A Bold Effort To Cure HIV—Using Crispr

Immune cells infected with HIV Photograph: BIOPHOTO ASSOCIATES/Science SourceImmune cells infected with HIVPhotograph: BIOPHOTO ASSOCIATES/Science Source

An experiment tests whether the gene-editing technology can stop the virus from replicating, which would ultimately wipe out the infection.

In July, an HIV-positive man became the first volunteer in a clinical trial aimed at using Crispr gene editing to snip the AIDS-causing virus out of his cells. For an hour, he was hooked up to an IV bag that pumped the experimental treatment directly into his bloodstream. The one-time infusion is designed to carry the gene-editing tools to the man’s infected cells to clear the virus.

Later this month, the volunteer will stop taking the antiretroviral drugs he’s been on to keep the virus at undetectable levels. Then, investigators will wait 12 weeks to see if the virus rebounds. If not, they’ll consider the experiment a success. “What we’re trying to do is return the cell to a near-normal state,” says Daniel Dornbusch, CEO of Excision BioTherapeutics, the San Francisco-based biotech company that’s running the trial.

HIV attacks immune cells in the body called CD4 cells and hijacks their machinery to make copies of itself. But some HIV-infected cells can go dormant—sometimes for years—and not actively produce new virus copies. These so-called reservoirs are a major barrier to curing HIV.

“HIV is a tough foe to fight because it’s able to insert itself into our own DNA, and it’s also able to become silent and reactivate at different points in a person’s life,” says Jonathan Li, a physician at Brigham and Women’s Hospital and HIV researcher at Harvard University who’s not involved with the Crispr trial. Figuring out how to target these reservoirs—and doing it without harming vital CD4 cells—has proven challenging, Li says.

While antiretroviral drugs can halt viral replication and clear the virus from the blood, they can’t reach these reservoirs, so people have to take medication every day for the rest of their lives. But Excision BioTherapeutics is hoping that Crispr will remove HIV for good.

Crispr is being used in several other studies to treat a handful of conditions that arise from genetic mutations. In those cases, scientists are using Crispr to edit peoples’ own cells. But for the HIV trial, Excision researchers are turning the gene-editing tool against the virus. The Crispr infusion contains gene-editing molecules that target two regions in the HIV genome important for viral replication. The virus can only reproduce if it’s fully intact, so Crispr disrupts that process by cutting out chunks of the genome.

In 2019, researchers at Temple University and the University of Nebraska found that using Crispr to delete those regions eliminated HIV from the genomes of rats and mice. A year later, the Temple group also showed that the approach safely removed viral DNA from macaques with SIV, the monkey version of HIV.

That was an important step toward testing the treatment in people, says Kamel Khalili, a professor of microbiology at Temple University who led the work and is a cofounder of Excision Biotherapeutics. “You don’t want to eliminate the viral genome but at the same time cause any disruption in another part of the human genome and then create another set of problems for the patients,” he says. “We had to make sure that we identified a region within HIV that did not overlap with the human genome.”

Dornbusch thinks this strategy will spare patients from serious side effects and “off-target” edits—unintentional cuts elsewhere in the genome that could cause problems such as cancer.

The regions targeted by the company’s Crispr therapy are also in a part of the genome that tends to stay the same even when HIV evolves. That’s important because the virus mutates rapidly, and the researchers don’t want a moving target.

This isn’t the first time scientists have tried to use gene editing in the hope of curing people with HIV, but other efforts have focused on a protective mutation in a gene called CCR5. In the 1990s, scientists found that people with this naturally occurring mutation didn’t get HIV when exposed to it. The mutation—known as delta 32—thwarts the virus’s ability to get inside immune cells. In 2009, California-based Sangamo Therapeutics used an older editing technology called zinc finger nucleases to add that protective mutation into patients’ T cells—an important part of the immune system. Those trials have had limited success.

In 2017, Chinese scientists combined Crispr with a bone marrow transplant in an attempt to cure a patient with HIV and leukemia. In a typical transplant, donor stem cells are transferred to a recipient to replace their cancerous blood cells. These cells go on to form new, healthy blood cells. To also address the patient’s HIV, researchers edited the donor stem cells with Crispr to disable CCR5. But after the transplant, only a small percentage of the patient’s bone marrow cells ended up with the desired edit.

