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Why We Still Don’t Have a Vaccine for the Common Cold

Bill Gourgey wrote . . . . . . . . .

Feeling yucky? Runny nose, scratchy throat? Maybe a cough, with light chills and aches, possibly a low-grade fever? We’ve all been there. Statistically, everyone comes down with these symptoms multiple times a year. These past few years, it would be tempting to blame some variant of the COVID-19 coronavirus, or SARS-CoV-2, for such symptoms. However, there’s also a strong possibility that it’s a distant cousin on the human virus family tree, one that is responsible for more sick days and visits to the doctor each year than any other pathogen—rhinovirus. Common cold symptoms can be caused by many viruses, but the odds you’re fighting a rhinovirus are high: the virus accounts for as much as half of all common colds.

Traditionally, there has been a certain seasonality to respiratory viruses in the US. Influenza tends to peak in fall and again in early spring, while common colds, such as respiratory syncytial viruses (RSVs), non-COVID coronaviruses, adenoviruses, and rhinoviruses pick up in mid-winter. But COVID-19 seems to have disrupted the normal pattern. “We typically see RSV at the peak of winter season,” says Richard Martinello, a respiratory virus specialist at Yale School of Medicine in Connecticut. “But our hospital’s already full. We’re trying to figure out where to put patients and how to care for them.” It’s not just RSV. “We’re actually seeing occasional kids with pretty severe rhinovirus infections,” Martinello adds, “and adults with severe rhinovirus infections in the hospital this year.”

Every year, we’re encouraged to get our annual flu shot—and it seems COVID vaccinations are headed down a similar path. Yet, we don’t get one for the common cold. With more than a billion cases each year in the US alone—far more than any other virus, including COVID-19 and the flu combined—it’s hard to overstate the uplift a universal common cold vaccine would have. The hunt for such a vaccine began more than half a century ago, as Popular Science reported in November 1955.

Dating back to the 19th century, a slew of vaccines have been developed for many of humanity’s most pervasive pathogens, from the very first vaccine in 1798 for smallpox to cholera and typhoid in 1896 to the COVID-19 vaccines in 2020—but no common cold vaccine.

In the 1950s, however, flush with the success of Jonas Salk’s polio vaccine, virologists were convinced it would be just a handful of years before the common cold would be eradicated by vaccine. In the 1955 Popular Science article, prolific virologist Robert Huebner estimated that a vaccine for the common cold might be available to the general public in as little as a year. While Huebner—who is credited with discovering oncogenes (genes with the propensity to cause cancer)—was successful in developing an adenovirus vaccine specifically for pharyngoconjunctival fever, he never fulfilled his quest for a common cold vaccine.

Although Popular Science’s story focused on Huebner’s 1953 discovery of adenovirus as a root cause for the common cold, it wasn’t until Winston Price’s 1956 discovery that virologists realized rhinovirus was the chief common-cold culprit. Since Price’s discovery, three species of rhinovirus have been discovered (A, B, and C), including more than 150 distinct strains. Plus, a majority of the known rhinovirus genomes have been sequenced in an effort to find commonalities that might serve as the basis for a universal vaccine.

“Considering there are more than 100 types of A and B rhinoviruses,” notes Yury Bochkov, a respiratory virus specialist at the University of Wisconsin School of Medicine and Public Health, “you would have to put all 100 types in one vial of vaccine in order to enable protection” against just A and B rhinoviruses. Add in all the C rhinovirus types (more than 50), then cram in RSV’s virus types (more than 40), and that same vaccine would have to be packed with more than 200 strains. Even then, it would only offer protection against about two-thirds of all common colds. “That was considered the major obstacle in development of those vaccines,” Bochkov says.

When it comes to manufacturing universal vaccines, scientists hunt for the lowest common denominator—a common trait that the vaccine can target—shared by all variants of a virus. Unfortunately, viruses aren’t that cooperative. Breaking them down to find common traits is not so easy. To trigger antibody production, human immune systems must be able to recognize those common viral traits as belonging to an intruder. That means the traits must be exposed, or on the surface of the virus. Traits locked inside the virus particle, or in its capsid structure, are not detectable until after the virus has begun to replicate, which is too late to avoid infection.

Antibodies, which are made of protein-based immunoglobulins such as IgM and IgG, are Y-shaped cells that continuously circulate through our blood, and latch onto invading pathogens, which are recognizable by certain sequences in their surface proteins. Antibodies are capable of disabling the invaders until the white blood cell, or leukocyte, troops can arrive to kill them. The goal of a universal vaccine is to not only find an antibody-triggering trait common across those many distinct types of the same virus, but also find a trait that is slow to mutate—or one that doesn’t mutate at all. In the cases of universal coronavirus and influenza vaccines currently under development, researchers have focused on more than just the surface protein, targeting other viral parts, such as the surface protein’s stalk, that are still detectable by our immune systems, but less likely to mutate from one variant to the next.

Viruses travel light, in other words they don’t carry around the machinery to replicate on their own. Instead, they use their surface proteins to bind to our bodies’ cells, then trick them into replicating virus particles. Coronaviruses, for instance, are known for their distinctive spike surface proteins, which became the focus of COVID-19 vaccines. Similarly, rhinoviruses have their own distinguishing surface protein shaped like a cloverleaf, which plays an essential role in the virus’s ability to hijack cells and replicate. Unfortunately, surface proteins tend to mutate quickly, enabling viruses to shapeshift and evade detection by our immune systems. That’s a chief reason why flu vaccines, and now COVID-19 vaccines, must be updated at least annually.

