Don't put your hopes on a vaccine it might never arrive

[Hypocrite-The]

Coronavirus has put a spotlight on a difficult medical question: Why do so few drugs kill viruses? - ABC News
The Conversation
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By Christine Carson and Rachel Rope
Posted 10h

Remdesivir is one antiviral researchers are investigating to treat COVID-19, but it has shown mixed results in clinical trials.(Reuters: Ulrich Perrey)
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As the end of the World War II neared, mass production of the newly developed antibiotic penicillin enabled life-saving treatment of bacterial infections in wounded soldiers.
Since then, penicillin and many other antibiotics have successfully treated a wide variety of bacterial infections.
But antibiotics don't work against viruses; antivirals do. Since the outbreak of the coronavirus pandemic, researchers and drug companies have struggled to find an antiviral that can treat SARS-CoV-2, the virus that causes COVID-19.
Why are there so few antivirals? The answer boils down to biology, and specifically the fact viruses use our own cells to multiply. This makes it hard to kill viruses without killing our own cells in the process.
Exploit our differences with bacteria
The differences between bacterial and human cells are what make antibiotics possible.
Bacteria are self-contained life forms that can live independently without a host organism. They are similar to our cells, but also have many features not found in humans.
For example, penicillin is effective because it interferes with the construction of the bacterial cell wall. Cell walls are made of a polymer called peptidoglycan. Human cells don't have a cell wall or any peptidoglycan.
So antibiotics that prevent bacteria from making peptidoglycan can inhibit bacteria without harming the human taking the medicine. This principle is known as selective toxicity.
Viruses use our own cells to replicate
Unlike bacteria, viruses cannot replicate independently outside a host cell. There is a debate over whether they are really living organisms at all.
To replicate, viruses enter a host cell and hijack its machinery. Once inside, some viruses lie dormant, some replicate slowly and leak from cells over a prolonged period, and others make so many copies that the host cell bursts and dies.
The newly replicated virus particles then disperse and infect new host cells.
An antiviral treatment that intervenes in the viral "life" cycle during these events could be successful. The problem is that if it targets a replication process that is also important to the host cell, it is likely to be toxic to the human host as well.
Killing viruses is easy. Keeping host cells alive while you do it is the hard part.
Successful antivirals target and disrupt a process or structure unique to the virus, thereby preventing viral replication while minimising harm to the patient. The more dependent the virus is on the host cell, the fewer targets there are to hit with an antiviral. Unfortunately, most viruses offer few points of unique difference that can be targeted.
Another complication is that different viruses vary from each other much more than different bacteria do. Bacteria all have double-stranded DNA genomes and replicate independently by growing larger and then splitting into two, similar to human cells.
But there is extreme diversity between different viruses. Some have DNA genomes while others have RNA genomes, and some are single-stranded while others are double-stranded. This makes it practically impossible to create a broad spectrum antiviral drug that will work across different virus types.
Antiviral success stories
Nevertheless, points of difference between humans and viruses do exist, and their exploitation has led to some success. One example is influenza A, which is one form of the flu.
Influenza A tricks human cells so it can enter them. Once inside our cells, the virus needs to "undress", removing its outer coat to release its RNA into the cell.