Then in 2018, Chinese scientist He Jiankui used Crispr to edit the CCR5 mutation into the genomes of twin baby girls to make them resistant to HIV. Fraught with ethical violations, the experiment was widely condemned by scientists. He’s research was suspended by the Chinese government, and he served a three-year prison sentence. While the twins were born healthy, only some of their cells were successfully edited, meaning the girls might in fact not be immune to HIV.

As of 2022, two people have now been cured of HIV after receiving bone marrow transplants from donors with the CCR5. Known as the Berlin patient and the London patient, both had cancer and received transplants to treat their disease. But these transplants aren’t a viable option for most people—they’re highly risky, and donors with the delta 32 mutation are scarce. But a third person was declared cured of HIV earlier this year after she received a new type of transplant involving umbilical cord blood.

The Excision trial will eventually enroll nine participants and test three dosage amounts to determine which is most effective. Investigators will measure each person’s viral load and CD4 count before receiving the therapy and after they stop taking antiretroviral drugs. The ultimate goal is to get viral loads down to an undetectable level—that is, less than 200 copies of HIV per milliliter of blood. At this level, HIV can’t be passed on through sex.

The challenge for Excision will be getting Crispr to enough cells to bring HIV down to undetectable levels. The company is using an engineered virus to shuttle the gene-editing components to patients’ HIV-infected CD4 cells. But so far, there’s little human data on how well Crispr works when it’s delivered directly to the body. “It’s possible that you get the virus to such low levels that if a person’s immune system were intact, they might be able to keep the virus at bay such that they don’t have to take antiretroviral therapy anymore,” says Rowena Johnston, vice president and director of research for amfAR, the Foundation for AIDS Research.

And even though these drugs are very effective, Johnston says, many people would rather be completely free of the virus. A single Crispr infusion—if it works—would eliminate the need for daily pills. “People with HIV still live with a lot of stigma and internalized shame,” she says. “I think a cure is something that addresses that much better than lifelong therapy, regardless of how easy that therapy becomes.”

Emily Mullin is a staff writer at WIRED, covering biotechnology. Previously, she was an MIT Knight Science Journalism project fellow and a staff writer covering biotechnology at Medium’s OneZero. Before that, she served as an associate editor at MIT Technology Review, where she wrote about biomedicine. Her stories have also… Read more

Source: A Bold Effort to Cure HIV—Using Crispr | WIRED



Human immunodeficiency virus infection and acquired immunodeficiency syndrome (HIV/AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV), a retrovirus. Following initial infection an individual may not notice any symptoms, or may experience a brief period of influenza-like illness .Typically, this is followed by a prolonged incubation period with no symptoms.

If the infection progresses, it interferes more with the immune system, increasing the risk of developing common infections such as tuberculosis, as well as other opportunistic infections, and tumors which are otherwise rare in people who have normal immune function. These late symptoms of infection are referred to as acquired immunodeficiency syndrome (AIDS).This stage is often also associated with unintended weight loss.

HIV is spread primarily by unprotected sex (including anal and vaginal sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Some bodily fluids, such as saliva, sweat and tears, do not transmit the virus. Oral sex has little to no risk of transmitting the virus.

Methods of prevention include safe sex, needle exchange programs, treating those who are infected, as well as both pre- and post-exposure prophylaxis.[4] Disease in a baby can often be prevented by giving both the mother and child antiretroviral medication. Known as the Berlin Patient and the London Patient, two individuals have been reported cured of AIDS and the United States’ National Institutes of Health (NIH) and the Gates Foundation have pledged $200 million focused on developing a global cure for AIDS.

While there is no broadly available cure or vaccine, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. Treatment is recommended as soon as the diagnosis is made.[17] Without treatment, the average survival time after infection is 11 years. In 2021, about 38 million people worldwide were living with HIV and 650,000 deaths had occurred in that year.

An estimated 20.6 million of these live in eastern and southern Africa. Between the time that AIDS was identified (in the early 1980s) and 2021, the disease has caused an estimated 40 million deaths worldwide. HIV/AIDS is considered a pandemic—a disease outbreak which is present over a large area and is actively spreading. HIV made the jump from other primates to humans in west-central Africa in the early-to-mid 20th century.