Fortunately for RSV, scientists have identified such commonalities. RSV is considered among the most dangerous of common cold viruses, especially for infants and children who are susceptible to respiratory tract infections. After a failed human trial in the 1960s that led to the death of two infants, it took another half century before scientists identified an immutable common trait—RSV’s surface fusion protein, or F protein, that binds to cells. Now, four different vaccines are already in the final third phase of human trials. “And they’re working,” Martinello notes, “they’re working amazingly well. It’s a very exciting time for RSV right now.”

But for a common cold vaccine to make a dent in annual infections, protection against rhinovirus must be developed, too. While progress has been made on RSV, the quest for a universal rhinovirus vaccine has received less attention. That may be changing.

Since the 1960s, there have been several human clinical trials of rhinovirus vaccine candidates, although none have been universal. Still, some results have been promising—one trial reduced symptomatic colds from 47 percent to 3.5 percent. However, the vaccines have only been effective on a few of the more than 150 strains. In the 2010s, researchers developed synthetic peptide immunogens capable of triggering immune responses in rabbits exposed to 48 different strains; peptides are the building blocks of proteins, which give cells their shape, and peptide immunogens attract antibodies, encouraging their production. In a 2019 study, researchers identified a way in mice to deprive rhinoviruses (and other viruses) of a specific enzyme they need to replicate.

In 2016, a 50-valent rhinovirus vaccine, or 50 strains in one shot, was successfully trialed in rhesus macaques, and a vaccine with 25 strains in mice. But even if such vaccines make it into human trials, that leaves more than 100 unaccounted-for rhinovirus strains.

“What if you could split [all the different strains] into several groups?” Bochkov says. “Then I think you would have higher chances of finding something that would be conserved within a group.” It’s like breaking fractions into similar groups and finding the least common denominator for each—or, in this case, separating out groups of strains with common traits and developing individual vaccines for each, which are all later combined into one super-packed vaccine. That’s precisely the direction research team’s like Bochkov’s are heading with rhinovirus species C. Once separate vaccines are developed for individual groups, they might be bundled into a single shot, which is called a polyvalent vaccine. This approach of targeting multiple strains in one shot has already been proven a successful way to control viral diseases. The annual flu vaccine, for instance, is a polyvalent vaccine designed to target three or four of the flu strains most likely to circulate in a given year. Similarly, the new bivalent COVID booster shots create an immune response to both the original strain of SARS-CoV-2, as well as recent Omicron strains.

Better tools for genome sequencing are also on the rise, including AI software that can be used to analyze surface proteins and predict possible mutations, like Google’s AlphaFold. This combined with mRNA platform technologies that expedite vaccine development makes Martinello and Bochkov optimistic that more respiratory virus vaccines will be developed in the coming years. “Maybe we’ll see a flu, COVID, RSV vaccine all combined in one,” Bochkov says, adding that “vaccination would be the way to go in fighting the common cold.”

Even as progress has been made on a universal flu vaccine and a universal coronavirus vaccine, the quest for a universal common cold vaccine has received less attention. That’s in part because public health efforts need to focus and allocate vaccine-development on the deadliest and most infectious pathogens first. As contagious as common cold viruses are—they spread through droplets that are airborne or left on surfaces—COVID-19 is at least 10 times deadlier than the flu, and the flu is deadlier than the common cold. Still, the common cold can lead to serious complications for people who are immunocompromised or have lung conditions, like asthma and chronic obstructive pulmonary disease.

While the search for a universal common cold vaccine began several decades ago, it is not likely to be fulfilled anytime soon, despite recent advances like the RSV vaccine trials. So, keep those tissues handy and wash your hands frequently. Wearing face masks as a prevention tactic isn’t exclusive to fighting COVID—they also work against the spread of other respiratory illnesses, including the common cold. “We have to be cognizant of what the risks are and thoughtful about how we protect ourselves from getting sick,” Martinello notes. “If you are sick, stay home, keep your kids home, because you know when you’re out and about that’s how that’s how things further spread.”

And when common cold vaccines do arrive, even if they’re virus-specific at first, don’t hesitate to get your jab.


Source : Popular Science


Self-Spreading Vaccine Research Could Spin Out of Control, Experts Warn

George Dvorsky wrote . . . . . . . . .

Imagine a future scenario in which a dangerous new virus is detected in chimpanzees. To prevent this virus from spreading to humans, biologists decide to deliberately infect scores of wild chimps with a transmissible vaccine—an infectious, lab-grown virus that immunizes, rather than harms, its host. The chimps, now vaccinated, no longer pose a threat to humans.

That solution sounds too good to be true, which is exactly the problem, as scientists warn in a new Policy Forum published today in Science. Self-spreading vaccines are potentially dangerous and difficult to manage, and are “genetically too unstable to be used safely and predictably outside contained facilities,” write the authors, led by Filippa Lentzos from King’s College London and Guy Reeves from the Max Planck Institute for Evolutionary Biology.

This is not just their opinion, the authors argue. Rather, it’s an “evidence-based norm” that’s been around for decades, but this “norm now seems to be challenged,” they write. The result is an increased potential for “risky research on lab-modified self-spreading viruses,” according to the report. This could lead to a normalization of the concept and eventual real-world use without the proper safeguards, the scientists argue.

“Self-spreading vaccine research continues to proceed despite a lack of new information that would compellingly refute long-standing evidence-based norms in virology, evolutionary biology, vaccine development, international law, public health, risk assessment, and other disciplines,” the biologists write.

