condition that they can’t treat.”
Ladines-Lim worked with U-M pediatrician and health care researcher Kao-Ping Chua, M.D., Ph.D., on the new studies. The one on outpatient prescribing by insurance status is in the Journal of General Internal Medicine and the one on trends in emergency department prescribing is in Antimicrobial Stewardship and Healthcare Epidemiology.

Building on previous research
Chua and colleagues recently published findings about trends in inappropriate antibiotic prescribing in outpatients under age 65, suggesting about 25% were inappropriate. But that number includes antibiotic prescriptions written for infectious conditions that antibiotics don’t help, such as colds, and antibiotic prescriptions that aren’t associated with any diagnoses that could be a plausible antibiotic indication.
The new studies add more nuance to that finding, by looking more closely at these two different types of inappropriate prescriptions.
Most antibiotic stewardship efforts to date have focused on reducing the use of the first type of inappropriate prescription — those written for infectious but antibiotic-inappropriate conditions like colds. The new studies show such patients still account for 9% to 22% of all antibiotic prescriptions, depending on the setting and age group.
But since doctors and other prescribers aren’t required to run a test for a bacterial infection or list a specific diagnosis in order to prescribe antibiotics, symptoms provide potential clues to why they might have written a prescription anyway.
So some of those 9% to 22% of all people receiving antibiotics may have also had a secondary bacterial infection that the clinician suspected based on symptoms.

However, it’s impossible to know.
As for those with no infection-related diagnoses or symptoms in their records who got antibiotics, the researchers suggest that clinicians may not have bothered to add these diagnoses or symptoms to the patient record inadvertently — or even deliberately, to try to avoid the scrutiny of antibiotic watchdogs.
But the researchers also speculate that the lower rate of diagnosis documentation in patients in the healthcare safety net may also have to do with the way healthcare organizations are reimbursed.
Often, clinics and hospitals receive a fixed amount from Medicaid to care for all their patients with that type of coverage. So they aren’t incentivized to create records that are as detailed as for privately insured patients, whose care traditionally is reimbursed under a fee-for-service model.
“This could actually be a matter of health equity if people with low incomes or no insurance are being treated differently when it comes to antibiotics,” says Ladines-Lim, who has also studied antibiotic use related to immigrant and asylum-seeker health and will soon begin a fellowship in infectious diseases.
He said that private and public insurers, and health systems, may need to incentivize accurate diagnosis coding for antibiotic prescriptions — or at least make it easier for providers to document why they’re giving them.
That might even include steps such as requiring providers to record the reason for antibiotic prescribing before prescriptions can be sent to pharmacies through electronic health record systems.
After all, Ladines-Lim said, physicians often have to list a diagnosis that justifies tests they order, such as CT scans or x-rays. With antibiotic resistance posing an international threat to patients who have antibiotic-susceptible conditions, similar steps to justify prescriptions of antibiotics might be advisable.
In addition to Ladines-Lim and Chua, the other authors of the two articles are Michael A. Fischer, M.D., M.S. of Boston Medical Center and Boston University, and Jeffrey A. Linder, M.D., M.P.H. of Northwestern University Feinberg School of Medicine.
The research was funded by a Resident Research Grant from the American Academy of Pediatrics, a Physician Investigator Award from Blue Cross Blue Shield Foundation of Michigan, and a Research Grant from the National Med-Peds Residents’ Association.

The latest findings from the Global Burden of Disease Study (GBD) 2021, published today in The Lancet, forecast that global life expectancy will increase by 4.9 years in males and 4.2 years in females between 2022 and 2050.
Increases are expected to be largest in countries where life expectancy is lower, contributing to a convergence of increased life expectancy across geographies. The trend is largely driven by public health measures that have prevented and improved survival rates from cardiovascular diseases, COVID-19, and a range of communicable, maternal, neonatal, and nutritional diseases (CMNNs).
This study indicates that the ongoing shift in disease burden to non-communicable diseases (NCDs) — like cardiovascular diseases, cancer, chronic obstructive pulmonary disease, and diabetes — and exposure to NCD-associated risk factors — such as obesity, high blood pressure, non-optimal diet, and smoking — will have the greatest impact on disease burden of the next generation.
As the disease burden continues to shift from CMNNs to NCDs and from years of life lost (YLLs) to years lived with disability (YLDs), more people are expected to live longer, but with more years spent in poor health. Global life expectancy is forecasted to increase from 73.6 years of age in 2022 to 78.1 years of age in 2050 (a 4.5-year increase). Global healthy life expectancy (HALE) — the average number of years a person can expect to live in good health — will increase from 64.8 years in 2022 to 67.4 years in 2050 (a 2.6-year increase).
To come to these conclusions, the study forecasts cause-specific mortality; YLLs; YLDs; disability-adjusted life years (DALYs, or lost years of healthy life due to poor health and early death); life expectancy; and HALE from 2022 through 2050 for 204 countries and territories.
“In addition to an increase in life expectancy overall, we have found that the disparity in life expectancy across geographies will lessen,” said Dr. Chris Murray, Chair of Health Metrics Sciences at the University of Washington and Director of the Institute for Health Metrics and Evaluation (IHME). “This is an indicator that while health inequalities between the highest- and lowest-income regions will remain, the gaps are shrinking, with the biggest increases anticipated in sub-Saharan Africa.”
Dr. Murray added that the biggest opportunity to speed up reductions in the global disease burden is through policy interventions aimed to prevent and mitigate behavioral and metabolic risk factors.