Tamiflu is one antiviral drug that is successful in slowing the spread of influenza in humans. So far we don’t have an antiviral that works effectively in COVID-19 patients.(Hannah Johnston, File Photo: Getty Images)
A viral protein called matrix-2 protein is key to this process, facilitating a series of events that releases the viral RNA from the virus particle. Once the viral RNA is released inside the host cell, it is transported to the cell nucleus to start viral replication.
But if a drug jams the matrix-2 protein, the viral RNA can't exit the virus particle to get to the cell nucleus, where it needs to be to replicate. So, the infection stalls. Amantadine and rimantadine were early antiviral successes targeting the matrix-2 protein.
Zanamivir (Relenza) and oseltamivir (Tamiflu) are newer drugs that have also had success in treating patients infected with influenza A or B.
They work by blocking a key viral enzyme, obstructing virus release from the cell, slowing the spread of infection within the body, and minimising the damage the infection causes.
We need to find what makes SARS-CoV-2 unique
A COVID-19 vaccine may be difficult to create. So testing antivirals to find one that can effectively treat COVID-19 remains an important goal.
Much depends on knowing the intricacies of the SARS-CoV-2 virus and its interactions with human cells. If researchers can identify unique elements in how it survives and replicates, we can exploit these points of weakness and make an effective antiviral treatment.
Christine Carson is a senior research fellow in the School of Biomedical Sciences at University of Western Australia and Rachel Rope is Associate Professor of Microbiology and Immunology at East Carolina University. This article originally appeared on The Conversation.

 

[nightsafari]

Everybody is just guessing. The experts are even worse because they have developed complex mathematical models but entering garbage parameters means that the output is an even bigger pile of garbage.

There is probably a shred of truth in each version of the possible outcome but whatever is published the end result is that the pandemic will burn itself out because in the history of mankind no pandemic has wiped out the human race. Genetic diversity ensures that this will not happen.

If a million or so die so what. Our own inventions eg the automobile kill 1.4 million annually but we still worship the car as a status symbol. Nobody considers it to be a killing machine.

This covid-19 headlines will just fade away after a while even if the virus doesn't and life will carry on.

you'd better not move to the country this assinine guy is PM of...

https://globalnews.ca/news/6857058/coronavirus-canada-science-vaccine-funding/

https://www.cbc.ca/news/politics/global-vaccine-pledge-trudeau-1.5554278

 

[Hypocrite-The]

 

[Hypocrite-The]

Everybody is just guessing. The experts are even worse because they have developed complex mathematical models but entering garbage parameters means that the output is an even bigger pile of garbage.

There is probably a shred of truth in each version of the possible outcome but whatever is published the end result is that the pandemic will burn itself out because in the history of mankind no pandemic has wiped out the human race. Genetic diversity ensures that this will not happen.

If a million or so die so what. Our own inventions eg the automobile kill 1.4 million annually but we still worship the car as a status symbol. Nobody considers it to be a killing machine.

This covid-19 headlines will just fade away after a while even if the virus doesn't and life will carry on.

Basically the data that came out of imperial college is crap. N they are the ones that caused the lockdown. N they are the cause of the economic destruction

 

[Pinkieslut]

Japan launches transparent body wrap bag to allow family members of the new crown deceased to see the last side of relatives wanted-Choose Japan launc
The new crown epidemic in Japan continues to develop in many places, and the treatment of the remains of patients who have died due to illness has also become a problem, because it is impossible for relatives to hold memorial services for them. Recently, Japan introduced a transparent sealed body wrap bag, claiming that this allows family members to participate in the corpse transport process, allowing them to see the last side of relatives.

According to a report by Japan ’s Yahoo on April 4, Japan had previously stipulated that the deceased should be cremated only 24 hours after death. However, because the body of the patient who died in the new crown may be infectious, the Japanese health department requires that it must be cremated within 24 hours, and family members cannot say goodbye for safety reasons.

In order to let the relatives of the deceased meet the last of their loved ones, the Kobe City Government of Hyogo Prefecture has launched a fully sealed transparent body bag, claiming that it can effectively close the body and avoid secondary infection.

The advantage of this is that the dead body of the new crown can be sealed, and at the same time it is transparent to see the relatives' faces. After sterilization, relatives can be involved in the delivery of corpses, including moving into a coffin for a farewell ceremony.

At the same time, by adopting such sealing measures, the funeral parlour would not need to kill all enemies in a comprehensive manner, and could normally arrange farewell ceremonies and conduct cremation work.

There are no patients who have died because of the new crown in Kobe City. However, the local government started to develop this kind of transparent corpse bag early in the outbreak. Several hospitals have already purchased them, and they are prepared for unexpected needs.