Vaccines that spread like a disease are an unquestionably powerful concept. They could be used to protect animals from disease and/or prevent them from harboring viruses dangerous to humans. In 2020, biologists Scott Nuismer and James Bull, both at the University of Idaho, argued for this very approach in a paper titled “Self-disseminating vaccines to suppress zoonoses.” (By self-disseminating virus, scientists mean a virus that has been artificially modified to perform a desired function while retaining its ability to spread between hosts.)

By leveraging the spreading power of viruses, scientists could create biological agents that proliferate quickly through a target population, with the viruses performing specific tasks, such as delivering vaccines or sterilizing invasive species. In the late 1980s, Australian researchers dabbled with lab-modified, contagious viruses, using multiple approaches to exterminate foxes, mice, and rabbits, according to the paper.

More conceptually—and certainly more controversially—this strategy could also be used to spread vaccines among humans.

As the paper points out, interest in this biotechnology has increased significantly over the past several years, with the European Union (through its Horizon 2020 program), the U.S. National Institutes of Health, and the U.S. Defense Advanced Research Projects Agency all currently running programs to explore a wide range of possible applications.

Lentzos, Reeves, and colleagues say it’s time to pump the brakes and consider the consequences of this research and all the moving parts needed to make such a thing work. It’s not immediately clear, they argue, that self-disseminating viruses can be contained or removed from an environment once released, or who would be responsible for the biocontrol agent, should the virus behave unexpectedly or cross national boundaries.

Advocates of the idea say these viruses could be modified to have short lifespans or be made incapable of mutating, but “it remains to be experimentally tested if [manipulations] could simultaneously limit viral replication transmissibility to the extent that they could be perceived as controllable while maintaining sufficient transmissibility to be considered useful as vaccines in continually dynamic environments,” according to the report.

As for using transmissible vaccines to limit the spread of diseases from animals to humans, the scientists say the “the vast majority of virus species that currently exist are undescribed by science,” making it “very difficult to imagine how the considerable effort necessary to develop and test self-spreading vaccines could identify and then prioritize single viral species circulating in wildlife.” That viruses are constantly mutating makes this task all the more onerous, they add.

In terms of what’s needed, the authors call for various safeguards, cost-benefit analyses, and measures such as regulatory oversight. This would involve “a concerted, global governance effort with coherent regional, national, and local implementation.” The essay suggests that national governments update their legislation and guidelines on the matter, while developers and funders of this research “articulate comprehensive and credible regulatory paths through which they believe the safety and efficacy of self-spreading approaches could be established.”

In an email, Bull, co-author of the 2020 paper advocating for research into this biotechnology, said the authors of the new report “raise several valid points,” and he agrees that “informed regulatory oversight is essential,” adding that “public acceptance is also essential.”

“Until we undertake preliminary studies of transmissible vaccines (in contained environments), we will have little evidence on which to base estimated risks and benefits,” Bull told Gizmodo. “It is to be expected that early papers on transmissible vaccines explore the theoretical possibilities, many of which will never be practical or, as further work may show, never be safe.”

In an effort to move ahead cautiously, Bull recommended conservative approaches, such as creating a vaccine from a benign virus that already exists in a target population, as opposed to modifying an otherwise harmful virus. Work into gene drives, a related technology in which modified organisms engineer an entire species, could also help. “Just as gene drive developers have responded to regulatory concerns and have invented new designs with limited potential for spread, it is expected that investment in laboratory studies of transmissible vaccines will also lead to methods that mitigate risks,” Bull argued.

The idea of transmissible vaccines might die on the vine, whether on account of technical issues, safety concerns, or lack of public acceptance. But, clearly, dedicated research attention is needed, since the potential benefits—and risks—are immense.


Source : GIZMODO


Read also at Bulletin of the Atomic Scientists

Scientists are working on vaccines that spread like a disease. What could possibly go wrong? . . . . .

Antibody-dependent Enhancement (ADE) and Vaccines

Immune responses to pathogens involve many cells and proteins of the immune system. Early during an infection, these responses are non-specific, meaning that although they are directed at the pathogen, they are not specific to it. This is called innate immunity. Within a few days, adaptive immunity takes over; this immunity is specific to the invading pathogen. Adaptive immune responses include antibodies. A major goal of antibodies is to bind to the pathogen and prevent it from infecting, or entering, a cell. Antibodies that prevent entry into cells are called neutralizing antibodies. Many vaccines work by inducing neutralizing antibodies. However, not all antibody responses are created equal. Sometimes antibodies do not prevent cell entry and, on rare occasions, they may actually increase the ability of a virus to enter cells and cause a worsening of disease through a mechanism called antibody-dependent enhancement (ADE).

What is ADE?

ADE occurs when the antibodies generated during an immune response recognize and bind to a pathogen, but they are unable to prevent infection. Instead, these antibodies act as a “Trojan horse,” allowing the pathogen to get into cells and exacerbate the immune response.

Importantly, when a vaccinated person subsequently gets infected, this is not automatically evidence of ADE. Specifically, if a vaccinated person gets infected with the pathogen against which the vaccine protects, three different scenarios can occur:

Mild illness – In this scenario, the person may experience some symptoms, but they are more of an inconvenience and last only a few days (typically about 1-3 days). For many respiratory and gastrointestinal infections (e.g., influenza, COVID-19, and rotavirus), this is common. These mild symptoms are evidence that the vaccine worked.