These findings build upon the results of the GBD 2021 risk factors study, also released today in The Lancet. This accompanying study found that the total number of years lost due to poor health and early death (measured in DALYs) attributable to metabolic risk factors has increased by 50% since 2000. Read more on the risk factors report at https://bit.ly/GBDRisks2021.
The study also puts forth various alternative scenarios to compare the potential health outcomes if different public health interventions could eliminate exposure to several key risk factor groups by 2050.
“We forecast large differences in global DALY burden between different alternative scenarios to see what is the most impactful on our overall life expectancy data and DALY forecasts,” said Dr. Stein Emil Vollset, first author of the study who leads the GBD Collaborating Unit at the Norwegian Institute of Public Health. “Globally, the forecasted effects are strongest for the ‘Improved Behavioral and Metabolic Risks’ scenario, with a 13.3% reduction in disease burden (number of DALYs) in 2050 compared with the ‘Reference’ (most likely) scenario.”
The authors also ran two more scenarios: one focused on safer environments and another on improved childhood nutrition and vaccination.
“Though the largest effects in global DALY burden were seen from the ‘Improved Behavioral and Metabolic Risk’ scenario, we also forecasted reductions in disease burden from the ‘Safer Environment’ and ‘Improved Childhood Nutrition and Vaccination’ scenarios beyond our reference forecast, said Amanda E. Smith, Assistant Director of Forecasting at IHME. “This demonstrates the need for continued progress and resources in these areas and the potential to accelerate progress through 2050.”
“There is immense opportunity ahead for us to influence the future of global health by getting ahead of these rising metabolic and dietary risk factors, particularly those related to behavioral and lifestyle factors like high blood sugar, high body mass index, and high blood pressure,” continued Dr. Murray.

A team led by investigators from Massachusetts General Hospital, a founding member of the Mass General Brigham healthcare system, used a new drug to save the life of a patient with immune thrombotic thrombocytopenic purpura (iTTP), a rare disorder characterized by uncontrolled clotting throughout the small blood vessels. The group describes the first clinical use of the drug for iTTP in the New England Journal of Medicine.
“The drug is a genetically engineered version of the missing enzyme in iTTP, and we showed that it was able to reverse the disease process in a patient with an extremely severe form of this condition,” said lead author Pavan K. Bendapudi, MD, an investigator in the Division of Hematology and Blood Transfusion Service at Massachusetts General Hospital and an assistant professor of Medicine at Harvard Medical School.
iTTP results from an autoimmune attack against an enzyme called ADAMTS13 that is responsible for cleaving a large protein involved in blood clotting. The current mainstay of therapy for this life-threatening blood disorder is plasma exchange, which removes the harmful autoantibodies and provides extra ADAMTS13. Plasma exchange induces a clinical response in most patients but can restore at best only about half of normal ADAMTS13 activity. By contrast, a recombinant form of human ADAMTS13 (rADAMTS13) offers the possibility of greatly increased ADAMTS13 delivery.
rADAMTS13 was recently approved for patients with congenital thrombotic thrombocytopenic purpura, which occurs in patients born with complete loss of the ADAMTS13 gene. It’s questionable whether rADAMTS13 could be effective in iTTP given the presence of inhibitory anti-ADAMTS13 autoantibodies, but Bendapudi and his colleagues received permission from the US Food and Drug Administration to utilize rADAMTS13 donated from the manufacturer under a compassionate use protocol in a dying patient with treatment-resistant iTTP.
“We found that rADAMTS13 rapidly reversed this patient’s disease process despite the current dogma that inhibitory autoantibodies against ADAMTS13 would render the drug useless in this condition,” said Bendapudi. “We were the first physicians to use rADAMTS13 to treat iTTP in the United States, and in this case it helped to save the life of a young mother.”
Bendapudi noted that the infused rADAMTS13 overwhelmed the inhibitory autoantibodies in the patient and reversed the thrombotic effects of iTTP. This impact was observed almost immediately upon administration of rADAMTS13, after daily plasma exchange had failed to induce remission.
“I think rADAMTS13 has the potential to replace the current standard of care in acute iTTP. We will need larger, well-designed trials to evaluate this possibility,” said Bendapudi.
A phase 2b randomized clinical trial of rADAMTS13 in iTTP was recently initiated.

