Why COVID-19 kills some people and spares others. Here’s what scientists are finding.

COVID-19 seems to hit some people harder than others, with some people experiencing only mild symptoms and others being hospitalized and requiring ventilation. Though scientists at first thought age was the dominant factor, with young people avoiding the worst outcomes, new research has revealed a suite of features impacting disease severity. These influences could explain why some perfectly healthy 20-year-old with the disease is in dire straits, while an older 70-year-old dodges the need for critical interventions.

These risk factors include:
Age
Diabetes (type 1 and type 2)
Heart disease and hypertension
Smoking
Blood type
Obesity
Genetic factors

Age

About 8 out of 10 deaths associated with COVID-19 in the U.S. have occurred in adults ages 65 and older, according to the U.S. Centers for Disease Control and Prevention (CDC). The risk of dying from the infection, and the likelihood of requiring hospitalization or intensive medical care, increases significantly with age. For instance, adults ages 65-84 make up an estimated 4-11% of COVID-19 deaths in the U.S, while adults ages 85 and above make up 10-27%. 

The trend may be due, in part, to the fact that many elderly people have chronic medical conditions, such as heart disease and diabetes, that can exacerbate the symptoms of COVID-19, according to the CDC. The ability of the immune system to fight off pathogens also declines with age, leaving elderly people vulnerable to severe viral infections, Stat News reported.RECOMMENDED VIDEOS FOR YOU…CLOSEVolume 0%PLAY SOUND

Related: Coronavirus in the US: Latest COVID-19 news and case counts

Diabetes

Diabetes mellitus — a group of diseases that result in harmful high blood sugar levels — also seems to be linked to risk of more severe COVID-19 infections. 

The most common form in the U.S. is type 2 diabetes, which occurs when the body’s cells don’t respond to the hormone insulin. As a result, the sugar that would otherwise move from the bloodstream into cells to be used as energy just builds up in the bloodstream. (When the pancreas makes little to no insulin in the first place, the condition is called type 1 diabetes.)

In a review of 13 relevant studies, scientists found that people with diabetes were nearly 3.7 times more likely to have a critical case of COVID-19 or to die from the disease compared with COVID-19 patients without any underlying health conditions (including diabetes, hypertension, heart disease or respiratory disease), they reported online April 23 in the Journal of Infection.

Even so, scientists don’t know whether diabetes is directly increasing severity or whether other health conditions that seem to tag along with diabetes, including cardiovascular and kidney conditions, are to blame. 

That fits with what researchers have seen with other infections and diabetes. For instance, flu and pneumonia are more common and more serious in older individuals with type 2 diabetes, scientists reported online April 9 in the journal Diabetes Research and Clinical Practice. In a literature search of relevant studies looking at the link between COVID-19 and diabetes, the authors of that paper found a few possible mechanisms to explain why a person with diabetes might fare worse when infected with COVID-19. These mechanisms include: “Chronic inflammation, increased coagulation activity, immune response impairment and potential direct pancreatic damage by SARS-CoV-2.”

Related: 13 coronavirus myths busted by science

Mounting research has shown the progression of type 2 diabetes is tied to changes in the body’s immune system. This link could also play a role in poorer outcomes in a person with diabetes exposed to SARS-CoV-2, the virus that causes COVID-19. 

No research has looked at this particular virus and immune response in patients with diabetes; however, in a study published in 2018 in the Journal of Diabetes Research, scientists found through a review of past research that patients with obesity or diabetes showed immune systems that were out of whack, with an impairment of white blood cells called Natural Killer (NK) cells and B cells, both of which help the body fight off infections. The research also showed that these patients had an increase in the production of inflammatory molecules called cytokines. When the immune system secretes too many cytokines,a so-called “cytokine storm” can erupt and damage the body’s organs. Some research has suggested that cytokine storms may be responsible for causing serious complications in people with COVID-19, Live Science previously reported. Overall, type 2 diabetes has been linked with impairment of the very system in the body that helps to fight off infections like COVID-19 and could explain why a person with diabetes is at high risk for a severe infection.

Not all people with type 2 diabetes are at the same risk, though: A study published May 1 in the journal Cell Metabolism found that people with diabetes who keep their blood sugar levels in a tighter range were much less likely to have a severe disease course than those with more fluctuations in their blood sugar levels. 