But even so, many funeral homes and funeral staff still hold a wait-and-see attitude, because the new coronavirus is too contagious, and even the remains may contaminate the funeral home, so the effectiveness of this body bag remains to be verified.

 

[Hypocrite-The]

Anti-viral drug trio found to shorten COVID-19 illness in mild cases: Study
A medical worker at Princess Margaret Hospital in Hong Kong
A medical worker wearing protective gear takes the temperature of a woman as she enters Princess Margaret Hospital in Hong Kong on Feb 4, 2020. (Photo: AFP/Anthony Wallace)
09 May 2020 09:17AM
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LONDON: A triple drug combination of antiviral medicines helped relieve symptoms in patients with mild to moderate COVID-19 infection and swiftly reduced the amount of virus in their bodies, according to results of a small trial in Hong Kong.

The trial, which involved 127 patients, compared those given the combination drug - made up of the HIV medicine lopinavir–ritonavir, the hepatitis drug ribavirin, and the multiple sclerosis treatment interferon beta - with a control group given just the HIV drug.

The findings, published in the Lancet medical journal, showed that on average, people who got the triple drug reached the point of no detectable virus five days earlier than those in the control group - at 7 days versus 12 days.

"Our trial demonstrates that early treatment of mild to moderate COVID-19 with a triple combination of antiviral drugs may rapidly suppress the amount of virus in a patient's body, relieve symptoms, and reduce the risk to health-care workers," said Kwok-Yung Yuen, a professor at the University of Hong Kong who co-led the research.

He said the lower risk to health workers would be due to the combination drug's effect in reducing 'viral shedding' - which is when the virus is detectable and potentially transmissible.

In the trial, all patients received standard hospital care as needed, including ventilation support, dialysis support, antibiotics and corticosteroids.

Kowk-Yung Yuen said the findings were "encouraging", but that the triple drug's effect now needed to be tested in larger numbers of patients and in people with more severe COVID-19 illness.

Independent experts agreed that the findings were positive, but said larger and more detailed studies would be needed.

This ... definitely justifies the consideration of adding interferon beta to the list of genuinely, evidence-based, promising treatments to be tested in further randomised trials," said Stephen Evans, a professor of pharmacoepidemiology at the London School of Hygiene & Tropical Medicine.

He said that long years of experience in treating the human immunodeficiency virus (HIV) that causes AIDS have shown that it is best treated with combinations of different drugs "and this could also be the case with COVID-19".

 

[Hypocrite-The]

Commentary: COVID-19 treatment researchers should be cooperating not trash-talking each other
No fair test of the two top contending treatments chloroquine and remdesivir has been conducted yet, says an observer.

fauci raoult
Anthony Fauci (L) and Didier Raoult (R). (Photo: AFP/JIM WATSON, AFP/GERARD JULIEN)
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OXFORD: Rivals Usain Bolt and Justin Gatlin trash-talked each other before the 2016 Olympics, with Bolt calling Gatlin “old man”, and Gatlin calling Bolt “middle aged”.

The banter was entertaining but vanished into insignificance when Bolt won. After the race, both athletes shook hands and accepted the result.

Something like trash-talking is happening in the race for a treatment for COVID-19, but – unlike with Bolt and Gatlin’s race, which decided the matter – there is no fair test of the two top contending treatments being conducted.

The two competing treatments getting the most press are chloroquine, or its cousin hydroxychloroquine (usually given with an antibiotic), and remdesivir. Like almost all medical treatments, they both have benefits and harms.

Hydroxychloroquine is promoted by world-renowned French virologist Didier Raoult, who looks like a rock star. Remdesivir is being endorsed by Donald Trump’s scientific adviser, Anthony Fauci.

Fauci claimed that Raoult’s treatment may have “no effect”, and Raoult returned the favour by accusing Fauci’s trial of “surprisingly” changing outcomes mid-stream (death rate was initially the primary outcome measure but this was replaced with the time it took patients to recover).

