Cells that can give you super immunity. There are certain immune cells that play a very important role in protecting us from severe illness, and COVID-19 has helped scientists realize their importance in fighting infection.
Cells that can give you super immunity
In October 2020, a team of virologists at Rockefeller University in New York began a year-long project to predict what dangerous strains of COVID-19 might emerge in the future.
While the nightmare of new strains had yet to occupy the minds of political leaders and citizens, scientists knew that COVID-19 would likely mutate in ways that would make it more contagious and pathogenic.
The goal of the Rockefeller scientists was to create a synthetic version of the COVID-19 spike protein (the protein the virus uses to enter our cells) that could evade all the protective antibodies known to be found in the blood of COVID-19 survivors.
Over the next 12 months, the researchers worked with different combinations of mutations on the surface of the spike protein to find a set of 20 mutations that seemed to make the virus specifically resistant to anything the immune system could throw at it. To test this set of mutations, they introduced it into a pseudotyped virus. A pseudovirus is a type of virus that is engineered not to have enough genetic material to replicate, allowing scientists to modify it and understand its behavior without the risk of escaping.
At first, everything went as expected. When the virologists exposed their engineered virus to blood samples taken from people who had either recovered from COVID-19 or had been vaccinated against the disease, the virus deftly evaded all of their antibodies.
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Cells that can give you super immunity
But then something amazing happened. When the researchers tested their engineered virus on the blood of people who had recovered from COVID-19 in 2020 and were vaccinated a few months later, their antibodies were able to bind to the virus and completely neutralize it.
“It was incredible to see,” says Michel Nussenzweig, a professor of molecular immunology at Rockefeller University and one of the scientists involved in the project. “One of the biggest lessons we’ve learned from the world is how the immune system responds differently depending on whether we’re naturally infected, vaccinated, or both.” (Of course, that doesn’t mean it’s a good idea to get infected on purpose, as any infection comes with risks.)
Over the past four months, Rockefeller’s team’s findings have been seen many times in real life. People who have recovered from a COVID-19 infection and then been vaccinated appear to be more resistant to the new strains, from delta to omicron.
Immunologists took blood samples from these people and found that they have an extraordinary type of immunity that the scientific community calls hybrid immunity. Not only do these people produce very high levels of antibodies (much more than those who are fully vaccinated), but they also produce a much more diverse range of antibodies that have a better chance of finding weak spots in the virus, even in highly mutated forms of COVID-19.
B cells were first discovered in the 1960s in chickens.
A recent study by scientists in Boston and South Africa showed that people who were infected with one of the types of COVID-19 before receiving two doses of the vaccine and a booster dose had greater immunity against Omicron. Omicron is the closest real-world species to the synthetic Rockefeller virus.
Nussenzweig says: When people previously infected with Covid-19 were vaccinated with the mRNA vaccine, they produced an antibody response that was three times greater than those vaccinated without prior infection.
But the reason these people show such strong responses has to do with a long-overlooked aspect of the immune system, a type of white blood cell called “memory B cells.”
For a long time, we knew little about memory B cells and how they behave; But through research on HIV, Ebola, and autoimmune diseases, and now COVID-19, we are beginning to understand how critical these cells are in determining our responses to infections and vaccines.
Cells that can give you super immunity
From chickens to HIV
In the 1890s, the German physiologist Emil von Bering (a man known as the savior of children for his Nobel Prize-winning research on the treatment of tetanus and diphtheria) proposed the existence of cells that could recover from past encounters with a particular infection. remember and produce antibodies when exposed to it again.
It took seventy years to prove von Bering’s ideas. In the 1960s, immunologists discovered that chickens whose bursa (synovial sac: one of the main immune organs in birds) had been destroyed by radiation lacked the special cells needed to produce antibodies. These cells became known as “bursal-derived cells” or “B cells”. By the mid-1970s, it was discovered that these cells form in the bone marrow in humans before migrating to the lymph nodes or spleen.
We now know that throughout life, we are constantly making new B cells. The body has about 10 billion B cells (the length of 100 football fields if you lined them up in a row), and each B cell contains receptors that recognize different antigens on the surface of the virus.
This is important because while B cells themselves do not attach to viruses, they can become plasma cells when they detect a threat. These plasma cells produce antibodies that recognize the same viral antigen as the primary B cell. Low diversity of B cells means fewer antibodies that may be able to neutralize the virus.
One thing that COVID-19 has revealed to immunologists is that people with a higher diversity of B cells are much better equipped to fight off new pathogens, especially new strains of COVID-19. This issue is also influenced by age, health conditions, and genetics. Ali Al-Badi, Associate Professor of Pathology and Immunology at Washington University School of Medicine says:
Everyone will have a different set of B cells that they use to respond to any infection. Even if you have siblings, they will have different B cell responses.