Scientists aren’t sure whether this elevated risk of a severe COVID-19 infection also applies to people with type 1 diabetes (T1D). A study coordinated by T1D Exchange — a nonprofit research organization focused on therapies for those with type 1 diabetes — launched in April to study the outcomes of T1D patients infected with COVID-19. When a person with T1D gets an infection, their blood sugar levels tend to spike to dangerous levels and they can have a buildup of acid in the blood, something called diabetic ketoacidosis. As such, any infection can be dangerous for someone with type 1 diabetes.

Heart disease and hypertension

People with conditions that affect the cardiovascular system, such as heart disease and hypertension, generally suffer worse complications from COVID-19 than those with no preexisting conditions, according to the American Heart Association. That said, historically healthy people can also suffer heart damage from the viral infection. 

The first reported coronavirus death in the U.S., for instance, occurred when the virus somehow damaged a woman’s heart muscle, eventually causing it to burst, Live Science reported. The 57-year-old maintained good health and exercised regularly before becoming infected, and she reportedly had a healthy heart of “normal size and weight.” A study of COVID-19 patients in Wuhan, China, found that more than 1 in 5 patients developed heart damage — some of the sampled patients had existing heart conditions, and some did not. 

In seeing these patterns emerge, scientists developed several theories as to why COVID-19 might hurt both damaged hearts and healthy ones, according to a Live Science report

In one scenario, by attacking the lungs directly, the virus might deplete the body’s supply of oxygen to the point that the heart must work harder to pump oxygenated blood through the body. The virus might also attack the heart directly, as cardiac tissue contains angiotensin-converting enzyme 2 (ACE2) — a molecule that the virus plugs into to infect cells. In some individuals, COVID-19 can also kickstart an overblown immune response known as a cytokine storm, wherein the body becomes severely inflamed and the heart could suffer damage as a result.

Smoking

People who smoke cigarettes may be prone to severe COVID-19 infections, meaning they face a heightened risk of developing pneumonia, suffering organ damage and requiring breathing support. A study of more than 1,000 patients in China, published in the New England Journal of Medicine, illustrates this trend: 12.3% of current smokers included in the study were admitted to an ICU, were placed on a ventilator or died, as compared with 4.7% of nonsmokers. 

Cigarette smoke might render the body vulnerable to the coronavirus in several ways, according to a recent Live Science report. At baseline, smokers may be vulnerable to catching viral infections because smoke exposure dampens the immune system over time, damages tissues of the respiratory tract and triggers chronic inflammation. Smoking is also associated with a multitude of medical conditions, such as emphysema and atherosclerosis, which could exacerbate the symptoms of COVID-19.

A recent study, posted March 31 to the preprint database bioRxiv, proposed a more speculative explanation as to why COVID-19 hits smokers harder. The preliminary research has not yet been peer-reviewed, but early interpretations of the data suggest that smoke exposure increases the number of ACE2 receptors in the lungs — the receptor that SARS-CoV-2 plugs into to infect cells. 

Many of the receptors appear on so-called goblet and club cells, which secrete a mucus-like fluid to protect respiratory tissues from pathogens, debris and toxins. It’s well-established that these cells grow in number the longer a person smokes, but scientists don’t know whether the subsequent boost in ACE2 receptors directly translates to worse COVID-19 symptoms. What’s more, it’s unknown whether high ACE2 levels are relatively unique to smokers, or common among people with chronic lung conditions.

Obesity

Several early studies have suggested a link between obesity and more severe COVID-19 disease in people. One study, which analyzed a group of COVID-19 patients who were younger than the age of 60 in New York City, found that those who were obese were twice as likely as non-obese individuals to be hospitalized and were 1.8 times as likely to be admitted into critical care. 

“This has important and practical implications” in a country like the U.S. where nearly 40% of adults are obese, the authors wrote in the study, which was accepted into the journal Clinical Infectious Diseases but not yet peer-reviewed or published. Similarly, another preliminary study that hasn’t yet been peer-reviewed found that the two biggest risk factors for being hospitalized from the coronavirus are age and obesity. This study, published in medRxiv looked at data from thousands of COVID-19 patients in New York City, but studies from other cities around the world found similar results, as reported by The New York Times.