Missing from this exchange is a call for a fair head-to-head test of the two treatments.

RAOULT’S HYDROXYCHLOROQUINE STUDY

Hydroxychloroquine is a cheap treatment for malaria, which some test-tube studies suggest inhibits the growth of viruses such as the novel coronavirus.

The spread of the coronavirus disease (COVID-19) in Porto Alegre
FILE PHOTO: A nurse shows a Hydroxychloroquine pill, amid the coronavirus disease (COVID-19) outbreak, at Nossa Senhora da Conceicao hospital in Porto Alegre, Brazil, April 23, 2020. REUTERS/Diego Vara
Raoult noticed that it appeared to be very effective in most of his COVID-19 patients. He conducted a few trials that seemed to show a large effect, but the trials were small (fewer than 80 patients) and it seemed to have serious side-effects in some patients.

Raoult claims that patients in his hospital wouldn’t have agreed to a “fair test” of his treatment against any other (or a placebo) because they wanted hydroxychloroquine. This may be true in his hometown of Marseilles, where he has celebrity status, but not elsewhere.

Also, the fact that he has fans in Marseilles should not have stopped him from publishing a protocol for a comparative trial.

Without a fair test, fans of remdesivir (and critics of hydroxychloroquine) will continue to find flaws with Raoult’s study.

READ: Ebola drug remdesivir used to treat COVID-19 patients in Singapore as part of clinical trials
FAUCI’S REMDESIVIR TRIAL

Remdesivir, a drug developed by Gilead Sciences, has been shown to work in monkeys, but it flopped in the first trial for treating humans with COVID-19.

Revealing the dangerously non-transparent nature of the science in this area, the World Health Organization (WHO) initially posted the results of the failed trial and subsequently took the data down. Simultaneously, Gilead Sciences accused the WHO of “misrepresenting” the trial.

Another trial that didn’t test the drug against a control group, reported by industry-funded authors, found that 36 of the 53 patients who took remdesivir had improved lung function.

Yet 60 per cent of the patients had at least one side-effect, including abnormal liver function.

FILE PHOTO: Investigational remdesivir vials are capped at a Gilead Sciences facility in La Verne
FILE PHOTO: Vials of investigational coronavirus disease (COVID-19) treatment drug remdesivir are capped at a Gilead Sciences facility in La Verne, California, U.S. March 18, 2020. Gilead Sciences Inc/Handout via REUTERS/File Photo
Most recently, the US National Institutes of Health funded a trial comparing remdesivir with placebos in 1,000 patients. The drug seemed to reduce the length of stay in hospital from 14 days – which was how long those who took a placebo were in hospital – to 11 days.

However, Fauci announced the results on national television before the study was reviewed, so nobody can confirm independently whether it was a fair test.

A problem with Fauci’s trial is that the protocol was changed after the trial started. Initially, they were supposed to measure death, which is barely susceptible to bias. They changed this to length of stay in hospital, which is more susceptible to bias.

Changing the protocol mid-stream is sometimes justified, but no rationale was provided.

Even if the trial of remdesivir versus placebo had no flaws, believers in hydroxychloroquine could say that their treatment would have fared better if it had been compared directly.

READ: Commentary: COVID-19 vaccine – why is it taking so long to develop one?
A FAIR SIDE-BY SIDE TRIAL

There is plenty more to the story of hydroxychloroquine and remdesivir. Last time I checked, there were almost 100 trials of either hydroxychloroquine or remdesivir registered worldwide.

The problem is that none of them amounts to a fair side-by-side trial. A fair comparative test of a treatment is (conceptually) no more complex than a 100m race. Such comparative tests are the heart of evidence-based medicine.

In brief, we need a randomised, double-blind trial that compares one treatment against another. Such a trial uses (something like) flipping a coin to decide who gets what.