AIDS was first recognized by the U.S. Centers for Disease Control and Prevention (CDC) in 1981 and its cause—HIV infection—was identified in the early part of the decade. HIV/AIDS has had a large impact on society, both as an illness and as a source of discrimination. The disease also has large economic impacts. There are many misconceptions about HIV/AIDS, such as the belief that it can be transmitted by casual non-sexual contact.The disease has become subject to many controversies involving religion, including the Catholic Church’s position not to support condom use as prevention. It has attracted international medical and political attention as well as large-scale funding since it was identified in the 1980s


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What We Know About Why Some People Never Get Covid 19

Americans who haven’t had covid-19 are now officially in the minority. A study published this week from the US Centers for Disease Control and Prevention (CDC) found that 58% of randomly selected blood samples from adults contained antibodies indicating that they had previously been infected with the virus; among children, that rate was 75%.

What is different about that minority of people that hasn’t yet gotten infected? Stories abound of close calls, of situations where people are sure they could have (or should have) gotten sick, but somehow dodged infection. Not all the questions are answered yet, but the question of what distinguishes the never-covid cohort is a growing area of research even as the US moves “out of the full-blown” pandemic. Here are the possibilities that scientists are considering to explain why some people haven’t contracted the virus.

They behave differently

We’ve seen it play out time and time again—some people adhere more strictly to protocols known to reduce transmission of the virus, including wearing a mask and getting vaccinated. Some people avoid large public settings and may have even been doing so before the pandemic, says Nicholas Pullen, a biology professor at the University of Northern Colorado. Then again, that doesn’t tell the whole story; as Pullen himself notes: “Ironically, I happen to be one of those ‘never COVIDers’ and I teach in huge classrooms!”

They’ve trained their immune systems

The immune system, as any immunologist or allergist can tell you, is complicated. Though vaccination against covid-19 can make symptoms more mild for some people, it can prevent others from contracting the illness altogether.

Growing evidence suggests that there may be other ways that people are protected against the virus even without specific vaccines against it. Some could have previously been infected with other coronaviruses, which may allow their immune systems to remember and fight similarly shaped viruses. Another study suggests that strong defenses in the innate immune system, barriers and other processes that prevent pathogens from infecting a person’s body, may also prevent infection.

An innate immune system that’s already not functioning as well due to other medical conditions or lifestyle factors such as sleep or diet may put a person at higher risk of getting sick from a pathogen. There’s not single answer here yet, but initial studies are intriguing and may offer avenues for future treatments for covid-19 and other conditions.

They’re genetically different

In the past, studies have found interesting associations between certain genetic variants and people’s susceptibility to communicable diseases such as HIV, tuberculosis, and the flu. Naturally, researchers wondered if such a variant could exist for covid-19. One June 2021 study that was not peer reviewed found an association between a genetic variant and lower risk of contracting covid-19; another large-scale study, focused on couples in which one person got sick while the other didn’t, kicked off in Oct. 2021.

“My speculation is that something will be borne out there, because it has been well observed that resistance embedded in genetic variation is selected in pandemics,” Pullen says. But most experts suspect that even if they are able to identify such a variant with some certainty, it’s likely to be rare. For now, it’s best for those who haven’t gotten covid to assume they’re as susceptible as anyone else. Whatever the reasons some people haven’t yet gotten sick, the best defense remains staying up to date with vaccinations and avoiding contact with the virus.

Source: What we know about why some people never get covid-19 — Quartz

“Being exposed to the SARS-CoV-2 virus doesn’t always result in infection, and we’ve been keen to understand why,” study author Rhia Kundu said in a statement, using the scientific name for the coronavirus. “We found that high levels of pre-existing T cells, created by the body when infected with other human coronaviruses like the common cold, can protect against COVID-19 infection.”

The study, which examined 52 people who lived with someone who contracted the coronavirus, found that those who didn’t get infected had significantly higher levels of T cells from previous common cold coronavirus infections. T cells are part of the immune system and believed to protect the body from infection. “Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against SARS-CoV-2 infection,” study author Ajit Lalvani said in a statement.

Researchers cautioned that the findings should not be relied upon as a protection strategy. “While this is an important discovery, it is only one form of protection, and I would stress that no one should rely on this alone,” Kundu said. “Instead, the best way to protect yourself against COVID-19 is to be fully vaccinated, including getting your booster dose.” And the findings on the subject have been inconsistent, with other studies actually suggesting that previous infection with some coronaviruses have the opposite effect.