A preliminary study from Shenzhen, China, which also hasn’t been peer-reviewed, found that obese COVID-19 patients were more than twice as likely to develop severe pneumonia as compared with patients who were normal weight, according to the report published as a preprint online in the journal The Lancet Infectious Diseases. Those who were overweight, but not obese, had an 86% higher risk of developing severe pneumonia than did people of “normal” weight, the authors reported. Another study, accepted into the journal Obesity and peer-reviewed, found that nearly half of 124 COVID-19 patients admitted to an intensive care unit in Lille, France, were obese.

It’s not clear why obesity is linked to more hospitalizations and more severe COVID-19 disease, but there are several possibilities, the authors wrote in the study. Obesity is generally thought of as a risk factor for severe infection. For example, those who are obese had longer and more severe disease during the swine flu epidemic, the authors wrote. Obese patients might also have reduced lung capacity or increased inflammation in the body. A greater number of inflammatory molecules circulating in the body might cause harmful immune responses and lead to severe disease.

Blood type

Blood type seems to be a predictor of how susceptible a person is to contracting SARS-CoV-2, though scientists haven’t found a link between blood type per se and severity of disease.

Jiao Zhao, of The Southern University of Science and Technology, Shenzhen, and colleagues looked at blood types of 2,173 patients with COVID-19 in three hospitals in Wuhan, China, as well as blood types of more than 23,000 non-COVID-19 individuals in Wuhan and Shenzhen. They found that individuals with blood types in the A group (A-positive, A-negative and AB-positive, AB-negative) were at a higher risk of contracting the disease compared with non-A-group types. People with O blood types (O-negative and O-positive) had a lower risk of getting the infection compared with non-O blood types, the scientists wrote in the preprint database medRxiv on March 27; the study has yet to be reviewed by peers in the field.

In a more recent study of blood type and COVID-19, published online April 11 to medRxiv, scientists looked at 1,559 people tested for SARS-CoV-2 at New York Presbyterian hospital; of those, 682 tested positive. Individuals with A blood types (A-positive and A-negative) were 33% more likely to test positive than other blood types and both O-negative and O-positive blood types were less likely to test positive than other blood groups. (There’s a 95% chance that the increase in risk ranges from 7% to 67% more likely.) Though only 68 individuals with an AB blood type were included, the results showed this group was also less likely than others to test positive for COVID-19. 

The researchers considered associations between blood type and risk factors for COVID-19, including age, sex, whether a person was overweight, other underlying health conditions such as diabetes mellitus, hypertension, pulmonary diseases and cardiovascular diseases. Some of these factors are linked to blood type, they found, with a link between diabetes and B and A-negative blood types, between overweight status and O-positive blood groups, for instance, among others. When they accounted for these links, the researchers still found an association between blood type and COVID-19 susceptibility. When the researchers pooled their data with the research by Zhao and colleagues out of China, they found similar results as well as a significant drop in positive COVID-19 cases among blood type B individuals.

Why blood type might increase or decrease a person’s risk of getting SARS-CoV-2 is not known. A person’s blood type indicates what kind of certain antigens cover the surfaces of their blood cells; These antigens produce certain antibodies to help fight off a pathogen. Past research has suggested that at least in the SARS coronavirus (SARS-CoV), anti-A antibodies helped to inhibit the virus; that could be the same mechanism with SARS-CoV-2, helping blood group O individuals to keep out the virus, according to Zhao’s team.

Genetic factors

Many medical conditions can worsen the symptoms of COVID-19, but why do historically healthy people sometimes fall dangerously ill or die from the virus? Scientists suspect that certain genetic factors may leave some people especially susceptible to the disease, and many research groups aim to pinpoint exactly where those vulnerabilities lie in our genetic code. 

In one scenario, the genes that instruct cells to build ACE2 receptors may differ between people who contract severe infections and those who hardly develop any symptoms at all, Science magazine reported. Alternatively, differences may lie in genes that help rally the immune system against invasive pathogens, according to a recent Live Science report.

For instance, a study published April 17 in the Journal of Virology suggests that specific combinations of human leukocyte antigen (HLA) genes, which train immune cells to recognize germs, may be protective against SARS-CoV-2, while other combinations leave the body open to attack. HLAs represent just one cog in our immune system machinery, though, so their relative influence over COVID-19 infection remains unclear. Additionally, the Journal of Virology study only used computer models to simulate HLA activity against the coronavirus; clinical and genetic data from COVID-19 patients would be needed to flesh out the role of HLAs in real-life immune responses.

