„Coronavirus Pandemic Update 82: Racial Disparities with „COVID-19 & Vitamin D“
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COVID-19 Update 82 with Roger Seheult, MD of https://www.medcram.com
There is an increasing amount of data that suggests that Black, Asian, and other minority ethnic groups are at an increased risk of COVID-19 deaths in the United States, England, and other European Countries. Dr. Seheult discusses how Vitamin D deficiency may play a role in this disparity. (This video was recorded June 10, 2020).“
Update: 16.6.2020:
„There is an increasing amount of data that suggests that Black, Asian, and other minority ethnic groups are at an increased risk of COVID-19 deaths in the United States, England, and other European Countries. Dr. Seheult discusses how Vitamin D deficiency may play a role in this disparity. (This video was recorded June 10, 2020).“
Conspiracy Revelation: 16.6.2020: India´s Death Toll rises and they have by far not so much sugar intake (200% up to 50% less than most other countries according to your stats..) So this might be an anomaly in your theory.
„International and UK data suggests that black Asian and minority ethnic groups are at increased risk for infection and death from Covid-19. We aimed to explore the risk of death in minority ethnic groups in England, using data reported by the NHS England. so how did they do that, let’s take a look at their methods nice thing about the NHS of course is that there’s easily able to get data and say
looked at deaths from the 1st of March up until the 21st of April of this year and they standardized the data looking
at the entire population of England to produce ethnic
specific standardized mortality ratios or SMRs for adjusted age and geographical region and so the data here shows that the largest total number of deaths in minority ethnic groups were: Indian and black Caribbean and that when they adjusted for region they found a lower risk of death for white Irish and for white British ethnic groups, but rather an increased risk of death for black African, Black Caribbean, Pakistani,
Bangladeshi and Indian minority ethnic groups.“
Kategorie: DNA-Tracking/NASA/NAVY
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Rockefeller: Ziel ist jedem Menschen dieser Welt einen RFID-Chip zu verpassen. NWO Aaron Russo
„Rockefeller: Ziel ist jedem Menschen dieser Welt einen RFID-Chip zu verpassen. NWO Aaron Russo“
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Genes May Leave Some People More Vulnerable to Severe Covid-19
„Genes May Leave Some People More Vulnerable to Severe Covid-19“
Conspiracy Revelation: 6.6.2020: Most people have this blood type…
„Geneticists have turned up intriguing links between DNA and the disease. Patients with Type A blood, for example, seem to be at greater risk.“
„By Carl Zimmer
June 3, 2020
Why do some people infected with the coronavirus suffer only mild symptoms, while others become deathly ill?
Geneticists have been scouring our DNA for clues. Now, a study by European scientists is the first to document a strong statistical link between genetic variations and Covid-19, the illness caused by the coronavirus.
Variations at two spots in the human genome are associated with an increased risk of respiratory failure in patients with Covid-19, the researchers found. One of these spots includes the gene that determines blood types.
Having Type A blood was linked to a 50 percent increase in the likelihood that a patient would need to get oxygen or to go on a ventilator, according to the new study.
The study was equally striking for the genes that failed to turn up. The coronavirus attaches to a protein called ACE2 on the surface of human cells in order to enter them, for example. But genetic variants in ACE2 did not appear to make a difference in the risk of severe Covid-19.
The findings suggest that relatively unexplored factors may be playing a large role who develops life-threatening Covid-19. “There are new kids on the block now,” said Andre Franke, a molecular geneticist at the University of Kiel in Germany and a co-author of the new study, which is currently going through peer review.
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Scientists have already determined that factors like age and underlying disease put people at extra risk of developing a severe case of Covid-19. But geneticists are hoping that a DNA test might help identify patients who will need aggressive treatment.
Figuring out the reason that certain genes may raise the odds of severe disease could also lead to new targets for drug designers.
As the pandemic gained momentum in February, Dr. Franke and his colleagues set up a collaboration with doctors in Spain and Italy who were struggling with a rising wave of Covid-19.