Otherwise, if people choose which treatment they are on, it could turn out that, say, younger, healthier people chose one treatment over another. That would be like giving one of the treatments a head start.

Successful drug tests may provide a better treatment for severe coronavirus cases, but until there
(Photo: AFP/Alberto PIZZOLI)
Blinding involves hiding knowledge of who got what (by making both treatments in the trial look the same). Blinding prevents people’s beliefs and expectations (which can influence outcomes) from influencing the outcome.

Fauci and Raoult know this, and they have chosen not to ask for a fair test.

There is a silver lining to this evidence cloud in the form of an Oxford-based trial called RECOVERY. RECOVERY compares several options for treating COVID-19, including hydroxychloroquine. However, it does not include remdesivir.

In a recent interview with the Financial Times, the lead researcher of RECOVERY claimed that there was not enough remdesivir available.

Also, the results of Fauci’s (unpublished) trial were not available at the time they designed the Oxford trial, so the RECOVERY researchers only had access to the earlier small trial in which remdesivir failed.

READ: Commentary: What if a COVID-19 vaccine doesn’t emerge?
THE BEST TREATMENT?

Sick patients are concerned with objective facts that can answer the question: “What is the best treatment for my COVID-19?”

Until a head-to-head study of the two drugs is conducted, this vital question will not be answered satisfactorily. Instead, we will continue to get biased opinions, sometimes fuelled by conspiracy theories that inform treatment decisions.

For the sake of patients, energy spent promoting these partisan opinions need to be redirected towards conducting fair tests. Until this happens, these readily available objective facts will be obscured beneath biased opinions.

As a result, more patients than necessary will remain ill and die.

 

[Hypocrite-The]

This just proves herd immunity is the best n the wuhan virus should b treated as the flu

Coronavirus restrictions are easing but that doesn't mean the pandemic is over, health experts warn - ABC News
Social distancing banner installed in Adelaide, which reads: "Protect yourselves and others".
In Australia, it will be up to individual states and territories to decide when to lift restrictions.(Getty Images: Moisseyev)
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As each day brings announcements of easing coronavirus restrictions, many Australians are feeling hopeful that life may soon return to normal — or some new version of that.

The National Cabinet has outlined a three-step plan to relax restrictions across the next several months.

By July, it's hoped that the whole country will reach the most relaxed "stage three", where people can return to work and gatherings of up to 100 will be allowed.

But with new cases of coronavirus still expected to emerge, and a potential vaccine at least 12 to 18 months away, what exactly does this 'new normal' look like — and how long will it last?

We want to avoid a 'second wave'
Predicting what will happen next with coronavirus in Australia and around the world is an almost impossible task, said Katherine Gibney, an infectious disease physician and medical epidemiologist at the Doherty Institute.

"A whole range of scenarios are possible," she said.

Australia's plan to gradually ease restrictions, with states and territories going at their own pace based on local incidence and distribution of the disease, was designed to do exactly that, she said.

But it would only work with "ongoing buy in"” from all Australians, which means everyone following social distancing rules and maintaining personal hygiene.

Occasional outbreaks, such as the recent one at the Melbourne meat processing company at the centre of Victoria's largest COVID-19 cluster, are likely to continue, she said.

This is why governments have scaled up COVID-19 testing, and bolstered the capacity of health authorities to trace cases and "trap" local outbreaks.

Second wave 'might not be as severe'
Overseas, some projections have suggested countries like the United States — which have been hit significantly harder by COVID-19 — may face a second deadlier wave later this year, or recurring outbreaks of equal size through to 2022.

Even countries previously praised for their success of containing the initial outbreak, such as Singapore and Japan, have re-entered partial lockdowns amid a surge in cases.

While it's unclear exactly what lies ahead, Dr Gibney said she expected initial COVID-19 outbreaks (rather than subsequent ones) to be the worst we would see.

"You would expect that even though they might have ongoing issues and a second wave in countries where they've had really huge outbreaks, that second wave might not be as severe," she said.