Originally published on Live Science.  

https://www.livescience.com/why-covid-19-coronavirus-deadly-for-some-people.html

Golden State Lockdown: Bay Area Extends Its Shelter-In-Place Order

On Wednesday, Bay Area health officials extended shelter-in-place orders through May, bringing their duration to 11 weeks. The new orders very minimally loosen restrictions to allow construction and some outdoor shops and activities, but most businesses remain closed. The announcement comes as California’s Covid-19 situation is looking better, in terms of infections, while the economic, social, and even health repercussions of its stay-at-home orders mounts. A rational cost-benefit analysis of the public-health response should encourage California and the Bay Area to begin a phased reopening.

The health situation in the Bay Area, and California as a whole, appears far from dire. Data on new Covid-19 cases show a clear flattening of the curve. The number of patients hospitalized for Covid-19 in the Bay Area has dropped almost every day for a week. According to the website rt.live, the effective reproduction number (known as Rt or Re) in California, and in almost every other state, is below 1, indicating a decline in infections. The seven-day average for new infections in the Bay Area is the lowest in a month. California’s 16 northernmost counties, with a population of more than 1 million, have seen only 181 confirmed cases — a lower known infection rate than South Korea’s.

Meantime, some 26 million people have filed for unemployment nationally over the past month, including 3.2 million in California, a crushing tide of layoffs that dwarfs prior job-loss records. Almost one-third of Americans did not pay their rent this month. Businesses everywhere are struggling, with small businesses faring the worst and museums and nonprofits in jeopardy, too. Transit agencies face enormous financial losses because of lost riders. Federal Reserve chairman Jerome Powell has said that the economy is deteriorating “with alarming speed.” In a tragic irony, hospitals that worried about an overflow of Covid-19 patients are now laying off workers due to cancellation of elective surgeries and also, perhaps, sick people avoiding treatment for fear of infection. Lines at food banks are staggering. People talk openly not just of recession but depression.

Luckily, recovery should be easier than from a typical recession, since this one is a forced abnormality. Millions of people could have their jobs back tomorrow if shelter-in-place orders were eased — and as the impact of the virus wanes, it makes sense to begin lifting them, as European nations such as Norway and Austria are doing, and as Texas has begun to do. Even New York, far harder hit than California, has tentatively scheduled an end to its statewide “pause” on May 15.

Yet California shows no inclination to ease up. The statewide order has no end date. Governor Gavin Newsom refuses to set one, saying only that the end is “weeks away.” Newsom has outlined criteria to lift the order, but some of his requirements—such as sufficient hospital capacity and progress toward a treatment—are unnecessary or unrealistic. The state’s 5,000 Covid-19 hospitalizations represent a small fraction of its approximately 75,000 staffed beds. A vaccine could be more than a year away and like the swine flu virus, Covid-19 may never even get a silver-bullet cure. Neither the Bay Area nor California have put together a clear plan for reopening.

Newsom is not the only one taking a hard line. Governor Phil Murphy of New Jersey has stated that there “is no cost that is too high to save any one precious life.” Some infectious-disease specialists argue that restrictions should remain in place until the infection rate is nearly zero. These are impossible standards to meet, and not applied to any other danger or disease. Governor Murphy has never ordered streets and highways closed despite more than one life lost each day in New Jersey car crashes. According to the CDC, swine flu has continued to kill about 7,500 Americans each year since the outbreak in 2009. We must accept that Covid-19 will probably never go away entirely.

For some observers, the idea of quantifying human life in economic terms sounds heartless. Yet we perform such cost-benefit analyses all the time, both as individuals—when we choose between riding a motorcycle or a station wagon—and as societies—when we choose whether to put more money into cancer research or into studies of rarer diseases. Every developed nation maintains value of statistical life (VSL) measures, for use in planning, transportation, and health policies.

There are social as well as economic costs. The effects of job losses and recession fall hardest on the poor and working class. People living paycheck-to-paycheck, or without savings, are suffering most. As the economy sinks, it takes with it the livelihoods and aspirations of tens of millions of Californians. It is reasonable to argue that we cannot destroy the economy trying to stop every possible Covid-19 death. When people can’t eat, that’s a health problem, too.