A major question that has come from the so-called ‘never COVID’ group is whether genetics plays a role in preventing infection. In fact, the question has spurred a team of international researchers to look for people who are genetically resistant to COVID-19 in the hopes that their findings could improve therapeutics. “What we are doing essentially is that we are testing the hypothesis that some people might not be able to get infected because of their genetic and inborn makeup, meaning that they might be genetically resistant to COVID,” says Spaan, who is a member of the COVID Human Genetic Effort.

The effort has sequenced genetic data from about 700 individuals so far, but enrollment is ongoing and researchers have received thousands of inquiries, according to Spaan. The study has several criteria, including laboratory test confirmation that the person has not had previous COVID-19 infection, intense exposure to the virus without access to personal protective equipment like masks and an unvaccinated status at the time of exposure, among others. So far, the group doesn’t know what the genetic difference could be – or if it even exists at all, though they believe it does.

“We do not know how frequent it is actually occurring,” Spaan says. “Is it like a super rare individual with a very, very rare mutation? Or is that something more common?” But the hypothesis is “embedded in human history,” according to Spaan. “COVID is not quite the first pandemic that we are dealing with,” Spaan says. “Humans have been exposed to viruses and other pathogens across time from the early beginning, and these infections have left an imprint on our genetic makeup.”

Those who haven’t gotten the coronavirus are “very much at risk,” says Murphy of Northwestern University. “I think every unvaccinated person is going to get it before this is over.” Experts stressed that research to determine why some people get COVID-19 while others don’t is still very much underway, and no one should rely on any of the hypotheses for protection. Instead, those who haven’t gotten the coronavirus should continue mitigation measures that have been proven to work, like vaccination and mask-wearing.

“You don’t ever want to have COVID,” Murphy says. “You just don’t know which people are going to get really sick from this and die or who’s going to get long COVID, which is hard to diagnose and difficult to treat and very real.” But with coronavirus cases on the rise and mitigation measures like mask mandates dropping left and right, it’s not an easy task.

COVID19: Face masks could return as cases spike Financial Mirror

06:48 Tue, 21 Jun
19:35 Mon, 20 Jun
21:11 Fri, 17 Jun

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Pandemic Endgame: What ‘Endemic’ Covid Means—And When We May Get There

Nearly two years into the pandemic, weary politicians and governments are pushing to treat Covid-19 like any other problematic but manageable illness like the seasonal flu, but experts warn the approach could be premature and paints an overly optimistic picture of what “living with Covid” actually means.

Despite the contagious omicron variant driving huge waves of infections, countries including the U.K., Denmark and Sweden have dropped almost all pandemic restrictions as leaders stress we must “learn to live” with the virus and transition from treating Covid-19 as a pandemic illness to an endemic one.

But “with few exceptions, politicians do not understand the meaning or significance of endemicity,” warns Dr. John Swartzberg, an infectious disease expert at the University of California at Berkeley school of public health, who told Forbes endemic means the “stable or constant presence of a disease” within a set area.

Dr. Aris Katzourakis, an evolutionary virologist at the University of Oxford, expressed a similar degree of uncertainty and told Forbes that while he couldn’t say how soon we might reach it, “it’s not going to be in 2022.”

Endemic doesn’t mean mild or infrequent disease either, both experts caution—”endemic means that it is with us to stay,” Halloran said—and many of the world’s biggest killers like malaria, tuberculosis and HIV are endemic.

What We Don’t Know

What endemic Covid would mean for our everyday lives. This would depend on “what level the endemicity arrives at,” Swartzberg said, meaning how common the disease will be. If Covid were to be endemic at a very high level, “we will be limited in our options,” he explained, and may have to keep on using social restrictions and non-pharmaceutical interventions like masks.

At a very low level, “life will return toward the pre-pandemic state.” We have some control over the level of endemicity through vaccination, Swartzberg said, which would also reduce the chance of a new variant emerging.

Key Background

Calls to just live with the coronavirus have been prevalent since the pandemic began and many—including a not-insignificant number of politicians at the highest levels of office like former President Donald Trump and Brazil’s Jair Bolsonaro—controversially compared it to seasonal flu to illustrate the point.