We're in 'early stages of epidemic'
While the rate of new infections remains low in Australia, globally, COVID-19 continues to spread rapidly, said James McCaw, a University of Melbourne epidemiologist.

"There are seven billion people on the planet, and there's been somewhere under 10 million infections," said Professor McCaw, who is part of the team producing models of the pandemic for the Australian Government.

Since the vast majority of Australians remain susceptible to COVID-19 (because so few of us have been infected), he said physical distancing measures, hand hygiene, and staying at home when sick remained critical.

So far, the virus has infected fewer than 1 per cent of us, but would likely go on to infect 70 to 80 per cent of the population if no measures were in place, Professor McCaw said.

"If people don't remain vigilant about minimising contact, then we will see the so-called large second wave, which would put us back to the start, and all of the excellent success to date would have essentially been squandered."

The easing of restrictions was not a sign that COVID-19 was over, he said, but rather the beginning of the next phase of managing it.

To do that successfully, Australia has to continue with its strategy of suppression, by maintaining low levels of community transmission, and keeping the virus reproduction number (the average number of people an infected person goes on to infect) below or close to 1.

Professor McCaw said although a potential vaccine would bring more protection, it wouldn't mean the end of coronavirus.

"We have an influenza vaccine that saves many thousands of lives every year, but the flu virus is still part of our society," he said.

"The coronavirus is becoming part of the world we live in."

Not clear if the virus will become seasonal
There is still so much scientists don't understand about SARS-CoV-2, said virologist Sacha Stelzer-Braid, which makes it difficult to predict what might happen next.

"All respiratory viruses behave in slightly different ways, so we can't make any assumptions about what this virus will do," Dr Stelzer-Braid said.

While some respiratory viruses like influenza are seasonal, others, like rhinovirus (the predominant cause of the common cold), occur all year round.

At this point, it's too early to say whether climate will affect coronavirus, despite speculation it might get worse as winter sets in.

"It might turn out to be something like the flu, where it kind of jumps from hemisphere to hemisphere depending on where the winter is," Dr Stelzer-Braid said.

"Having said that, they get influenza in tropical countries as well."

A transmission electron microscope image of SARS-CoV-2, the virus that causes COVID-19.
While the flu virus mutates rapidly, coronaviruses tends to be slower.(NIAID-RML)
Kirsty Short, a virologist at the University of Queensland, said despite the many uncertainties, it was clear that without further intervention, SARS-CoV-2 was very unlikely to disappear on its own.

"It would be possible in countries with really low rates to get rid of the virus, but it wouldn't be sustainable because you would just have to completely shut your borders for an indefinite period," Dr Short said.

"When you think about eradicating a virus, it's no small feat. There is only one virus we have successfully eradicated from the world with intervention — that was smallpox."

Like all viruses, SARS-CoV-2 has acquired mutations and will continue to do so (as the virus replicates, it makes mistakes copying its genetic code).

But Dr Short said the number of mutations so far had been very low, and that the virus appeared reasonably stable, despite reports a second 'more contagious' strain had emerged.

Unlike seasonal influenza, which mutates so rapidly we need a different vaccine each year, she said there was no evidence of any significant mutations to the new coronavirus that would change the virus's behaviour.

Health system is now prepared for COVID-19 patients
When it comes to how well prepared our health system is to handle any potential outbreaks, intensive care specialist Steve Webb said Australia was in an enviable position.

"The government and public health authorities have done an absolutely stunning job with protecting us from a major outbreak," said Professor Webb, who works at the frontline of COVID-19 at Royal Perth Hospital.

"We're one of the very few countries around the world to be in the situation that we are at the moment."

The efforts of the Australian public had helped hospitals buy time to adequately prepare, he said.

Intensive care units now had plans to expand their capabilities if necessary, including for "double or perhaps even triple the number of patients" they would normally see.

"There's lots of personal protective equipment available … and the systems, processes and policies have been put in place," Professor Webb said.