The doctors took blood samples from 1,610 patients who needed an oxygen supply or had to go on a ventilator. Dr. Franke and his colleagues extracted DNA from the samples and scanned it using a rapid technique called genotyping.
The researchers did not sequence all three billion genetic letters in the genome of each patient. Instead, they looked at nine million letters. Then the researchers carried out the same genetic survey on 2,205 blood donors with no evidence of Covid-19.
The scientists were looking for spots in the genome, called loci, where an unusually high number of the severely ill patients shared the same variants, compared with those who were not ill.
Two loci turned up. In one of these sites is the gene that determines our blood type. That gene directs production of a protein that places molecules on the surface of blood cells.
It’s not the first time Type A blood has turned up as a possible risk. Chinese scientists who examined patient blood types also found that those with Type A were more likely to develop a serious case of Covid-19.
No one knows why. While Dr. Franke was comforted by the support from the Chinese study, he could only speculate how blood types might affect the disease. “That is haunting me, quite honestly,” he said.
He also noted that the locus where the blood-type gene is situated also contains a stretch of DNA that acts as an on-off switch for a gene producing a protein that triggers strong immune responses.
The coronavirus triggers an overreaction of the immune system in some people, leading to massive inflammation and lung damage — the so-called cytokine storm. It is theoretically possible that genetic variations influence that response.
A second locus, on Chromosome 3, shows an even stronger link to Covid-19, Dr. Franke and his colleagues found. But that spot is home to six genes, and it is not yet possible to say which of them influences the course of Covid-19.
The Coronavirus Outbreak
Frequently Asked Questions and Advice
Updated June 5, 2020
How many people have lost their jobs due to coronavirus in the U.S.?
The unemployment rate fell to 13.3 percent in May, the Labor Department said on June 5, an unexpected improvement in the nation’s job market as hiring rebounded faster than economists expected. Economists had forecast the unemployment rate to increase to as much as 20 percent, after it hit 14.7 percent in April, which was the highest since the government began keeping official statistics after World War II. But the unemployment rate dipped instead, with employers adding 2.5 million jobs, after more than 20 million jobs were lost in April.
Will protests set off a second viral wave of coronavirus?
Mass protests against police brutality that have brought thousands of people onto the streets in cities across America are raising the specter of new coronavirus outbreaks, prompting political leaders, physicians and public health experts to warn that the crowds could cause a surge in cases. While many political leaders affirmed the right of protesters to express themselves, they urged the demonstrators to wear face masks and maintain social distancing, both to protect themselves and to prevent further community spread of the virus. Some infectious disease experts were reassured by the fact that the protests were held outdoors, saying the open air settings could mitigate the risk of transmission.
How do we start exercising again without hurting ourselves after months of lockdown?
Exercise researchers and physicians have some blunt advice for those of us aiming to return to regular exercise now: Start slowly and then rev up your workouts, also slowly. American adults tended to be about 12 percent less active after the stay-at-home mandates began in March than they were in January. But there are steps you can take to ease your way back into regular exercise safely. First, “start at no more than 50 percent of the exercise you were doing before Covid,” says Dr. Monica Rho, the chief of musculoskeletal medicine at the Shirley Ryan AbilityLab in Chicago. Thread in some preparatory squats, too, she advises. “When you haven’t been exercising, you lose muscle mass.” Expect some muscle twinges after these preliminary, post-lockdown sessions, especially a day or two later. But sudden or increasing pain during exercise is a clarion call to stop and return home.
My state is reopening. Is it safe to go out?
States are reopening bit by bit. This means that more public spaces are available for use and more and more businesses are being allowed to open again. The federal government is largely leaving the decision up to states, and some state leaders are leaving the decision up to local authorities. Even if you aren’t being told to stay at home, it’s still a good idea to limit trips outside and your interaction with other people.
What’s the risk of catching coronavirus from a surface?