“Breakthrough illness” – Traditionally, this term has been reserved for vaccinated people who get more severely ill, requiring hospitalization or experiencing untoward outcomes, such as disease complications (e.g., pneumonia) or death. In this case, the vaccine may not have worked at all or it did not induce high enough levels of immunity to effectively stop an infection.

ADE – In this scenario, the antibodies that the vaccine generated actually help the virus infect greater numbers of cells than it would have on its own. In this situation, the antibodies bind to the virus and help it more easily get into cells than it would on its own. The result is often more severe illness than if the person had been unvaccinated. ADE can occur after disease and has on occasion been identified following vaccination, as described below. Any vaccine that has been found to cause ADE has stopped being used or, more recently as described below for dengue vaccine, been recommended only for those who will not be affected by ADE. Evidence of ADE has not emerged for COVID-19 vaccines even though concerns have been raised.

Is ADE caused by a disease?

Most diseases do not cause ADE, but one of the best studied examples of a pathogen that can cause ADE is dengue virus. Dengue virus is one of the most common infections in the world, infecting hundreds of millions and killing tens of thousands of people each year. Unlike viruses like measles or mumps that only have one type, dengue virus has four different forms, called “serotypes.” These serotypes are very similar, but slight differences among them set the stage for ADE. If a person is infected by one serotype of dengue virus, they typically have mild disease and generate a protective immune response, including neutralizing antibodies, against that serotype. But, if that person is infected with a second serotype of dengue virus, the neutralizing antibodies generated from the first infection may bind to the virus and actually increase the virus’s ability to enter cells, resulting in ADE and causing a severe form of the disease, called dengue hemorrhagic fever.

Is ADE caused by vaccines?

On a few occasions ADE has resulted from vaccination:

Respiratory syncytial virus (RSV) — RSV is a virus that commonly causes pneumonia in children. A vaccine was made by growing RSV, purifying it, and inactivating it with the chemical formaldehyde. In clinical trials, children who were given the vaccine were more likely to develop or die from pneumonia after infection with RSV. As a result of this finding, the vaccine trials stopped, and the vaccine was never submitted for approval or released to the public.

Measles — An early version of measles vaccine was made by inactivating measles virus using formaldehyde. Children who were vaccinated and later became infected with measles in the community developed high fevers, unusual rash, and an atypical form of pneumonia. Upon seeing these results, the vaccine was withdrawn from use, and those who received this version of the vaccine were recommended to be vaccinated again using the live, weakened measles vaccine, which does not cause ADE and is still in use today.

Both the RSV and measles vaccines that caused ADE were tested in the 1960s. Since then, other vaccines have successfully been created by purifying and chemically inactivating the virus with formaldehyde, such as hepatitis A, rabies, and inactivated polio vaccines. These more recent vaccines do not cause ADE.

A more recent example of ADE following vaccination comes from dengue virus:

Dengue virus — In 2016, a dengue virus vaccine was designed to protect against all four serotypes of the virus. The hope was that by inducing immune responses to all four serotypes at once, the vaccine could circumvent the issues related to ADE following disease with dengue virus. The vaccine was given to 800,000 children in the Philippines. Fourteen vaccinated children died after encountering dengue virus in the community. It is hypothesized that the children developed antibody responses that were not capable of neutralizing the natural virus circulating in the community. As such, the vaccine was recommended only for children greater than 9 years of age who had already been exposed to the virus.

Other viral vaccines that target multiple types of a virus have been safely used, including vaccines against polio (3 types), rotavirus (5 types), and human papillomavirus (9 types).

Should I be concerned that my child will develop ADE after receiving a vaccination?

Today’s routinely recommended vaccines do not cause ADE. If they did, like those described above, they would be removed from use. Phase III clinical trials are designed to uncover frequent or severe side effects before a vaccine is approved for use. Find out more about how vaccines are developed and approved for use.

Can the new COVID-19 vaccines cause ADE?

Neither COVID-19 disease nor the new COVID-19 vaccines have shown evidence of causing ADE. People infected with SARS-CoV-2, the virus that causes COVID-19, have not been likely to develop ADE upon repeat exposure. This is true of other coronaviruses as well. Likewise, studies of vaccines in the laboratory with animals or in the clinical trials in people have not found evidence of ADE.

Following the experience with dengue vaccine, early during the COVID-19 pandemic, concerns about ADE were top of mind. During this time, a few scientists tried to predict whether ADE would occur by evaluating genes for similarities and differences. While this was a useful approach at a time when we did not have much information about what might happen in people, we have since accumulated several lines of clinical evidence that confirm ADE is not an issue for COVID-19 or the vaccines:

People who are infected with SARS-CoV-2, or its variants, do not become more susceptible to ADE.

Many vaccinated people have been exposed to the virus, and its variants, and most of them have developed no disease or mild symptoms. A very small number have experienced more severe disease (“breakthrough infection”), and these individuals have not shown evidence of ADE.

Unfortunately, some people continue to spread misinformation suggesting that ADE is an ongoing concern for COVID-19 vaccines; however, scientists and clinicians are continuing to monitor COVID-19 infections and, to date, no evidence to validate this concern has emerged.


Source : The Children’s Hospital of Philadelphia

What the Polio Vaccines Can Teach Us About the COVID Ones

Peter Skurkiss wrote . . . . . . . . .

Prior to the 1950s, paralytic polio was a scourge. FDR was crippled from it while in his 30s, the March of Dimes was started to combat it, and photos of rows and rows of children in iron lungs were common in the media. From this situation, vaccines were developed to combat the disease.