As we age, two things happen to the B cell response. First, the body begins to produce a smaller pool of B cells, meaning they are less likely to have receptors that recognize antigens on the new virus. More importantly, they take longer to mobilize against the threat, so deadly pathogens can overwhelm it before the immune system can kick in. These are the factors that make younger people who have underlying diseases more vulnerable to Covid-19.
But when your body fights an infection or you receive a vaccine, it triggers a clever immunological trick. Some B cells become memory B cells, which can circulate in the bloodstream for decades, ready to reactivate and mount an antibody response if the virus returns.
Such antibodies also play a role in suppressing chronic infections such as the Epstein-Barr virus, which remain latent in the body for most of our lives. It seems that these viruses can reactivate after the body is weakened (this seems to happen in some patients with prolonged COVID).
the response of memory B cells. One thing immunologists have learned from studies of Ebola survivors is that severe infections seem to stimulate far greater numbers of memory B cells than vaccines alone.
Nussenzweig says: When you have a bad infection, your body’s cells produce a lot of viruses. The virus is present throughout the respiratory system, nose, lungs, upper airways, and mucous membranes. The entire immune system plays a role in the response and response to all elements of the virus, so this is one possible reason why natural infections may induce better immune system memory.
Over the past six months, Nussenzweig has been studying the subtle differences between natural infection caused by COVID-19 and vaccination. By isolating memory B cells from people who had been infected or vaccinated at different points in time, he found that natural infection appears to produce memory B cells that evolve continuously. This means they produce antibodies that are more likely to protect against new strains of the virus. The important thing that the immunologists found was that this effect occurred more strongly when people were infected and then vaccinated.
Scientists are now looking to understand whether we can tailor vaccine regimens so that they alone can induce a combined immune response. Success in doing this can provide humanity with an important weapon against new strains of Covid-19 and future outbreaks.
Cells that can give you super immunity
The next world
In 2007, a group of researchers at Oregon Health & Science University began a mission to understand why the immune response to some infections or vaccines seems to be more durable than to other infections and vaccines.
The researchers compared antibodies produced by a series of common vaccine technologies: measles vaccine (which delivers a weakened form of the whole virus), tetanus and diphtheria vaccines (which contain viral antigens), and antibodies produced by common pathogens such as Epstein-Barr virus or Cytomegalovirus.
The resulting article showed that the half-life of antibodies varies greatly depending on the type of virus or vaccine. While the antibodies produced to suppress cytomegalovirus remain in the body almost indefinitely, the response to tetanus declines after a few years. “These results showed us that the cellular programming that gives rise to memory B cells is very different depending on the nature of the infection or the immunogen,” said John Wray, director of the Institute of Immunology at the University of Pennsylvania.
Now, COVID-19 provides a unique opportunity to compare different vaccine technologies for the same virus to understand what elicits the most durable and effective immune response by observing how memory B cells respond over time.
So far, messenger RNA vaccines, such as those made by Pfizer, Moderna, and Novartis, seem to work best, although researchers are still trying to figure out exactly why. “These vaccines produce a stronger memory B-cell response,” says Elbedi. “If you compare it to, for example, the flu vaccine, you’ll see that the response is at least ten times greater.”
The interesting discovery of combinatorial immunity in recent months has led scientists to analyze different regimens of the Covid-19 vaccine to see if combinations of different vaccines can induce a similarly strong immune response.
The first solid data on this will come in 2022, Nussenzweig says, and could help us figure out how best to use vaccines and booster doses against other viruses, from influenza to HIV.
He says: We will have a huge amount of clinical and immunological data, based on which we will find the best methods. For example, would giving an uninfected person a booster dose in addition to the antibodies already in circulation boost their memory B cells? Does this make people do better in dealing with the next covid infection? We can put all of this together and say, for example, what we should have done was give everyone the mRNA vaccine. The best number of vaccine doses is this amount and the best interval between doses is this size.
Vary predicts that increasing our understanding of B cells through the study of COVID-19 could also have advantages in the field of cancer immunotherapy.
B cells make antibodies against specific parts of tumors in the same way they do against viruses. B cells also cooperate with other components of the immune system, such as T cells and dendritic cells, to create the right environment for tumor attack, and one of the goals of future immunotherapies is to stimulate the interaction between these cells. “This small three-cell interaction is associated with a better outcome for all cancer treatments,” Vary says. “Whenever that happens, you get a better result.”