Touching contaminated objects and then infecting ourselves with the germs is not typically how the virus spreads. But it can happen. A number of studies of flu, rhinovirus, coronavirus and other microbes have shown that respiratory illnesses, including the new coronavirus, can spread by touching contaminated surfaces, particularly in places like day care centers, offices and hospitals. But a long chain of events has to happen for the disease to spread that way. The best way to protect yourself from coronavirus — whether it’s surface transmission or close human contact — is still social distancing, washing your hands, not touching your face and wearing masks.
What are the symptoms of coronavirus?
Common symptoms include fever, a dry cough, fatigue and difficulty breathing or shortness of breath. Some of these symptoms overlap with those of the flu, making detection difficult, but runny noses and stuffy sinuses are less common. The C.D.C. has also added chills, muscle pain, sore throat, headache and a new loss of the sense of taste or smell as symptoms to look out for. Most people fall ill five to seven days after exposure, but symptoms may appear in as few as two days or as many as 14 days.
How can I protect myself while flying?
If air travel is unavoidable, there are some steps you can take to protect yourself. Most important: Wash your hands often, and stop touching your face. If possible, choose a window seat. A study from Emory University found that during flu season, the safest place to sit on a plane is by a window, as people sitting in window seats had less contact with potentially sick people. Disinfect hard surfaces. When you get to your seat and your hands are clean, use disinfecting wipes to clean the hard surfaces at your seat like the head and arm rest, the seatbelt buckle, the remote, screen, seat back pocket and the tray table. If the seat is hard and nonporous or leather or pleather, you can wipe that down, too. (Using wipes on upholstered seats could lead to a wet seat and spreading of germs rather than killing them.)
How do I take my temperature?
Taking one’s temperature to look for signs of fever is not as easy as it sounds, as “normal” temperature numbers can vary, but generally, keep an eye out for a temperature of 100.5 degrees Fahrenheit or higher. If you don’t have a thermometer (they can be pricey these days), there are other ways to figure out if you have a fever, or are at risk of Covid-19 complications.
Should I wear a mask?
The C.D.C. has recommended that all Americans wear cloth masks if they go out in public. This is a shift in federal guidance reflecting new concerns that the coronavirus is being spread by infected people who have no symptoms. Until now, the C.D.C., like the W.H.O., has advised that ordinary people don’t need to wear masks unless they are sick and coughing. Part of the reason was to preserve medical-grade masks for health care workers who desperately need them at a time when they are in continuously short supply. Masks don’t replace hand washing and social distancing.
What should I do if I feel sick?
If you’ve been exposed to the coronavirus or think you have, and have a fever or symptoms like a cough or difficulty breathing, call a doctor. They should give you advice on whether you should be tested, how to get tested, and how to seek medical treatment without potentially infecting or exposing others.
How do I get tested?
If you’re sick and you think you’ve been exposed to the new coronavirus, the C.D.C. recommends that you call your healthcare provider and explain your symptoms and fears. They will decide if you need to be tested. Keep in mind that there’s a chance — because of a lack of testing kits or because you’re asymptomatic, for instance — you won’t be able to get tested.
One of those gene candidates encodes a protein known to interact with ACE2, the cellular receptor needed by the coronavirus to enter host cells. But another gene nearby encodes a potent immune-signaling molecule. It is possible that this immune gene also triggers an overreaction that leads to respiratory failure.
Dr. Franke and his colleagues are part of an international effort called the Covid-19 Host Genetics Initiative.
A thousand researchers in 46 countries are collecting DNA samples from people with the disease. They are now beginning to post data on the initiative’s website.
Andrea Ganna, a genetic epidemiologist at the University of Helsinki, said that initiative’s collected data were beginning to point to a single spot on Chromosome 3 as a potentially important player.
It’s not common for genetic variants to emerge out of studies of so few people, said Jonathan Sebat, a geneticist at the University of California, San Diego, who was not involved in the new study.
“We were all hoping optimistically this was one of those situations,” Dr. Sebat said.