Polio is caused by one of three types of poliovirus that can cause paralysis and death. In the 1950s, two vaccines were independently developed to combat it, one by Jonas Salk and the other by Albert Sabin. Polio was eradicated, and today those vaccines are thought of as miracle drugs. But were they?

In the early 1950s, Salk was the first to come out with a vaccine. His was designed to treat all three polio viruses at once. His approach seemed basic enough. It was to grow polioviruses in the lab, kill them, and then inject healthy children with the dead viruses. The idea was that the dead viruses could not reproduce, so they could not harm the children. The children’s immune system, however, would detect the injected viruses and produce effective antibodies against them, thus creating immunity against polio.

Just prior to beginning mass inoculations, samples of the Salk vaccine were sent to the National Institutes of Health (NIH) for safety testing.

There, when bacteriologist Dr. Bernice Eddy injected the vaccine into her monkeys, some of them fell down paralyzed. She concluded that the virus was not entirely dead as promised. Instead, the virus was active and could reproduce in its host. Eddy sounded the alarm and presented her findings. A debate ensued in the corridors of power. Advocates for caution were overruled, and the mass inoculation proceeded on schedule.

The inoculation of children began in 1955. Within days, some injected children were coming down with polio. Some were even spreading the disease to family members. Subsequent investigations determined that the vaccine had caused 40,000 cases of polio, leaving 200 children with varying degrees of paralysis and ten dead. Alton Ochsner, a professor of surgery at Tulane Medical School, was such a strong proponent of proceeding with the inoculation program that he gave vaccine injections to his grandchildren to prove that it was safe. Ochsner’s grandson died from polio a few months later, and his granddaughter contracted polio but survived.

This fiasco has become known as the Cutter incident. It’s named after the manufacturer of the vaccine. The vaccine was recalled and retested for safety, but the damage had already been done in the mind of the public.

Let’s continue to the second version of the polio vaccine, the Sabin.

In 1957, inactivated poliovirus vaccine (IPV) and live but weakened oral poliovirus vaccines (OPV) were prepared in primary cell cultures derived from rhesus monkey kidneys.

According to the American Association for Cancer Research, it was later determined that the vaccines made from these cultures were contaminated with the infectious cancer-causing virus SV40. The Centers for Disease Control & Prevention estimates that up to 30 percent of the polio vaccines administered from 1957 to 1963 contained this cancer-causing monkey virus. Dr. Eddy was involved in the discovery of that, too, despite being shunted off to other research after her first discovery.

Did this result in a cancer epidemic? Some believe that it did, as there was a sharp rise in soft tissue cancer in the following decades. The medical establishment disagrees, saying only a “small” number of cancer cases can be traced to the polio vaccines. In any event, it was a fact that a cancer-causing virus was present in the polio vaccines and that the government kept the public in the dark. This was done to avoid mass hysteria and to prevent the wrecking of the public’s confidence in medicine and vaccines in particular.

One result of the damage caused by these initial polio vaccines is that strict new safety regulations and procedures were instituted. Also, legislation was passed to exempt vaccine manufacturers from civil damages due to the side-effects of their vaccines. 42 U.S. Code 300aa-22 — Standard of responsibility states: “No vaccine manufacturer shall be liable in a civil action for damages arising from a vaccine-related injury or death associated with the administration of a vaccine after October 1, 1988.”

Polio is practically unknown today. But is that because of the vaccines or other factors? Note, polio is spread by contact with infected feces, which often happens from poor hand-washing. It can be spread from eating or drinking contaminated food or water. In some cases, it can be spread when an infected person coughs or sneezes infected droplets into the air. It would seem that as hygiene improved and sanitation got better, polio would diminish. This was all known in the 1950s.

Whatever the case, a takeaway lesson from the early polio vaccines is that haste makes waste. Back then, those vaccines were rushed out to the public without being adequately tested due to panic over the disease. One has to wonder if the same sort of thing isn’t happening today with the COVID vaccines. There are similarities between what happened then and what’s unfolding now, chief among them political pressure for a magic-bullet cure. Is it possible or even likely that political pressure has compromised the safety protocols and standard procedures at the FDA and Big Pharma which are there to ensure only safe vaccines are issued for public use? Time will tell.


Source : American Thinker

How Does the Johnson & Johnson Vaccine Compare to Other Coronavirus Vaccines?

Maureen Ferran wrote . . . . . . . . .

1. How does the Johnson & Johnson vaccine work?

The Johnson & Johnson vaccine is what’s called a viral vector vaccine.

To create this vaccine, the Johnson & Johnson team took a harmless adenovirus – the viral vector – and replaced a small piece of its genetic instructions with coronavirus genes for the SARS-CoV-2 spike protein.

After this modified adenovirus is injected into someone’s arm, it enters the person’s cells. The cells then read the genetic instructions needed to make the spike protein and the vaccinated cells make and present the spike protein on their own surface. The person’s immune system then notices these foreign proteins and makes antibodies against them that will protect the person if they are ever exposed to SARS-CoV-2 in the future.

The adenovirus vector vaccine is safe because the adenovirus can’t replicate in human cells or cause disease, and the SARS-CoV-2 spike protein can’t cause COVID–19 without the rest of the coronavirus.

This approach is not new. Johnson & Johnson used a similar method to make its Ebola vaccine, and the AstraZeneca-Oxford COVID-19 vaccine is also an adenovirus viral vector vaccine.