There are even direct health reasons to reopen. After six weeks of shelter-in-place, cracks are appearing in California. San Francisco police broke up an illegal nightclub, surely not the only infraction. More people are circulating outside, and the size of the groups suggests that it’s no longer just roommates walking together. People are more likely to take risks the longer their confinement lasts. Far better to begin a gradual reopening, with a highly publicized campaign to encourage mitigation measures, such as wearing masks.

Another public health reason to begin to lift restrictions is that if stay-at-home orders ruin the lives of millions, they will be much harder to implement in the future. A future disease could be worse than Covid-19—the fatality rate of SARS, in 2003, was 11 percent—but resentment over a “Covid recession” might make it much harder to get people to cooperate next time.

California led the nation in shutting down, but the state is lagging the country, and the world, in opening back up. New Zealand planned its successful lockdown on the scientific basis of two incubation cycles, or 28 days. The sequence lasted slightly longer, but after 33 days, the country began a phased reopening this week. Operating on the same parameters, California could have started lifting restrictions last week. Instead of waiting four more weeks, it should start a phased reopening now.

The stay-at-home orders have been very successful and given California a relatively low infection rate despite one of the earliest exposures. Most people have complied, and local officials should trust them to behave responsibly as restrictions lift, rather than trying to micromanage their activity. And all phases of reopening would include continuing effective mitigation measures—washing hands, wearing masks, social distancing, self-isolation of at-risk people, and tracking and quarantining of those testing positive for Covid-19.

Each region of the United States has experienced the pandemic differently; a phased reopening would work differently in each place. The current approach—where largely healthy Northern California lives under the same restrictions as harder-hit Los Angeles—is not tenable. It’s time to begin the gradual lifting of shelter-in-place orders before these orders do more damage than the illness they were issued to fight.

Phillip Sprincin is a veteran of the United States Marine Corps who lives in the San Francisco Bay Area.

This article was originally published by City Journal Online.

Any COVID Response Excluding Herd Immunity Doomed For Failure

A cursory study of diseases shows that defeating COVID-19 through social distancing, mass testing, and a hoped-for vaccination is impractical, and has no expiration date.

There is no practical “exit strategy” to Democrats’ shut-down measures

Any health care response that excludes exposure to and surviving COVID-19 – the same way hundreds of thousands, if not millions of Americans, contract and recover from influenza each year – is incomplete. If this is a “war against an invisible enemy,” as President Trump declares, then young, healthy people need to “serve” in this national crusade by contracting and recovering from COVID-19 to build “herd immunity,” for their own future safety and to weaken COVID-19’s deadly impact when it assuredly returns some day. “Herd immunity” simply describes strengthening one’s own, personal immune system, which naturally fights diseases such as COVID-19, while also benefiting society as a whole.

President Trump needs to fire germophobes Drs. Anthony Fauci and Deborah Birx and get a “second opinion” by hiring new health care advisers who recognize this reality.

So far, the argument against the extreme social distancing mandates required by the nation’s almost overwhelmingly Democratic governors has been that the economic and societal catastrophe created will be far worse than the impact of COVID-19 to the population. But now more than six weeks into this nightmare of restricted liberties and quarantine edicts, the country ought to open for business as soon as possible for health reasons, too.

Social distancing and all the other precautions to avoiding contracting COVID-19 have merit, but can’t alone succeed even if Democratic governors would rule by executive order indefinitely. This is where the dishonesty begins: There is no practical “exit strategy” to Democrats’ shut-down measures.

Despite vaccinations, flu kills 30,000 to 60,000 Americans each year

Even if a vaccination were discovered tomorrow to combat coronavirus, it’s unlikely that it would eradicate COVID-19 forever based on what we already know about other viruses, such as the flu, which is that they mutate and continue to kill even with vaccinations.

Despite vaccinations, flu kills 30,000 to 60,000 Americans each year and we do not shut the economy for the flu. What we do is vaccinate vulnerable elderly people and children and hope for the best. And when one considers that it took decades of research and testing to find cures for viral diseases such as polio, measles and chicken pox, we don’t have that time to wait, while our country falls apart and people’s businesses and lives are ruined.

Both COVID-19 and influenza cause lower respiratory illness that leads to death, sometimes from pneumonia. Others who die from COVID-19 had heart disease or diabetes. The point is that it’s not so simple to determine a cause of death.