Though symptoms between the two diseases are similar, the comparison misleadingly downplayed the severity of the coronavirus and showed ignorance of the death toll influenza exacts every year (up to 650,000 people worldwide).

Calls to treat Covid-19 as a more predictable and regular illness grew in popularity as restrictions continued into a second year of the pandemic and vaccines were rolled out and gained new momentum with the rapid spread of the delta and then the omicron variant. Though the latter variant caused higher rates of infection—which reached record levels in many countries—there were relatively low levels of hospitalization and deaths compared to previous waves.

In addition to parts of Europe, leaders in many states are renewing the push to return to normal, with a number of governors feeling it’s time to treat Covid as endemic.

Chief Critic

Tedros Adhanom Ghebreyesus, the leader of the World Health Organization, warned last week against countries lifting restrictions and claiming victory over the virus prematurely. “This virus is dangerous, and it continues to evolve before our very eyes,” he said. Continued restrictions are vital to stop transmission of the virus, he added, in response to countries relaxing measures.

What To Watch For

“Stealth” omicron BA.2. A close relative of the omicron variant—known as BA.2 and called “stealth omicron” by some scientists—is more infectious than the original omicron variant and is rapidly overtaking it in some parts of the world. It does not appear to cause more serious disease, as with the original variant, though experts warn it could lead to more hospitalizations and deaths with more people getting infected.

Follow me on Twitter. Send me a secure tip.

I am a London-based reporter for Forbes covering breaking news. Previously, I have worked as a reporter for a specialist legal publication covering big data and as a freelance journalist and policy analyst covering science, tech and health. I have a master’s degree in Biological Natural Sciences and a master’s degree in the History and Philosophy of Science from the University of Cambridge. Follow me on Twitter @theroberthart or email me at rhart@forbes.com 

Source: Pandemic Endgame: What ‘Endemic’ Covid Means—And When We May Get There



Europe is entering the “plausible endgame” of the coronavirus pandemic, a director of the World Health Organization has said. Dr Hans Kluge, WHO regional director for Europe, said the region had recorded 12 million new COVID-19 cases in the last week, with 30% of all cases since the pandemic began being reported this year.

But he said “for now, the number of deaths across the region is starting to plateau”. He said there is an “opportunity to take control of transmission” because many are immune to Omicron through either natural infection or vaccination.

Dr Kluge said there is a “favourable seasonal pause as we move out of winter”, while the “lower severity of the Omicron variant” is also helping. “This context, that we have not experienced so far in this pandemic, leaves us with the possibility for a long period of tranquillity and a much higher level of population defence against any resurge in transmission, even with a more virulent variant,” he said.

“This period of higher protection should be seen as a ceasefire that could bring us enduring peace.”

More contents:

Don’t Treat Covid Like Flu, WHO Says, As Nations Ditch Restrictions And Live With Virus (Forbes)

COVID-19: endemic doesn’t mean harmless (Nature)

We’re Thinking About Endemicity All Wrong (Atlantic)

Pfizer sees revenues double to $81bn thanks to COVID-19 vaccine

COVID-19: Hundreds of thousands probably died due to ‘bad behaviour’ from politicians over AstraZeneca vaccine, says Oxford scientist

Sir Keir Starmer in the clear over claim he broke lockdown with office beer

How Humans Could Live Two Years Longer: Cut Air Pollution

You can’t see particles smaller than 2.5 microns. But they kill 3.4 million people a year. Climate change is going to have profound consequences on human health and survival. Most obviously, a hotter world means more heat stroke and other heat-caused deaths.

A recent study on the mortality cost of climate change found that every 4,434 metric tons of carbon dioxide emitted — about the combined lifetime emissions of 3.5 Americans, the study estimates — will cause a heat-related death this century.

But the situation is even worse than that number suggests. Danny Bressler, the environmental economist who authored the paper, notes his estimate leaves out some other potential climate-related deaths, like those from flooding and reduced food supply. He’s just estimating what higher temperatures alone will do, writing that he “does not consider likely mortality co-benefits of stricter climate policies, such as decreases in particulate matter pollution.”

That’s a technical way of putting it. Here’s a simpler way: When we burn fossil fuels, not all the resulting pollution goes up high into the atmosphere. Some of it accumulates in the air that we breathe every day.