While a vaccine is ultimately what is needed to combat COVID-19, he said in the interim, the development of effective drug treatments will also help to reduce the burden of the disease.

 

[Hypocrite-The]

There is a treatment for the wuhan virus...

 

[Hypocrite-The]

'The Lancet's got a bit of form, here': How did a retracted study on hydroxychloroquine get through peer review?
A bottle of hydroxychloroquine tablets
The Lancet retracted its study into hydroxychloroquine after its authors said independent reviewers could not verify the information.(AP: David J Phillip)
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Scientists around the world are resuming trials of the controversial drug hydroxychloroquine for possible use against COVID-19, after the retraction of a heavily criticised study into its effects and side-effects.

When the study was first published in the highly influential medical journal The Lancet, it prompted the World Health Organisation (WHO) to pause trials on the drug, which has long been used for preventing or treating malaria, as well as lupus.

Now the paper has been retracted, and the WHO trials are back on, after several of the paper's authors said they were not able to verify the contents of a database at the heart of the study.

So how did a paper of this size, with such apparent flaws, make it through peer review to publication in The Lancet? And how badly did it stall progress on assessing the drug's worth in the fight against coronavirus?

What was the study published in The Lancet?
The observational study was published in The Lancet on May 22 and described data purportedly collected from 671 hospitals around the world, including 96,000 COVID-19 patients, some of whom were treated with hydroxychloroquine.

It claimed that those treated with hydroxychloroquine or the related chloroquine had a higher risk of death and heart rhythm problems than patients who were not given the medicines.

WHO briefing
The WHO has now resumed trials on hydroxychloroquine.(AP: Salvatore Di Nolfi)
As a result of the study, a number of clinical trials were put on hold.

But many scientists voiced concern about the study following its publication. Nearly 150 doctors signed an open letter to The Lancet questioning the article's conclusions, and calling for the peer review comments that preceded publication to be released.

Company which gathered the data did 'not have the capacity to do this'
The data was gathered by a Chicago-based company called Surgisphere, a company that many experts suggested was too small to be capable of handling such an immense data set.

"This tiny company does not seem to have the capacity or the personnel to be able to do this," ABC medical expert Dr Norman Swan said on the Coronacast podcast.

"This was exposed by The Guardian, particularly in Australia, because it was shown that the Australian data they used could not have been right … The figures just did not add up for Australia."

For example, the research paper cited 73 deaths from COVID-19 in Australia by April 21, when official case counts only reported 67 deaths by the same date.

Critics also pointed out that the sheer scale of the data set seemed too good to be true.

"If you actually look at what they're claiming that they've done, is that they've integrated a huge amount of de-identifying data from patients, which is very hard to do," Dr Swan explained.

"A lot of the hospitals that they could have done it from don't have the capacity to do it.

The Guardian reported that Surgisphere's "handful of employees" included a science fiction writer and an adult-content model.

The company's founder, Dr Sapan Desai, was one of the study's authors. Requests for comment from Reuters to Dr Desai and Surgisphere were not immediately answered.

In the retraction notice, the study's co-authors — excluding Dr Desai — said Surgisphere would not give the reviewers the full data, citing confidentiality and client agreements.

The Lancet's notice said "there are many outstanding questions about Surgisphere and the data that were allegedly included in this study", adding that institutional reviews of the company's research collaborations were urgently needed.

Data from Surgisphere is also the subject of another recent coronavirus study in the New England Journal of Medicine, which has also been retracted.

'The Lancet's got a bit of form, here': How did the study get through peer review?
Dr Swan says while peer review is still a relied-upon fundamental of the scientific method, it is not foolproof.

Hydroxychloroquine tablets are displayed on a dark surface
Dr Norman Swan says the busy environment in which COVID-19 papers are being rushed to press may have contributed to The Lancet's study slipping through the cracks.(AP: John Locher)
"The Lancet's got a bit of form here. They were the ones who published the Wakefield study into the measles-mumps-rubella vaccine, claiming it causes autism," he said.