2. How effective is it?

The FDA’s analysis found that, in the U.S., the Johnson & Johnson COVID-19 vaccine was 72% effective at preventing all COVID-19 and 86% effective at preventing severe cases of the disease. While there is still a chance a vaccinated person could get sick, this suggests they would be much less likely to need hospitalization or to die from COVID-19.

A similar trial in South Africa, where a new, more contagious variant is dominant, produced similar results. Researchers found the Johnson & Johnson vaccine to be slightly less effective at preventing all illness there – 64% overall – but was still 82% effective at preventing severe disease. The FDA report also indicates that the vaccine protects against other variants from Britain and Brazil too.

3. How is it different from other vaccines?

The most basic difference is that the Johnson & Johnson vaccine is an adenovirus vector vaccine, while the Moderna and Pfizer vaccines are both mRNA vaccines. Messenger RNA vaccines use genetic instructions from the coronavirus to tell a person’s cells to make the spike protein, but these don’t use another virus as a vector. There are many practical differences, too.

Both of the mRNA-based vaccines require two shots. The Johnson & Johnson vaccine requires only a single dose. This is key when vaccines are in short supply.

The Johnson & Johnson vaccine can also be stored at much warmer temperatures than the mRNA vaccines. The mRNA vaccines must be shipped and stored at below–freezing or subzero temperatures and require a complicated cold chain to safely distribute them. The Johnson & Johnson vaccine can be stored for at least three months in a regular refrigerator, making it much easier to use and distribute.

As for efficacy, it is difficult to directly compare the Johnson & Johnson vaccine with the mRNA vaccines due to differences in how the clinical trials were designed. While the Moderna and Pfizer vaccines are reported to be approximately 95% effective at preventing illness from COVID–19, the trials were done over the summer and fall of 2020, before newer more contagious variants were circulating widely. The Moderna and Pfizer vaccines might not be as effective against the new variants, and Johnson & Johnson trials were done more recently and take into account the vaccine’s efficacy against these new variants.

4. Should I choose one vaccine over another?

Although the overall efficacy of the Moderna and Pfizer vaccines is higher than the Johnson & Johnson vaccine, you should not wait until you have your choice of vaccine – which is likely a long way off anyway. The Johnson & Johnson vaccine is nearly as good as the mRNA-based vaccines at preventing serious disease, and that’s what really matters.

The Johnson & Johnson vaccine and other viral-vector vaccines like the one from AstraZeneca are particularly important for the global vaccination effort. From a public health perspective, it’s important to have multiple COVID-19 vaccines, and the Johnson & Johnson vaccine is a very welcome addition to the vaccine arsenal. It doesn’t require a freezer, making it much easier to ship and store. It’s a one-shot vaccine, making logistics much easier compared with organizing two doses per person.

As many people as possible need to be vaccinated as quickly as possible to limit the development of new coronavirus variants. Johnson & Johnson is expected to ship out nearly four million doses as soon as the FDA grants emergency use authorization. Having a third authorized vaccine in the U.S. will be a big step towards meeting vaccination demand and stopping this pandemic.


Source : The Conversation

Denmark, Norway Temporarily Suspend AstraZeneca COVID Shots After Blood Clot Reports

Nikolaj Skydsgaard and Jacob Gronholt-Pedersen wrote . . . . . . . . .

Health authorities in Denmark and Norway said on Thursday they had temporarily suspended the use of AstraZeneca’s COVID-19 vaccine shots after reports of the formation of blood clots in some who have been vaccinated.

The move comes after Austria stopped using a batch of AstraZeneca shots while investigating a death from coagulation disorders and an illness from a pulmonary embolism.

Danish health authorities said the country’s decision to suspend the shots for two weeks came after a 60-year old woman in Denmark, who was given an AstraZeneca shot from the same batch that was used in Austria, formed a blood clot and died.

Danish authorities said they had responded “to reports of possible serious side effects, both from Denmark and other European countries.”

“It is currently not possible to conclude whether there is a link. We are acting early, it needs to be thoroughly investigated,” Health Minister Magnus Heunicke said on Twitter.

The vaccine would be suspended for 14 days in Denmark.

“This is a cautionary decision,” Geir Bukholm, director of infection prevention and control at the Norwegian Institute of Public Health (FHI), told a news conference.

FHI did not say how long the suspension would last.

“We … await information to see if there is a link between the vaccination and this case with a blood clot,” Bukholm said.

Also on Thursday, Italy said it would suspend use of an AstraZeneca batch that was different to the one used in Austria.

Some health experts said there was little evidence to suggest the AstraZeneca vaccine should not be administered and that the cases of blood clots corresponded with the rate of such cases in the general population.

“This is a super-cautious approach based on some isolated reports in Europe,” Stephen Evans, professor of pharmacoepidemiology at the London School of Hygiene & Tropical Medicine, told Reuters.

“The problem with spontaneous reports of suspected adverse reactions to a vaccine are the enormous difficulty of distinguishing a causal effect from a coincidence,” he said, adding that the COVID-19 disease was very strongly associated with blood clotting.

AstraZeneca on Thursday told Reuters in a written statement the safety of its vaccine had been extensively studied in human trials and peer-reviewed data had confirmed the vaccine was generally well tolerated.

The drugmaker said earlier this week its shots were subject to strict and rigorous quality controls and that there had been “no confirmed serious adverse events associated with the vaccine”. It said it was in contact with Austrian authorities and would fully support their investigation.