And it kills us. A lot of us. The Global Burden of Disease study, a common benchmark for public health work, estimates that 3.4 million people die prematurely every year due to air pollution. More recent research puts the total even higher, at 10 million a year. A recent paper suggested that 90 percent of the world’s population lives in areas with air pollution higher than World Health Organization guidelines (guidelines that the organization itself is toughening).

The particles in question here are invisible to the naked eye — but their effects are anything wood


The public health threat of particulate matter

This problem goes by a lot of different names — “air pollution,” “low air quality,” “PM 2.5 pollution” — but it is directly tied to our climate problem.

Burning fossil fuels, in a car or steel mill or power plant, produces carbon dioxide and methane, but it also produces other pollutants. The term “PM 2.5” refers to particles smaller than 2.5 microns (or 0.0025 millimeters — tinier than a grain of sand) suspended in the air. Sometimes colloquially called “soot,” PM 2.5 usually comes from burning stuff: wood in fireplaces, propane in generators, coal in power plants, and gasoline in cars.

But PM 2.5 pollution doesn’t just emanate from controlled combustion. Fossil fuels also contribute to PM 2.5 emissions indirectly: Global warming is increasing the frequency and severity of wildfires, which subject people to huge quantities of particulate matter. The largest wildfire in California’s history, the Camp Fire of 2018, led PM 2.5 levels in the nearby city of Chico to increase by about 12 times the EPA limit.

This all matters because PM 2.5 emissions are extremely deadly. Because PM 2.5 particles are so small, they can easily reach the lungs and even the bloodstream, and long-term exposure can cause a variety of serious health problems, like lung cancer, emphysema, strokes, heart attacks, and cognitive decline.

And we have very good causal evidence that high levels of exposure to PM 2.5 pollution lead to a decline in overall health and life expectancy. Some of the early convincing evidence came from the US, particularly an influentialSix Cities Study” released in 1993. That study found significant relationships between levels of air pollution and overall mortality, driven by higher rates of lung cancer and other lung diseases and heart disease.

A more recent and methodologically strong set of research has focused on China, specifically its “Huai River policy” instituted in the 1950s. The Chinese Communist government had promised free heating in wintertime as a new state-provided benefit, but lacked the resources to offer the benefit nationally. Instead, it only gave free or heavily subsidized coal for heating to households north of the Huai River. The Huai roughly bisects eastern China; Beijing is several hundred miles to its north, and Shanghai slightly to its south.

That meant communities north of the river were exposed to much more particulate pollution from burning coal than communities to the south. Retrospective work comparing lifespans above and below the Huai River suggested that these emissions were incredibly deadly, directly reducing life expectancy by five and a half years for people north of the river compared to those living south of it.

Air pollution is costing millions of lives — and more

Worldwide pollution isn’t quite as bad as it was north of the Huai, but it’s not great either. The University of Chicago’s Air Quality Life Index, which regularly estimates the human toll of particulate pollution, this fall issued a report estimating that the average person on Earth loses 2.2 years of life expectancy due to particulate pollution, compared to a scenario in which every country followed WHO guidelines.

“Alcohol use reduces life expectancy by 9 months; unsafe water and sanitation, 7 months; HIV/AIDS, 4 months; malaria, 3 months; and conflict and terrorism, just 7 days,” researchers Ken Lee and Michael Greenstone write in the report. “Thus, the impact of particulate pollution on life expectancy is comparable to that of smoking, almost three times that of alcohol and drug use and unsafe water, five times that of HIV/AIDS, and 114 times that of conflict and terrorism.”

By their count, lowering air pollution levels below those specified in WHO guidelines would enable people currently alive to enjoy 17 billion more years on Earth, collectively.

And that’s a relatively conservative figure. Shortly after the report’s release, the World Health Organization set stricter guidelines for particulate pollution. Its prior standard, undergirding the UChicago analysis, was that particulate concentration in the air we breathe should be kept to under 10 micrograms (µg, or a millionth of a gram) per cubic meter of air. The new threshold, developed due to evidence that even lower concentrations can be harmful to human health, is half that: 5 µg/m³.

Cutting global air pollution down to that new, lower threshold would save even more millions of life-years.