Knowing how to best activate the immune system also plays a large role in enabling healthcare systems to respond quickly and reduce mortality when the next outbreak occurs. Most scientists believe that the occurrence of subsequent deaths is inevitable. “There will be a next time,” Nussenzweig says. Three SARS viruses have emerged in the past 20 years and have caused major problems. “We don’t know what the next pathogen that will cause death will be, but we have to be ready for it.”
The study that first showed the benefits of ADHD
In a new study, it has been hypothesized that some genetic traits associated with attention deficit hyperactivity disorder (ADHD) can actually be beneficial by increasing exploratory behaviors.
The study that first showed the benefits of ADHD
While current diagnostic definitions of attention-deficit/hyperactivity disorder (ADHD) are relatively new, the condition has been recognized and defined by clinicians under various names for centuries.
According to NA, recent genetic studies have shown that this disease is highly hereditary, which means that most people with this disease genetically inherited it from their parents.
Depending on the diagnostic criteria, between 2% and 16% of children can be classified as having ADHD. In fact, the increase in diagnosis rates in recent years has led some doctors to argue that the disease is overdiagnosed.
What is relatively clear, however, is that the behavioral traits that underlie ADHD have potentially been genetically present in human populations for a long time, leading some researchers to speculate on the evolutionary advantages of this What could be the conditions?
Imagine you are part of a wandering tribe of early humans. Your group comes across a field full of one type of fruit and everyone is faced with one big question. Do you settle on a farm and exploit its fruit supply until it’s all gone, or do you quickly pick up what you can and continue exploring for more diverse foods?
This opposition to exploitation or exploration is fundamental to the survival of all animals. At what point does the risk of staying in one place outweigh the risk of moving to find what’s next?
In the early 2000s, a team of scientists studied the genetics of a unique tribe of people in northern Kenya. This tribe, known as Ariaal, has traditionally been incredibly nomadic and nomadic since ancient times, and they have continued to live in this way. Some members of the Arial tribe settled down during the 20th century and adopted modern farming methods, while others continued to live as nomadic herders.
Scientists compared the genetic and health differences between these two groups of the Arial tribe and discovered something incredibly interesting. In general, all people of the Arial tribe carry a unique genetic mutation called DRD4/7R. This genetic trait has previously been commonly identified in people with ADHD.
This genetic mutation in today’s children who have been diagnosed with ADHD is generally associated with restlessness and distraction, and in those children of the Ariel tribe who were used to the behaviors of staying still settling down, and avoiding moving, this gene was associated with health. Poor and disruptive behaviors in class were related. But in Aryalees who still lived a traditional nomadic life, this gene mutation was associated with better nutritional health and strength.
The DRD4/7R mutation is associated with increased food and drug cravings, novelty seeking, and ADHD symptoms, explained Dan Eisenberg, lead author of the 2008 study. It is possible that in a nomadic environment, a boy with this gene mutation would be able to more effectively defend livestock against invaders or find water and food sources, but these same tendencies may be limited to fixed jobs such as setting up a school, farming, or selling goods. not useful
So an interesting hypothesis emerged. Whether the genetic traits of ADHD can be somewhat beneficial to a tribe, as it predisposes some individuals to “exploration” What appears in modern times as unrest and restlessness could actually have been beneficial to tribes that were looking for food.
David Barak from the University of Pennsylvania along with a team of colleagues tested this hypothesis experimentally. They produced a unique game where players were given eight minutes to collect as many berries as possible by hovering over a bush. Each time they picked berries from a bush, the player’s harvest was reduced slightly, but if they went to a new bush, there was a time penalty.
So what did most players do? Did they stick to the original bush? Or risk wasting time trying another plant to see if it bears more fruit? The same basic question, exploration or exploitation?
About 450 people participated in this experiment and all were simultaneously screened for ADHD symptoms. Not surprisingly, the researchers found that people with higher ADHD scores reached out to new plants sooner than others, but more importantly, people with ADHD tended to collect a larger volume of berries overall.
In a recently published study, Barak and his colleagues noted that participants without ADHD traits tended to overeat individual plants.
Finally, looking at the optimal withdrawal strategy for this game, it was found that players with high ADHD scores were more successful overall.
“We found that participants who screened positive for ADHD gave up the bushes more easily and achieved higher rates of reward than participants who screened negative,” the researchers wrote in their conclusion. Given that participants stayed more on a plant in general, those with high ADHD scores made more exploratory decisions, consistent with the predictions of optimal search theory, and thus behaved more optimally.
It should be noted that these findings do not represent a definitive verdict on the possible evolutionary benefits of ADHD, but they provide compelling and plausible reasons why a small percentage of humans still have these traits.