Previous attempts to find any genetic loci that varied significantly between sick people and healthy ones have failed. Dr. Sebat speculated that the new study succeeded because the researchers focused only on people who had respiratory failure and were clearly vulnerable to serious forms of Covid-19.
“They had the ideal cohort,” he said.
New studies, such as the one Dr. Sebat is running in California, will allow scientists to see if the two loci really do matter as much as they seem to now.
The geneticists may be able to zero in on exactly which gene in each locus affects the disease, he said. And researchers will most likely find many other genes with subtler influences on the course of Covid-19.
Genetics and the Coronavirus“
Source: https://www.nytimes.com/2020/06/03/health/coronavirus-blood-type-genetics.html
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Chemtrails – Wie eine Weltregierung unser Wetter kontrolliert
https://youtu.be/WXpeouDwp18
„Kontext: ChemtrailWikipediaVerbrecher-Lügipedia korrigiert…
Der Begriff Chemtrails, gelegentlich auch Giftwolken, und wird im Zusammenhang mit einer seit den 1990er Jahren verbreiteten und bewiesenen Verschwörungsrealität.“
„Chemtrails – Wie eine Weltregierung unser Wetter kontrolliert.“
„75.400 Aufrufe•29.04.2017“
„Zum ersten mal bemerkte ich es 2002, ein Freund machte
mich vor seinem Büro darauf aufmerksam, wie ungewöhnlich langlebig die ..Streifen sind, es ärgerte mich. Unser
einst tiefblauer Himmel war inzwischen komplett vernebelt durch künstlich geschaffene Wolken, die das Sonnenlicht
blockierten. Schließlich fand sie heraus, dass sie mit ihren Sorgen nicht allein war, auf hunderten von Internetseiten gab es Schilderungen zu den langlebigen beständigen ..Streifen.“
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U.S Buys 300 Million Covid Vaccines from Gates-Affiliated Drug Maker
Conspiracy Revelation: 3.6.2020: The worst pharma mafia company in the world… „AstraZeneca121 = 112 = 211 = The Destroyers“
(They anagram number copy the Deep Underground Base 211 of the Antarctica Mars Slave Colony Corp. Nazis – no coincidence here)
I survived their Directed Energy Weapons / Zion-NSA-DIA-CIA-Arpa-Pentagon / Tesla Scalar Weapons / Neurowarfare and Skynet assaults (incl. their UN Nazi DoD CFR USAF Crime Syndicate NWO MIAC ShadowGov affiliates in 2011)…
„U.S Buys 300 Million Covid Vaccines from Gates-Affiliated Drug Maker
By David Sidman May 25, 2020 , 1:04 pm
„He who deals deceitfully shall not live in my house; he who speaks untruth shall not stand before my eyes. (Psalm 101:7)“
„AstraZeneca sign at British-Swedish multinational pharmaceutical and biopharmaceutical company campus – south San Francisco, California, USA – 2020 (courtesy: Shutterstock)
Washington has purchased nearly a third of the initial one billion doses of AstraZeneca’s experimental coronavirus vaccine.
The U.S. Department of Health has agreed to provide up to US$1.2 billion to fast-track AstraZeneca’s vaccine development while securing 300 million doses for the entire US reports MDLinx. The vaccine is being developed from a laboratory at Oxford University.
“This contract with AstraZeneca is a major milestone in Operation Warp Speed’s work toward a safe, effective, widely available vaccine by 2021,” U.S. Health Secretary Alex Azar said.
AstraZeneca is collaborating with Microsoft, to launch an artificial intelligence (AI) ‘Factory for Health’. One of the startups in the ‘factory’ is Kap Code. The tech company created a tool based on a method of hypnosis called Neuro-Linguistic Programming (NLP). The start-up scans social media posts and uses that data to better understand patient experiences. Microsoft was founded by Gates. He is now among the company’s top shareholders.
Jean-Philippe Courtois is the President of Microsoft Global Sales and used to to be on AstraZeneca’s board.
The drug-maker also teamed up with Glaxo-Smith Klein to provide a “proprietary libraries of molecular compounds” for screening with the coronavirus Therapeutics Accelerator, an initiative of the Bill & Melinda Gates Foundation.