Closing elementary schools and colleges in the United States to combat COVID-19 was a big mistake. Young people are the least likely to die from COVID 19, and would have greatly contributed to developing “herd immunity.” This alone cannot solve the problem of COVID-19 transmission, but would greatly contribute to reducing the number of “hosts” in which the virus could “live.”

Viruses can’t survive without a host, and the more people possessing coronavirus antibodies, the sooner COVID-19 will “die”

The death data so far show that the overwhelming number of the people “killed” by COVID-19 had compromised immune systems or were older and sick, and that nearly no children have died. Once children and young adults survive COVID-19, they likely will have the antibodies to protect them in the future when COVID-19 or another coronavirus returns.

Viruses can’t survive without a host, and the more people possessing coronavirus antibodies, the sooner COVID-19 will “die,” even though it’s not technically “alive” from a scientific perspective.

Everything in this article was gleaned from well-known, mainstream disease-combating websites, such as from the federal government’s Centers for Disease Control and Prevention. The “I’m no doctor” line comes from a comedian Brian Regan skit about visiting a hospital and being asked stupid questions by the staff about why he was there.

We were told at the beginning that social distancing was to “flatten the curve” so as not to overwhelm the health care system with COVID-19 cases. However, that has morphed into we cannot open the economy until we have testing and a vaccine, which frankly will never be adequate to the Democrats who want to defeat President Trump this November, hence the politics of this “crisis.”

The media tells us that COVID-19 is “really bad,” and “much worse than the flu.” It may be worse, but they are Fake News and a mouthpiece of the Democratic National Committee. It is a partisan press, the same way that it was at the beginning of the country, and no American ought to take the Washington Post, or the New York Times, or CNN seriously on any topic.

We are alive, but we are not living

Right now, we don’t have to care whether the number of COVID-19 deaths has been exaggerated or whether the Chinese created it as part of biological warfare. There will be time for that later, but we do have to have a plan that works, which we do not have now.

We cannot ignore the Democrats and Deep State motivation to destroy Donald Trump’s presidency, and their obvious delight that COVID-19 and their draconian response to it presents them with their latest, best opportunity to do so, but which will also fail. In this regard, the Democrats and the Deep State are Wiley E. Coyote to Donald Trump’s Roadrunner.

We are alive, but we are not living. In New York City, people wait in line to enter grocery stores; all the concrete “parks” are closed to street basketball. Even so, yesterday, I saw two Dominican teen boys hop the fence to play.

Everybody has to do their part in this “war” against the pandemic: People have to get the virus and survive it and build herd immunity. Boris Johnson, the prime minister of England, contracted COVID-19 and recovered, everyone else can and ought to as well.

There is more to life than trying to avoid getting sick

Doctors are great; the whole “white lab coat” thing. But there is more to life than trying to avoid getting sick, and that’s what we are doing right now. That’s not sustainable or even desirable.

We need to stop telling people to “stay safe,” but rather “be smart.” We need healthy people, including children, to become infected and recover and develop the antibodies to minimize their future susceptibility of contracting the disease and using those antibodies to discover an effective vaccine. As said before, healthy people who survive will likely experience minimum to less severe symptoms while they become immune to hosting the virus.

We are not South Korea, which has a homogeneous population and culture, and can require a complete lock down of their country to combat COVID-19. In the United States, we have individual liberties. We have to be smart and solve this with American ingenuity. There is no solution in social distancing without opening the economy, protecting the vulnerable, developing herd immunity, while waiting for a vaccine that may or not arrive soon. And even then, people are doing to die, like they have for time immemorial, because that’s the nature of life on Earth. And it is a twisted, dystopian ideology to think that “hunkering down” and hoping for an as-yet-undiscovered vaccine can save all of us. It can’t.

https://canadafreepress.com/article/any-covid-response-excluding-herd-immunity-doomed-for-failure

Australia lab may have found Covid-19 cure Queensland University to launch human trials of two-drug treatment that has apparently cured virus-infected patients

Stanford University School of Medicine reported on Friday that a former  malaria treatment known as chloroquine may have been effective in treating the disease in China and Singapore.

There is also anecdotal evidence that the redundant AIDS drug remdesivir may have worked in treating patients in China, the initial epicenter of the now global pandemic. )

SYDNEY – Australian researchers have been given the green light to start human trials of a promising drug treatment for the novel coronavirus after raising funds from donors in a remarkable global appeal. 