"At times the Lancet's peer review has been called into question, but peer review is not perfect. No journal's above all this.

"But it looks as if what's happened here — I've done a lot of reporting on scientific misconduct in the past, if this is what this turns out to be — is that you co-opt people who are busy but have a good reputation, and you put their names on the paper that beguiled the reviewers, saying, 'Oh, well, if that person's put on, it must be OK'.

"And I suspect that's how this has slipped through in a busy environment where people are rushing COVID-19 papers to press."

Why is hydroxychloroquine getting so much attention?
You can thank the President of the United States for the drug's notoriety.

US President Donald Trump gestures with his hands.
President Donald Trump told reporters he was taking zinc and hydroxychloroquine on May 18.(AP: Evan Vucci)
Donald Trump has repeatedly promoted hydroxychloroquine's use, calling it a "game changer" in the fight against coronavirus.

He said he had taken the drug himself to try and prevent infection, despite the well-known side effects.

Mr Trump claimed he had been taking the drug after a number of White House staffers became infected with COVID-19.

Observational studies v randomised clinical trials
Criticism over the quality of its data led to the Lancet study's withdrawal.

A close-up of a silver package of pills, with red writing, held by a hand.
The WHO halted its trials on hydroxychloroquine as a result of The Lancet's study.(AP: Rafiq Maqbool)
The Lancet study was a "retrospective observational" study, using a data set from Surgisphere.

Retrospective observational studies, which look backwards and examine exposures to suspected risks or protections, are more prone to error than prospective studies.

Randomised studies, on the other hand, are seen as the gold standard in research. These studies randomly assign a treatment to one group of people and a dummy to another group, so that the two can be compared.

The Lancet study simply used a large amount of hospital data — now called into question — to see what effects hydroxychloroquine had on some patients that were administered the drug, compared to those who were not.

"The study itself (and most commentators) concluded that high-quality randomised controlled trials of hydroxychloroquine in COVID-19 were needed — especially to clarify possible harms and establish which COVID-19 patients would benefit," said Professor Andrew McLachlan, head of the Sydney Pharmacy School at the University of Sydney.

"All the ongoing randomised controlled trials involve careful screening and monitoring of well-known adverse effects (on heart rhythm and eye toxicity).

"The numerous trials should continue; they can be conducted safely and when complete will answer the important question of whether hydroxychloroquine is a safe and effective drug to treat or prevent COVID-19 in the global pandemic."

The Lancet's study caused ripple effects
The WHO's decision to halt its trials on hydroxychloroquine as a result of the study had knock-on effects across the medical profession.

The United Kingdom's COPCOV trial, which was investigating whether hydroxychloroquine could prevent healthcare workers contracting COVID-19, was put on hold just a week after launch.

French company Sanofi also temporarily stopped recruiting for its study into the drug. Both the UK and French studies have yet to resume.

However, the UK Recovery Trial only paused briefly before proceeding after making safety checks, and has signed up about 4,500 recruits. Swiss pharmaceutical company Novartis has also continued with its trial.

Is hydroxychloroquine receiving too much research attention?
The notoriety surrounding hydroxychloroquine may have contributed to the sheer volume of studies surrounding the anti-malarial drug.

But that volume poses a problem of research balance in the race to find treatments for coronavirus, says Paul Glasziou, professor of Evidence Based Medicine at Bond University.

"As we calculated over a decade ago, there's a lot of waste that occurs in research, but we're seeing that waste accelerated or expanded by what's happening," Professor Glasziou told the Health Report on Radio National.

"The pace of research has been staggering. One example of that is the Oxford trial, randomised trials.

"Actually, what we need is a greater diversity of things being studied, including combinations of drugs.

"So it's been this lack of coordination, I think of people jumping on one bandwagon, but without seeing that we actually need a range of things."