The foundation’s CEPI is also funding drug-maker Moderna for a Covid vaccine. Moderna has strategic alliances for development programs with AstraZeneca.
Oxford University, where the vaccination is being developed, has also enjoyed funding from the Bill and Melinda Gates fund for disease research.
The British-based pharmaceutical giant also boasts a scandal-ridden history. This includes a 2014 lawsuit whereby Astrazeneca was caught faking conferences and bribing doctors in Russia and China to buy their drugs. The company was forced to pay. Earlier in 2010, Astrazeneca was caught offering kickbacks to doctors to prescribe their Seroquel drug to patients with disorders that the drug wasn’t even tested for. The company was forced to cough up $520 million in damages.“
Source: https://www.breakingisraelnews.com/150881/u-s-buys-300-million-covid-vaccines-from-gates-affiliated-drug-maker/ -
Why Immunity to the Novel Coronavirus Is So Complicated
„Why Immunity to the Novel Coronavirus Is So Complicated“
„Why Immunity to the Novel Coronavirus Is So Complicated
Some immune responses may be enough to make a person impervious to reinfection, but scientists don’t yet know how the human body reacts to this new virus
SARS-CoV-2_scanning_electron_microscope_image.jpg
A scanning electron microscope image of SARS-CoV-2, the coronavirus that causes COVID-19. (NIAID / flickr)
By Katherine J. Wu
SMITHSONIANMAG.COM
MAY 26, 2020
Even before the blood left his arm, André Valleteau suspected he knew what his doctors would find.
Just weeks before, the 27-year-old from Toronto had tested positive for SARS-CoV-2, the coronavirus that causes COVID-19. The symptoms hit him hard: headache, cough, sore throat and fatigue that relegated him to his bed 15 hours a day. “It didn’t matter how many times I napped,” he says. “I was tired until the next time I napped again.”
Valleteau, a researcher coordinator at a pharmaceutical company, spent two weeks self-isolating and recovering, then decided he wanted to help others do the same. He contacted a local researcher and offered up his blood—along with the disease-fighting antibodies that likely teemed within. Indeed, Valleteau’s blood tested positive for antibodies against SARS-CoV-2, and a team of scientists is now studying molecules from patients like Valleteau in the hopes they can inform the development of drugs or vaccines to vanquish the virus.
Antibodies, which the body makes in response to dangerous microbes like SARS-CoV-2, are crucial for defending against disease. Many can glom onto pathogens and subdue them before they have a chance to encounter vulnerable human cells. Antibodies are also evidence: Some COVID-19 tests target these molecules because they show that someone has previously been infected with SARS-CoV-2. (And as previously reported, the possibility of false negatives or false positives, which are more common with some tests than others, can sometimes muddle attempts to pinpoint past infections.)
Even then, while a positive antibody test (also called a serology test) can say a lot about the past, it may not indicate much about a person’s future. Researchers still don’t know if antibodies that recognize SARS-CoV-2 prevent people from catching the virus a second time—or, if they do, how long that protection might last.
Immunity isn’t binary, but a continuum—and having an immune response, like those that can be measured by antibody tests, doesn’t make a person impervious to disease. “There’s this impression that ‘immunity’ means you’re 100 percent protected, that you’ll never be infected again,” says Rachel Graham, an virologist studying coronaviruses at the University of North Carolina’s Gillings School of Global Public Health. “But having immunity just means your immune system is responding to something”—not how well it’s poised to guard you from subsequent harm.
It takes a symphony of cells
In discussions of immunity, antibodies often end up hogging the spotlight—but they’re not the only weapons the body wields against invaders. The sheer multitude of molecules at work helps explain why “immunity” is such a slippery concept.
When a pathogen infiltrates the body, the immune system mounts a defense in two acts. First comes the innate immune response, a blunt, broad-acting ensemble that attacks any invader that doesn’t resemble a normal-looking human cell. Slower but more specific is the adaptive immune response, a second wave of assailants the body custom-builds to recognize unique features of the infectious microbe.