The European Union’s drug regulator, the European Medicines Agency (EMA), said on Wednesday there was no evidence so far linking AstraZeneca to the two cases in Austria.

It said the number of thromboembolic events – marked by the formation of blood clots – in people who have received the AstraZeneca vaccine is no higher than that seen in the general population, with 22 cases of such events being reported among the 3 million people who have received it as of March 9.

EMA was not immediately available for comment on Thursday.

Four other countries – Estonia, Lithuania, Luxembourg and Latvia – have stopped inoculations from the batch while investigations continue, the EMA said.

The batch of 1 million doses went to 17 EU countries.

Swedish authorities said they did not find sufficient evidence to stop vaccination with AstraZeneca’s vaccine. Sweden has found two cases of “thromboembolic events” in connection with AstraZeneca’s vaccine and about ten for the Pfizer-BioNTech vaccine.

“We see no reason to revise our recommendation,” Veronica Arthurson, head of drug safety at the Swedish Medical Products Agency, told a news conference. “There is nothing to indicate that the vaccine causes this type of blood clots.”

Spain on Thursday said it had not registered any cases of blood clots related to AstraZeneca’s vaccine so far and would continue administering the shots.


Source : Reuters

Chart of the Day: Should COVID-19 Vaccination Be Mandatory?

Source : Statista

How Many People Need to Get a COVID-19 Vaccine in Order to Stop the Coronavirus?

Pedro Mendes wrote . . . . . . . . .

It has been clear for a while that, at least in the U.S., the only way out of the coronavirus pandemic will be through vaccination. The rapid deployment of coronavirus vaccines is underway, but how many people need to be vaccinated in order to control this pandemic?

I am a computational biologist who uses data and computer models to answer biological question at the University of Connecticut. I have been tracking my state’s COVID-19 epidemic with a computer model to help forecast the number of hospitalizations at the University of Connecticut’s John Dempsey Hospital.

This type of computer model and the underlying theory can also be used to calculate the vaccination rates needed to break the chain of transmission of the coronavirus. My estimate is that for the entire U.S., roughly 70% of the population needs to be vaccinated to stop the pandemic. But variation in how people behave in different parts of the country, as well as open questions on whether the vaccine prevents infection entirely or just prevents people from getting sick, add a degree of uncertainty.

Cutting off transmission

Clinical trials have shown that once a person gets vaccinated for the coronavirus, they won’t get sick with COVID-19. A person who doesn’t get sick can still be infected with the coronavirus. But let’s also assume that a vaccinated person can’t spread the virus to others, though researchers still don’t know if this is true.

When enough of the population is vaccinated, the virus has a hard time finding new people to infect, and the epidemic starts dying out. And not everyone needs to be vaccinated, just enough people to stop the virus from spreading out of control. The number of people who need to be vaccinated is known as the critical vaccination level. Once a population reaches that number, you get herd immunity. Herd immunity is when there are so many vaccinated people that an infected person can hardly find anyone who could get infected, and so the virus cannot propagate to other people. This is very important to protect people who cannot get vaccinated.

The critical vaccination level depends on how infectious the disease is and how effective the vaccine is. Infectiousness is measured using the basic reproduction number – R0 – which is how many people an infected person would spread the virus to on average if no protective measures were in place.

The more infectious a disease is, the larger the number of people who need to be vaccinated to reach heard immunity. The higher the effectiveness of the vaccine, the fewer people need to be vaccinated.

Not the same everywhere

R0 values differ from place to place because their populations behave differently – social interactions are not the same in rural and urban locations, nor in warm climates compared to cold ones, for example.

Using the data on positive cases, hospitalizations and deaths, my model estimates that Connecticut currently has an R0 of 2.88, meaning that, on average, every infected person would pass the virus on to 2.88 other people if no mitigation measures were in place. Estimates at the county level range from 1.44 in rural Alpine, California to 4.31 in urban Hudson, New Jersey.

But finding an R0 value for the entire U.S. is especially tricky because of the diversity of climates and because the virus has affected different areas at different times – behavior has been far from uniform. Estimates vary from 2.47 to 8.2, though most researchers place R0 for the entire U.S. around 3.

While R0 varies by location and between estimates, the effectiveness of the vaccines is constant and well known. The Pfizer-BioNTech and Moderna vaccines are 95% and 94.5% effective at preventing COVID-19, respectively.

Using values for vaccine effectiveness and the R0, we can calculate the critical vaccination level. For Connecticut, with an R0 of 2.88, 69% of the population needs to be vaccinated. For the entire U.S., with R0 of 3, this would be 70%. In New York City, with an estimated R0 of 4.26 this would be 80%.

A lot of uncertainty

While the math is relatively simple, things get complicated when you consider important questions for which epidemiologists still have no answers.

First, the formula for critical vaccination level assumes that people interact randomly. But in the real world, people interact in highly structured networks depending on work, travel and social connections. When those contact patterns are considered, some researchers found critical vaccination levels to be considerably smaller compared to assuming random interactions.

Unfortunately, other unknowns could have an opposite effect.

Vaccine trials clearly show that vaccinated people don’t get sick with COVID-19. But it is still unknown whether the vaccines prevent people from getting mild infections that they could pass on to others. If vaccinated people can still be infected and pass on the virus, then vaccination will not provide herd immunity – though it would still prevent serious disease and reduce mortality drastically.

A final question that remains to be answered is how long immunity to the coronavirus lasts after a person is vaccinated. If immunity wanes after a few months, then each individual will need repeated vaccinations.