And the harms of particulate pollution are not limited to life expectancy. Patrick Collison, the entrepreneur and cofounder of Stripe, has taken a research interest in this topic and has a useful compendium of recent work on air pollution harms. Among the studies he highlights:

  • A very small increase in particulate pollution (specifically an increase in PM 2.5 concentration of 1µg/m³) causes, by one estimate, a 0.8 percent reduction in GDP that year, mostly because air pollution increases absenteeism and reduces productivity.
  • Alzheimer’s diagnoses triple when long-term air pollution exposure is substantially increased (by 10 µg/m³). Parkinson’s and dementia diagnoses increase too.
  • Air pollution reduces cognitive functioning in young people. Applying US air pollution standards to China would substantially raise test scores on both reading and math in the latter country, from the median to the 63rd and 58th percentiles respectively.
  • Chess players, baseball umpires, and stock traders all perform worse at their jobs when exposed to more air pollution. Those jobs are unusually easy to quantify, but it stands to reason that people’s performance at other jobs suffers too.

Even if air pollution doesn’t kill you, it probably impedes your cognitive functioning, makes you poorer, and increases your susceptibility to brutal diseases like Alzheimer’s.

How combating climate change can extend life expectancy

Air pollution is a tough problem, but the good news is that we can help solve it by solving another tough problem. Actions to combat global warming can also dramatically cut air pollution deaths.

In 2018, a team of earth scientists at Duke and Columbia universities modeled what would happen to air pollution deaths if the world actually acted to confront climate change. They considered a scenario where 180 fewer gigatons of CO2 are emitted by 2100. That’s roughly the reductions needed to keep warming to 2ºC or below — the goal of the Paris climate agreement.

If we reduce emissions that much, we would prevent about 110 million to 196 million premature deaths by 2100. Averaged over the 80-year period the paper considers, that’s 1.4 million to 2.5 million deaths per year averted. (The improvements would need time to take effect, so more lives would be saved later in the century than in the next 10 years or so.)

The good news is that governments have regulatory levers for reducing air pollution deaths — and some are pulling them. The UChicago Air Quality Life Index report estimates that since 2013, China has reduced air pollution by 29 percent, for an average lifespan extension of 1.5 years for each of its citizens (assuming there’s no backsliding on pollution).

The passage of a stronger version of the Clean Air Act in the US, similarly, was followed by a 50 percent reduction in particulate pollution between 1970 and 1979, aided by a slow economy. Economists Kenneth Chay and Michael Greenstone have estimated that the Clean Air Act caused an immediate and sharp decline in infant mortality in the US.

By their figures, some 1,300 fewer infants died in 1972 than would have if the Clean Air Act amendments of 1970 hadn’t passed. What’s more, research from economists Adam Isen, Maya Rossin-Slater, and W. Reed Walker suggests that the Clean Air Act amendments led children to have higher earnings as adults than they would have had if they’d been exposed to prior levels of pollution.

There are also things you can do at an individual level to mitigate your air pollution intake. My colleague Rebecca Leber wrote about a tool that lets you investigate air quality where you live, and you can help prevent emissions from harming yourself or your loved ones with an electric air purifier (I have two running in my apartment).

But air pollution is not an individual problem, any more than climate change is. The long-term solutions involve setting much stricter regulations or higher taxes targeting particulate emissions, and replacing common sources like coal plants with solar, nuclear, or wind power.

The Biden administration is moving in the right direction. The Environmental Protection Agency, under Biden’s appointee Michael Regan, is reviewing its air quality standards, last reevaluated in 2012, in response to “the strong body of scientific evidence [which] shows that long- and short-term exposures to fine particles (PM2.5) can harm people’s health, leading to heart attacks, asthma attacks, and premature death.” A scientific panel at the EPA has signaled support for lowering the amount of PM 2.5 allowed in the air by as much as a third.

But this is also a global problem that hits the developing world even harder. Spreading green tech to emerging economies like India and Brazil is not just a climate necessity. It’s a public health necessity too.

Dylan Matthews

Source: How humans could live two years longer: Cut air pollution – Vox


More contents:

Researchers Warn of Heightened Risk of HIV With Certain COVID-19 Vaccines

As the race to approval of a safe and effective vaccine for coronavirus disease 2019 (COVID-19) continues, a group of researchers is warning some of these vaccines could make patients more susceptible to contracting HIV.