This second wave includes antibodies, which are manufactured by immune cells called B cells. Some antibodies are potent weapons that curb a microbe’s capacity to latch onto and enter cells, while others simply flag germs or infected cells for destruction by other parts of the immune system. The former category, called neutralizing antibodies, are necessary to combat most of the pathogens that plague humans, and their production is generally considered a hallmark of a good vaccine, says Sallie Permar, a virologist and vaccine expert at Duke University says.
GettyImages-1214741192.jpg
A laboratory technician holds a bag with samples ready for COVID-19 testing, including blood for an antibody test, at SOMOS Community Care site in Washington Heights Latino community. (Lev Radin/Pacific Press/LightRocket / Getty Images)
Although antibodies have a short lifespan, disappearing from the blood after a few weeks or months, the immune system retains some of the B cells that produce them. If the same germ returns, these cellular factories will whip up a big batch of antibodies to wage a second war. But antibodies alone aren’t enough to quash an infection, says Diane Griffin, an immunologist at Johns Hopkins University’s Bloomberg School of Public Health. “You need an orchestra of responses [for protection] to really be effective.”
T cells—another subset of the adaptive response—are often left out of conversations about immunity.
“You can’t have a great antibody response without T cells,” says Akiko Iwasaki, a virologist and immunologist at Yale University. Among a slew of helpful functions, T cells help young B cells mature into antibody-making machines. “These things really go hand in hand.”
T cells are also formidable fighters in their own right. In a bid to stop the spread of a pathogen throughout the body, some T cells will trigger infected cells to self-destruct. Others linger after an illness has resolved, patrolling tissues so germs can’t reestablish a foothold. (One of the reasons that HIV is such a devastating diagnosis is that the virus destroys some of the body’s T cells.)
Studies of other coronaviruses, including the ones that cause SARS and MERS, show that T cells play integral roles in stamping out sickness, says Stephanie Langel, a virologist and immunologist at Duke University. It’s likely that the same will hold true for SARS-CoV-2. Compared to antibodies, however, T cells—which often hole up in hard-to-reach tissues like the lungs—are more difficult to extract and analyze. That makes T-cell detection unlikely to play much of a role in clinical tests for immune responses against SARS-CoV-2. For researchers, though, T cells “represent a wealth of knowledge” about how our immune systems deal with the new coronavirus, Langel says.
Antibodies aren’t perfect
Even the most sensitive laboratory tests have their limits, and finding antibodies against SARS-CoV-2 is no guarantee that those molecules are high-quality defenders or that a person is protected from reinfection.
Most commercially available antibody tests search a person’s blood for antibodies that can recognize SARS-CoV-2’s spike protein, the molecule the virus uses to attach to human cells. Some (but not all) of these assessments can tell how many antibodies a person is producing—the more the better, generally speaking. But typical tests don’t determine whether the antibodies are neutralizing. To come to that conclusion, researchers must mix antibodies with viruses and check whether they stop the pathogens from invading human cells in a laboratory under strict safety protocols.
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A T cell (blue) engages its target cell for destruction. (Alex Ritter, Jennifer Lippincott Schwartz and Gillian Griffiths, National Institutes of Health / flickr)
Though non-neutralizing antibodies can play less direct roles in incapacitating a pathogen, many are duds that have no effect on microbes. Some may even chauffeur active viruses into healthy cells, inadvertently accelerating infection. “Essentially, the antibody helps the virus replicate,” Permar says. This rare phenomenon, called antibody-dependent enhancement, has been observed with the viruses that cause dengue and Zika.
Why antibodies can be so inconsistent is still a mystery, in part because laboratory experiments can’t recreate the conditions these molecules experience in the body, says Marcia Goldberg, a microbiologist at Harvard University. “It’s really important to actually test how well antibodies are working in people.” (One way to do so involves administering antibodies to patients battling COVID-19, something that’s being trialed in hospitals around the world.)