Covid-19 patients will be given two drugs previously used to treat AIDS and malaria at about 50 hospitals in Australia, with tests expected to start by the end of this month. The drugs reportedly eradicated the virus in lab tests.

“There have already been patients treated with these in Australia and there’s been successful outcomes, but it hasn’t been done in a controlled or comparative way,” said David Paterson, director of the Center for Clinical Research at Queensland University, which is leading the trials.

“What we want to do at the moment is a large clinical trial across Australia, looking at 50 hospitals, and what we’re going to compare is one drug versus another drug, versus the combination of the two drugs,” he said.

Stanford University School of Medicine reported on Friday that a former  malaria treatment known as chloroquine may have been effective in treating the disease in China and Singapore.

There is also anecdotal evidence that the redundant AIDS drug remdesivir may have worked in treating patients in China, the initial epicenter of the now global pandemic.

Trial data of the drug’s use, however, has not been made available by China. Scientists have dismissed a widely quoted online report that about 12,000 patients have been completely cured of Covid-19 in China after taking chloroquine.

Paterson said laboratory tests using a combination of the two drugs had indicated that they might provide a “cure” from the virus.

“It’s a potentially effective treatment. Patients would end up with no viable coronavirus in their system at all after the end of therapy,” he said.

The March 18 decision to go ahead with the human tests was only made after the researchers made an extraordinary global appeal for donations to cover the funding cost, estimated at A$750,000 (US$451,415).

There is an urgent push to develop effective Covid-19 treatments because a vaccine for widespread use is not expected to be developed for at least 18 months.

More than 30 academic institutions and pharmaceutical companies are collaborating in the search for a vaccine under a program coordinated by the Oslo-based non-profit group the Coalition for Epidemic Preparedness.

Labs in Australia, the US and the United Kingdom are already testing the first batches of vaccine “candidates” on animals, using some “prototype” pathogen platforms that were developed for severe acute respiratory syndrome (Sars) and Middle East respiratory syndrome (Mers) outbreaks in 2002-04 and 2012.

However, they were ultimately not needed to treat those diseases.

The Seattle-based Kaiser Permanente Washington Research Institute began human trials of a possible vaccine on March 16, and two other research programs, at the University of Queensland and Imperial College London, expect to start trials on patients within weeks.

Three or four potential vaccines will be developed, with the most promising version to be chosen for distribution. 

Research efforts received a boost on March 17 when Melbourne’s Peter Doherty Institute for Infection and Immunity announced it had succeeded in mapping how the body’s immune system fights back against the virus.

Published in the monthly peer-reviewed Nature Medicine journal, the research revealed that victims are recovering from the illness in the same way they would from the flu.

“This [discovery] is important because it is the first time where we are really understanding how our immune system fights novel coronavirus,”  said Katherine Kedzierska, who co-authored the journal article.

The team tracked the recovery of a 47-year-old woman from Wuhan, the original hotspot of the virus in China, who had mild-to-moderate symptoms from the virus and had no pre-existing health issues. She was admitted to a hospital in Australia and fully recovered within two weeks.

Kedzierska said that specific cells identified with influenza patients were spotted in her bloodstream three days before her health began to improve.

“We found in this patient at three days we could see emergence of immune cells in the blood. The immune cell populations we have seen emerging before patients recover are the same cells we see in influenza.

“Based on our experience with patients with influenza, we could predict recovery and that’s exactly what happened in Covid-19,” she said.

“This information will allow us to evaluate any vaccine candidate, as in an ideal world the vaccine should mimic our body’s immune response.”

Researchers are keen to isolate immune responses because these were a key factor in fighting SARS. Having blood markers will enable hospitals to screen out the 20% of patients who present with more severe symptoms.

“Then you could say upfront, this would be a severe case, or this will probably be a milder case,” said Doherty researcher Carolien van de Sandt. “Then you could alter their care to what the patient might need.”

The center has been given additional funding, some contributed by the Chinese billionaire Jack Ma, to expand the immune mapping to a bigger pool of patients, in part to monitor later phases of the recovery process.

“We know we can generate immune responses to the virus,” Kedzierska said. “The next question is whether that immune response gives people immunity for weeks or months or years so we are protected.”

The study’s findings are being shared with other research laboratories, she said.