A new study of prion diseases, using a human cerebral organoid model, suggests there is a substantial species barrier preventing transmission of chronic wasting disease (CWD) from cervids — deer, elk and moose — to people. The findings, from National Institutes of Health scientists and published in Emerging Infectious Diseases, are consistent with decades of similar research in animal models at the NIH’s National Institute of Allergy and Infectious Diseases (NIAID).
Prion diseases are degenerative diseases found in some mammals. These diseases primarily involve deterioration of the brain but also can affect the eyes and other organs. Disease and death occur when abnormal proteins fold, clump together, recruit other prion proteins to do the same, and eventually destroy the central nervous system. Currently, there are no preventive or therapeutic treatments for prion diseases.
CWD is a type of prion disease found in cervids, which are popular game animals. While CWD has never been found in people, a question about its transmission potential has lingered for decades: Can people who eat meat from CWD-infected cervids develop prion disease? The question is important because during the mid-1980s and mid-1990s a different prion disease — bovine spongiform encephalopathy (BSE), or mad cow disease — emerged in cattle in the United Kingdom (U.K.) and cases also were detected in cattle in other countries, including the United States. Over the next decade, 178 people in the U.K. who were thought to have eaten BSE-infected beef developed a new form of a human prion disease, variant Creutzfeldt-Jakob Disease, and died. Researchers later determined that the disease had spread among cattle through feed tainted with infectious prion protein. The disease transmission path from feed to cattle to people terrified U.K. residents and put the world on alert for other prion diseases transmitted from animals to people, including CWD. CWD is the most transmissible of the prion disease family, showing highly efficient transmission between cervids.
Historically, scientists have used mice, hamsters, squirrel monkeys and cynomolgus macaques to mimic prion diseases in people, sometimes monitoring animals for signs of CWD for more than a decade. In 2019, NIAID scientists at Rocky Mountain Laboratories in Hamilton, Montana, developed a human cerebral organoid model of Creutzfeldt-Jakob Disease to evaluate potential treatments and to study specific human prion diseases.
Human cerebral organoids are small spheres of human brain cells ranging in size from a poppy seed to a pea. Scientists grow organoids in dishes from human skin cells. The organization, structure, and electrical signaling of cerebral organoids are similar to brain tissue. They are currently the closest available laboratory model to the human brain. Because organoids can survive in a controlled environment for months, scientists use them to study nervous system diseases over time. Cerebral organoids have been used as models to study other diseases, such as Zika virus infection, Alzheimer’s disease, and Down syndrome.
In the new CWD study, the bulk of which was done in 2022 and 2023, the research team validated the study model by successfully infecting human cerebral organoids with human CJD prions (positive control). Then, using the same laboratory conditions, they directly exposed healthy human cerebral organoids for seven days with high concentrations of CWD prions from white-tailed deer, mule deer, elk, and normal brain matter (negative control). The researchers then observed the organoids for up to six months, and none became infected with CWD.
This indicates that even following direct exposure of human central nervous system tissues to CWD prions there is a substantial resistance or barrier to the propagation of infection, according to researchers. The authors acknowledge the limitations of their research, including the possibility that a small number of people may have genetic susceptibility that was not accounted for, and that emergence of new strains with a lesser barrier to infection remains possible. They are optimistic that the inference of these current data is that humans are extremely unlikely to contract a prion disease because of inadvertently eating CWD-infected cervid meat.