Even antibodies with known neutralizing powers aren’t foolproof. Donna Farber, an immunologist at Columbia University who studies T-cell responses against airway viruses, says that some patients with high levels of neutralizing antibodies in their blood still succumb to COVID-19, another hint that other parts of the immune system are needed to reliably defeat this disease.
That’s why antibody tests shouldn’t be overinterpreted, Iwasaki says. One common misconception is that a positive antibody test means a person no longer has the virus in their system, which isn’t necessarily the case. Antibodies are often roused about a week into a new infection, potentially overlapping with a pathogen’s tenure in the body. Diagnostic tests that search for the virus’ genetic material can help tease that timeline apart, but even these assessments can yield incorrect results.
“So much nuance is being lost by just saying ‘serology [antibody] positive’ and ‘serology [antibody] negative,’” Iwasaki says.
A range of responses
A person who has recovered from their first brush with a new pathogen like SARS-CoV-2 may travel one of several immunological routes, Goldberg says—not all of which end in complete protection from another infection.
One possibility is that the immune system does a great job of cataloguing the invader’s unique features. That intel will get stored in an army of B and T cells that will rally to fight the second time a germ comes around. B cells in particular play a starring role in this scenario, pumping out neutralizing antibodies that can sequester and disable a pathogen before it even has the chance to enter a host cell, Iwasaki says. This phenomenon, called sterilizing immunity, make people essentially resistant to reinfection. The body may rouse this reaction in response to microbes like the virus that causes measles, which tends to be a one-and-done infection for most people.
SARS-CoV-2.jpg
A scanning electron microscope image of SARS-CoV-2, the coronavirus that causes COVID-19. (NIAID / flickr)
But not all pathogens prompt such a robust response—and not everyone reacts the same way to a given microbe. People can experience varying shades of partial protection in the wake of an infection, Goldberg says. In some cases, a bug might infect a person a second time but struggle to replicate in the body, causing only mild symptoms (or none at all) before it’s purged once more. The person may never notice the germ’s return. Still, even a temporary rendezvous between human and microbe can create a conduit for transmission, allowing the pathogen to hop into another susceptible individual.
Under rarer circumstances, patients may experience symptoms that are similar to, or perhaps even more severe, than the first time their body encountered the pathogen.
That doesn’t mean people are doomed to experience the same diseases over and over. “The word ‘immune’ makes it sound like the virus gets close to your body, hits a wall, and has to turn away and go find someone else,” says Allison Roder, a virologist at New York University. But even partial protection from the immune system will curtail the amount of pathogen in a person’s body, and, by extension, the likelihood of transmission.
None of these protective states are necessarily permanent or mutually exclusive. A person’s immunity to a pathogen can wane over the course of months or years, eventually dropping below a threshold that leaves them susceptible to disease once again. Researchers don’t yet know whether that will be the case for SARS-CoV-2. The widespread deployment of accurate antibody tests, which can track both where the virus has been and how people are faring after having it, may help answer that question. Scientists are also trying to determine the antibody levels that correlate with protection against reinfection and how durable those responses are over time.
Finding those answers will be a boon for vaccine development, Permar says. “The dream of every vaccine is to be able to say, ‘We need this level of antibody.’ Then vaccines can chase that endpoint. Until we know that benchmark… we’re operating in the dark.”
So far, early studies in both humans and animals suggest exposure to SARS-CoV-2 marshals a strong immune response. But until researchers have more clarity, Graham advises continued vigilance—even for those who have gotten positive results from antibody tests, or have other reason to believe they were infected with COVID-19.
Valleteau, who has received clinical confirmation the coronavirus is no longer in his system, is still practicing physical distancing, frequently washing his hands and wearing protective gear like face coverings. He’s also taking extra precautions around the patients he works with, many of whom have diabetes, a condition that can increase the risk of complications from COVID-19.“
Source: https://www.smithsonianmag.com/science-nature/coronavirus-immunity-complicated-180974970/