In the 21st century, we may have pathologized ADHD as a negative disorder, but this could simply be because these characteristics no longer fit the world we have constructed. So in a different context, a person with ADHD may be the savior of a society with their restless exploration of new fields.
This new study is published in the journal Proceedings of the Royal Society B.
Flu-killer cells have been discovered in the lungs
A hidden army of flu-killer cells has been discovered in the lungs. A group of “University of California Riverside” researchers in their new research have discovered a group of virus-eating cells in the lung that can fight influenza.
A hidden army of flu-killer cells has been discovered in the lungs
Scientists have long thought of the fluid-filled sac around our lungs as merely a barrier to external damage, but new research shows that this sac also contains powerful virus-eating cells that enter when an influenza infection occurs.
According to ScienceMag, these cells should not be confused with phages that infect bacteria. These cells, called macrophages, are immune cells produced in the body.
“Juliet Morrison” (Juliet Morrison), a virologist at, “The University of California Riverside” (UC Riverside) and head of this research said: Macrophages swallow bacteria, viruses, cancer cells, and dying cells. They grab and destroy anything that looks alien. We were surprised to find them in the lungs because no one had seen anything like that before.
In this research, it is explained how macrophages leave the external cavity and enter the lungs during influenza. They reduce inflammation there and lower the level of disease. “This research shows that it’s not just what happens in the lung that matters, but what happens outside the lung as well,” Morrison said. Cells not normally associated with the lung can have important effects on lung disease and health.
He added: Since this structure contains liquid, it prevents the lungs from collapsing. Despite this, researchers haven’t thought much about the fact that it might contain an entire organ. Our research may change this perception.
Researchers initially sought to answer a more general question. The question was which type of cells are present in the lung when you get influenza? They obtained existing data on lung-related genes from research on mice that either died or survived the flu. Then, they mined the data using an algorithm to predict the types of cells that change in the lungs during influenza. “We analyzed the data to determine which immune cells were present in the lung tissues,” Morrison said. That’s when I realized that maybe we have an unknown external source of cells in the lung.
Then, using a laser-based method, the researchers tracked the macrophages entering the mice’s lungs and found out what would happen if they took these cells out. “When you take them out of the mouse lung, you see disease progression and increased lung inflammation,” Morrison continued.
Morrison hopes the research will encourage other scientists to re-evaluate data sets from older studies. He added: Our method was to make a new use of the available information and finally we were able to see something new.
In their future research, the research group hopes to understand which protein tells the macrophages to move into the lungs. Once the protein signals are identified, it may be possible to discover drugs that increase macrophage numbers or activity.
A strategy to strengthen the human defense system against infection rather than developing another antiviral drug could provide a treatment for influenza that is effective for a longer period of time. Morrison is interested in host therapy because antibiotic and antiviral drug resistance is a growing problem.
This problem occurs when microbes, such as bacteria and fungi, gain the ability to defeat drugs designed to kill them. Improper use and overdose of drugs accelerate this problem. According to the report of the “American Center for Disease Control and Prevention” (CDC), more than 2.8 million drug-resistant infections occur in this country every year, and as a result, more than 35 thousand people die.
“If we can boost what’s killing the infection in us, we’re probably going to have a better outcome and be less likely to become resistant to the drug,” Morrison said. The immune system is very complex, but our best long-term job is to work with what we have instead of chasing treatment-evasive viruses.
This research was published in the journal “PNAS”.
Why do we get old?
Aging is an inevitable fate for all living organisms and many scientists are trying to reverse this process by discovering effective factors. Now a new study shows that DNA damage may be the main cause of aging. So why do we get old?
Why do we get old?
Processes and pathways that run smoothly in our youth begin to fail as we age. Over time, these breaks build up and lead to symptoms like loss of muscle mass, weakened immune systems, memory problems, and more that we will all experience in the future.
According to Forbes, what we see on the skin is reflected at the genetic level, creating obvious differences between young and old adults, but the exact reasons for these age-related genetic changes have not been well understood. A new study suggests that DNA damage may be to blame for aging. So why do we get old?
The genetic fingerprint of aging
Genes make the world go round. It sounds like an exaggeration, but it’s true. Each of the processes we depend on for life is somehow shaped by genes. Remember that genes serve as blueprints for protein production. Without proteins, everything stops, and ultimately, they are molecules that perform functions.