It is hard to say with certainty how many people need to be vaccinated in order to end this pandemic. But even so, the arrival of COVID-19 vaccines has been the best news in 2020. In 2021, as a large proportion of individuals in the U.S. get the vaccine, the country will be heading toward the critical vaccination level – whatever it may be – so that life can start to return to normal.


Source : The Conversation

Israel Walks Back Reported Virus Czar Claim that Pfizer 1st Dose Less Effective

The Health Ministry on Friday walked back apparent claims by Israel’s virus czar that the first dose of Pfizer’s vaccine provides less protection against COVID-19 than the US pharmaceutical firm had initially indicated it would, saying his words had been quoted out of context.

Earlier this week, Army Radio reported that Nachman Ash had, in a meeting with health officials, noted that many people have gotten infected between the first and second Pfizer shots and questioned the effectiveness of the vaccine after just one dose. The data on the protective effect against the virus of the first dose is “lower than Pfizer presented,” he was quoted saying.

Pfizer says its vaccine, produced with BioNTech, is around 52% effective after the first dose, and increases to about 95% a number of days after the second dose.

In a statement issued Friday, the Health Ministry said reports regarding the czar’s comments were “out of context and not accurate.”

“The vaccination campaign in Israel started a month ago… during a surge in morbidity and mortality in the country, which makes it hard to evaluate vaccination effectiveness without biases,” the ministry said. “Initial evaluation reveals some protective effects of the vaccine and those are carefully studied by the Health Ministry.”

“The commissioner said we have yet to see a decrease in the number of severely ill patients. As the second dose is given these days to at-risk populations we expect to see the full protective impact of the vaccine,” the statement said.

The Health Ministry also announced Friday that it had broken a record in daily vaccinations on Thursday, with 244,000 Israelis getting inoculated.

Ministry figures showed 2,441,379 Israelis have received the first vaccine dose and 850,811 of them the second.

Israel is leading the world in vaccination on a per capita basis, according to the Oxford-based Our World in Data.

More than a month into Israel’s vaccination campaign, Health Ministry officials had hoped to see a dramatic drop in daily infections and serious cases, but there is no such trend at this time. The more contagious virus variants — particularly the British strain — are being blamed for the difficulty in bringing down illness rates and easing the heavy load on hospitals, despite the lockdown and mass vaccinations.

The ministry also reported a slight decline in daily coronavirus infections, as Israel’s worst outbreak since the pandemic began appeared to ease after weeks of strict lockdown rules.

According to the ministry, 7,099 new cases were confirmed Thursday, after peaking at over 10,100 earlier in the week. Along with another 1,228 cases since midnight, the total number of infections recorded in Israel reached 585,746.

The drop in daily cases came as testing levels also further decreased, though the positive test rate fell to 8.9 percent.

The death toll stood at 4,245, with 27 fatalities recorded Thursday.

The ministry said there were 82,029 active cases, with 1,845 patients hospitalized for COVID-19. Of those, 1,128 were in serious condition, with 310 on ventilators.


Source : The Times of Israel


Read also:

Nachman Ash reportedly says it’s not certain vaccines can protect against mutated coronavirus strains; 12,400 Israelis were infected with virus after receiving 1st shot . . . . .

British Scientists Developing World’s First Covid-19 Vaccine Smart Patch

Emily Brown wrote . . . . . . . . .

Scientists from Swansea University in Wales are striving to develop the first coronavirus vaccine ‘smart patch’.

The patch will use microneedles to both administer the coronavirus vaccine and monitor its efficacy for the patient by tracking the body’s immune response.

The research team plans to develop a prototype by the end of March, in the hope it can be put forward for clinical trials and ultimately released to the public, as part of the effort to tackle the coronavirus outbreak.

Scientists at Swansea’s IMPACT research centre hope to carry out human clinical studies in partnership with Imperial College London with the aim of making the device commercially available within three years.

Using polycarbonate or silicon millimetre-long microneedles, the smart patch can penetrate the skin to administer a vaccine. It can be held in place with a strap or tape for up to 24 hours, during which time it simultaneously measures a patient’s inflammatory response to the vaccination by monitoring biomarkers in the skin.

Once the vaccine has been administered, the device is scanned to produce a data reading that can provide an understanding about the efficacy of the vaccine and the body’s response to it.

Those involved in the project received Welsh government and European funding as part of the global response to overcome the coronavirus pandemic, though scientists hope the smart patch could also be used to treat other infectious diseases, the BBC reports.

Medical engineering lecturer Dr Sanjiv Sharma explained the body’s production of immunoglobulins – antibodies that form a critical part of our immune defences – are ‘good markers’ of showing the efficacy of vaccination.

Discussing the smart patch, Sharma said the scientists expect to see the production of immunoglobulins in response to the self-administration of the device.

He continued:

This low-cost vaccine administration device will ensure a safe return to work and management of subsequent Covid-19 outbreaks.

Beyond the pandemic, the scope of this work could be expanded to apply to other infectious diseases as the nature of the platform allows for quick adaption to different infectious diseases.

There are currently no other devices commercially available that provide vaccines in this manner, though Sharma said the patch is similar to ‘continuous glucose monitoring sensors’ used by people with diabetes.

The device may serve as a more desirable way for people who are scared of injections to receive the vaccine, as PhD student Olivia Howells explained the patch does not penetrate as deeply as needles. Howells added that the patches are cheaper than hypodermic needles, meaning they could be useful in countries struggling with resources for vaccination.


Source : Uilad