Writing in The Lancet, the researchers are urging caution when it comes to the use of adenovirus type-5 (Ad5) vectored vaccines for COVID-19, recalling their research from a decade ago on an Ad5 vectored vaccine in 2 HIV vaccine trials.

“On the basis of these findings, we are concerned that use of an Ad5 vector for immunisation against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) could similarly increase the risk of HIV-1 acquisition among men who receive the vaccine,” wrote the researchers. “Both the HIV and COVID-19 pandemics disproportionately affect vulnerable populations globally. Roll-out of an effective SARS-CoV-2 vaccine globally could be given to populations at risk of HIV infection, which could potentially increase their risk of HIV-1 acquisition.”

There are several clinical trials assessing Ad5 vectored vaccine candidates underway, including by China’s CanSino Biologics and California-based ImmunityBio.

The group’s ”cautionary tale” stems from the Step and Phambili phase 2b trials that studied the efficacy of an Ad5 vectored HIV-1 vaccine in preventing HIV infection. Across both international studies, they found that the vaccine actually increased the risk of HIV among the vaccinated men.

The findings from the Phambili study, in particular, have important implications for the use of the vaccines in COVID-19, according to the researchers, as findings from this study showed that heterosexual men receiving the Ad5 vectored vaccine faced a consistently increased risk of HIV infection. Notably, this increased risk appeared to be limited to men, with women not having an observed increase of infection in the study.

In the Step trial, the risk of acquiring HIV was particularly high among men who were uncircumcised and Ad5 seropositive men who reported having unprotected anal sex with a partner who was HIV seropositive or who had unknown serostatus as baseline.

Of note, the vaccine in both studies did not have the HIV envelope. Meanwhile, in another study that used a DNA prime and an Ad5 vector, both of which had the HIV envelope, there was no observed increase in HIV infection.

The reason for the observed increase in HIV risk remains uncertain, although several follow-up studies have suggested a potential explanation, according to the researchers.

“The vaccine was highly immunogenic in the induction of HIV-specific CD4 and CD8 T cells; however, there was no difference in the frequency of T-cell responses after vaccination in men who did and did not later become infected with HIV in the Step Study,” they wrote. “These findings suggest that immune responses induced by the HIV-specific vaccine were not the mechanism of increased acquisition.

Participants with high frequencies of preimmunisation Ad5-specific T cells were associated with a decreased magnitude of HIV-specific CD4 responses and recipients of the vaccine had a decreased breadth of HIV-specific CD8 responses, suggesting that pre-existing Ad5 immunity might dampen desired vaccine-induced responses.”

Other exploratory studies have indicated that the vaccine enhances HIV replication in CD4 T cells or that Ad5-specific CD4 T cells could be more susceptible to HIV infection.

Jaime Rosenberg


Buchbinder SP, McElrath MJ, Dieffenback C, Corey L. Use of adenovirus type-5 vectored vaccines: a cautionary tale. Lancet. Published online October 19, 2020.doi:10.1016/S0140-6736(20)32156-5

Source: http://ajmc.com




A new paper warns the link between COVID-19 vaccines and HIV risk.

Mayo Clinic

Nearly half of people in the U.S. diagnosed with HIV, the virus that causes AIDS, are over 50, according to the Centers for Disease Control and Prevention (CDC). HIV damages the body’s immune system, and interferes with the body’s ability to fight infection and disease. Does that make it more difficult to fight off COVID-19? Dr. Stacey Rizza, an infectious diseases specialist at Mayo Clinic, says, “We know that anybody who has a suppressed immune system may have an altered response to the virus that causes COVID-19. We know that older people whose immune systems are a little weaker, and people who have medical issues or organ diseases, are going to generally do worse with the infection.

If somebody has HIV and their immune system is weaker, meaning they’re not on therapy, or they’re earlier on in their therapy and their CD4 count is still low, they may be at risk of having a worse reaction to the virus. We will learn more about SARS-CoV-2 on people living with HIV over time.” Read more: https://newsnetwork.mayoclinic.org/di… More health and medical news on the Mayo Clinic News Network. https://newsnetwork.mayoclinic.org/ Journalists: Clean and nat sound versions of this pkg available for download at https://newsnetwork.mayoclinic.org/ Register (free) at https://newsnetwork.mayoclinic.org/re…

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