Whether a protein is produced when, where, and how much it is produced is precisely regulated by a process called gene expression. Gene expression is essentially a genetic on/off switch. For example, when a person becomes ill due to a viral infection, their body begins to turn on genes related to the immune response, thereby mobilizing the appropriate immune cells to help defend against the threat. When gene expression is properly regulated, cell function proceeds smoothly, but if the balance is disturbed, genes that should be off may remain on, and vice versa. Also, too much or too little protein may be produced.
Aging is characterized by a specific pattern of gene expression. In a sense, it can be said that aging has a specific genetic fingerprint. Just like a thief leaves his fingerprints at a crime scene, age leaves its mark, and this is true of all animal species, from tube worms to humans.
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Changes in gene expression associated with aging have been known for some time, but answering what triggers these changes in the first place has been surprisingly difficult. We know what aging looks like at the genetic level, but we don’t know why it happens.
From DNA to RNA
Protein production is a complex, multi-step process, and as with any complex process that has multiple moving parts, there is room for error. In fact, the findings of this new research show that changes in gene expression with age may be related to defects in protein production. It seems that damage to DNA is associated with damage to an important step called “transcription”.
Proteins are made from RNA, but our genes are stored in the form of DNA. Therefore, DNA must first be converted into RNA. In technical language, this work is called transcription. Why is this genetic procedure needed? Our DNA is stored in the nucleus of cells and does not leave this area of the cell to minimize damage, but protein production takes place in the cytoplasm. Therefore, genetic information must reach the cytoplasm from the nucleus.
This is where mRNA, or to be more precise, “messenger RNA” (mRNA) comes into play. While DNA is used for long-term storage, messenger RNA serves as a single-use set of genetic instructions. A messenger RNA encodes a copy of a specific gene and transfers it from the nucleus to the cytoplasm; Where the gene can be converted into a protein. The process is similar to copying part of a rare book that you need but can’t get out of the library.
The body even has its own genetic photocopying machine called RNAi polymerase II, or RNAPII. Arane polymerase II is a complex of several proteins that, depending on the gene that needs to be transcribed, attaches to a specific segment of DNA and then moves along the target gene, delivering a copy of the complementary arane. The resulting RNA strand, called the transcript, is the precursor to the messenger RNA.
In this study, Akos Gyenis, Jiang Chang, and their colleagues at the Erasmus MC Medical Center in the Netherlands discovered that in older mice, RNAi polymerase II often fails when transcribing DNA into Arani starts to stop. Analyzing the livers of two-year-old mice, they found that up to 40% of all polymerase II arane complexes were stopped. Additionally, each stalled set likely blocks three others behind it, causing the DNA strands to line up until the blockage is resolved. The researchers found that larger genes were particularly susceptible to these issues, leading to a bias towards the expression of small genes.
When transcription stops, gene expression also stops. As a result, many cellular pathways begin to fail. They are deprived of the proteins they need to function properly. This includes all pathways that malfunction with age. In other words, the genetic fingerprint created by interrupted transcription is the same as that created by aging, suggesting that they are closely related. Pathways affected include those involved in nutrient sensing, cellular debris clearance, energy metabolism, immune system function, and the ability of cells to cope with injury. All of these things play a vital role in shaping longevity.
In the next step, the researchers sought to understand the cause of the arrest of Aran polymerase II in aged mice. Their suspicions led to DNA damage that was spontaneous and internal. Gene expression patterns in cells exposed to DNA-damaging agents are very similar to those seen during normal aging. Premature aging disorders such as Cockayne syndrome are also characterized by DNA damage. Normal DNA repair mechanisms malfunction and result in the stalling of polymerase II at sites of damage known as lesions. Considering these similarities, scientists speculated that DNA damage could also be involved in normal aging.
To test their hypothesis, the researchers looked at genetically modified mice that lacked the normal DNA repair system and were prone to DNA damage. These mice showed many features of premature aging; Including their life span which was significantly shortened. As expected, the transcription speed was significantly lower in these mice compared to the healthy group.
Although we have a good understanding of how gene expression changes with age, we do not fully understand what causes these genetic changes. This situation is just like looking at the symptoms of a disease without knowing the root cause. This new research suggests one possible mechanism is the DNA damage that accumulates in RNAi polymerase II as it attempts to transcribe the template strand into RNAi. When RNAi polymerase II hits a site of damage, it stalls and interferes with transcription, disrupting several important cellular pathways.
Although this research does not yet have any immediate therapeutic implications, research of this type helps us better understand the inner workings of the aging process. The deeper our understanding, the more likely it is to develop effective drug interventions. Until then, it’s best to avoid behaviors that pose a risk of DNA damage, such as smoking and exposure to UV rays. Temporary programmed caloric restriction may also help reduce transcriptional pressure.
This research was published in “Nature Genetics” magazine.
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