The COVID-19 pandemic is over, but the virus that caused it is still here, sending thousands of people to the hospital each week and spinning off new variants with depressing regularity. The virus’s exceptional ability to change and evade immune defenses has led the World Health Organization (WHO) to recommend annual updates to COVID-19 vaccines.
But some scientists worry that the remarkable success of the first COVID-19 vaccines may work against updated versions, undermining the utility of an annual vaccination program. A similar problem plagues the annual flu vaccine campaign; immunity elicited by one year’s flu shots can interfere with immune responses in subsequent years, reducing the vaccines’ effectiveness.
A new study by researchers at Washington University School of Medicine in St. Louis helps to address this question. Unlike immunity to influenza virus, prior immunity to SARS-CoV-2, the virus that causes COVID-19, doesn’t inhibit later vaccine responses. Rather, it promotes the development of broadly inhibitory antibodies, the researchers report.
The study, available online in Nature, shows that people who were repeatedly vaccinated for COVID-19 — initially receiving shots aimed at the original variant, followed by boosters and updated vaccines targeting variants — generated antibodies capable of neutralizing a wide range of SARS-CoV-2 variants and even some distantly related coronaviruses. The findings suggest that periodic re-vaccination for COVID-19, far from hindering the body’s ability to recognize and respond to new variants, may instead cause people to gradually build up a stock of broadly neutralizing antibodies that protect them from emerging SARS-CoV-2 variants and some other coronavirus species as well, even ones that have not yet emerged to infect humans.
“The first vaccine an individual receives induces a strong primary immune response that shapes responses to subsequent infection and vaccination, an effect known as imprinting,” said senior author Michael S. Diamond, MD, PhD, the Herbert S. Gasser Professor of Medicine. “In principle, imprinting can be positive, negative or neutral. In this case, we see strong imprinting that is positive, because it’s coupled to the development of cross-reactive neutralizing antibodies with remarkable breadth of activity.”
Imprinting is the natural result of how immunological memory works. A first vaccination triggers the development of memory immune cells. When people receive a second vaccination quite similar to the first, it reactivates memory cells elicited by the first vaccine. These memory cells dominate and shape the immune response to the subsequent vaccine.
In the case of the flu vaccine, imprinting has negative effects. Antibody-producing memory cells crowd out new antibody-producing cells, and people develop relatively few neutralizing antibodies against the strains in the newer vaccine. But in other cases, imprinting can be positive, by promoting the development of cross-reactive antibodies that neutralize strains in both the initial and subsequent vaccines.

To understand how imprinting influences the immune response to repeat COVID-19 vaccination, Diamond and colleagues including first author Chieh-Yu Liang, a graduate student, studied the antibodies from mice or people who had received a sequence of COVID-19 vaccines and boosters targeting first the original and then omicron variants. Some of the human participants also had been naturally infected with the virus that causes COVID-19.
The first question was the strength of the imprinting effect. The researchers measured how many of the participants’ neutralizing antibodies were specific for the original variant, the omicron variant or both. They found that very few people had developed any antibodies unique to omicron, a pattern indicative of strong imprinting by the initial vaccination. But they also found few antibodies unique to the original variant. The vast majority of neutralizing antibodies cross-reacted with both.
The next question was how far the cross-reactive effect extended. Cross-reactive antibodies, by definition, recognize a feature shared by two or more variants. Some features are shared only by similar variants, others by all SARS-CoV-2 variants or even all coronaviruses. To assess the breadth of the neutralizing antibodies, the researchers tested them against a panel of coronaviruses, including SARS-CoV-2 viruses from two omicron lineages; a coronavirus from pangolins; the SARS-1 virus that caused the 2002-03 SARS epidemic; and the Middle Eastern Respiratory Syndrome (MERS) virus. The antibodies neutralized all the viruses except MERS virus, which comes from a different branch of the coronavirus family tree than the others.
Further experiments revealed that this remarkable breadth was due to the combination of original and variant vaccines. People who received only the vaccines targeting the original SARS-CoV-2 variant developed some cross-reactive antibodies that neutralized the pangolin coronavirus and SARS-1 virus, but the levels were low. After boosting with an omicron vaccine, though, the cross-reactive neutralizing antibodies against the two coronavirus species increased.
Taken together, the findings suggest that regular re-vaccination with updated COVID-19 vaccines against variants might give people the tools to fight off not only the SARS-CoV-2 variants represented in the vaccines, but also other SARS-CoV-2 variants and related coronaviruses, possibly including ones that have not yet emerged.
“At the start of the COVID-19 pandemic, the world population was immunologically naïve, which is part of the reason the virus was able to spread so fast and do so much damage,” said Diamond, also a professor of molecular microbiology and of pathology & immunology. “We do not know for certain whether getting an updated COVID-19 vaccine every year would protect people against emerging coronaviruses, but it’s plausible. These data suggest that if these cross-reactive antibodies do not rapidly wane — we would need to follow their levels over time to know for certain — they may confer some or even substantial protection against a pandemic caused by a related coronavirus.”