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One Year Since Reporting Started on COVID-19, Here’s What We Do (And Still Don’t) Know

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A year ago, I wrote an article for The Conversation about a mysterious outbreak of pneumonia in the Chinese city of Wuhan, which transpired to be the start of the COVID-19 pandemic.


At the time of writing, very little was known about the disease and the virus causing it, but I warned of the concern around emerging coronaviruses, citing SARS, MERS and others as important examples.

Since then – and every day since – we continue to learn so much about SARS-CoV-2 and COVID-19, finding new ways to control the pandemic and undoubtedly keep us safer in the decades that will follow.

Here is what we have learned since last January and what we still need to learn.

Lessons learned

Initially, the disease that we now call COVID-19 was described in terms of a lung inflammation, or pneumonia, in older people. But we now know that SARS-CoV-2 infection can result in a wide range of symptoms in people of all ages, spanning from no symptoms at all to systemic inflammation and death.

And then there are the lingering symptoms that many suffer from – so-called “long COVID“. We are also beginning to tease apart the different phases of the disease, the damage caused to organs (such as the heart and brain), and the role of co-infections with bacteria and fungi.


In January 2020, there was limited evidence of human-to-human transmission. If there was, it was thought to be similar to its cousin virus SARS-CoV-1, which causes SARS, in that infection spreads relatively late in the disease, when symptoms are at their peak.

Yet early studies showed that spread between people was highly efficient for SARS-CoV-2, and that it could happen fast and before the worst of the symptoms began. This made it hard to control without sensitive and specific tests using the now-famous PCR test.

Social distancing, hygiene and masks would help limit the spread alongside isolation and quarantine.

At first, there were no treatments or vaccines against COVID-19, apart from support in hospital, such as providing oxygen when patients had difficulty breathing or antibiotics when they catch a secondary bacterial infection.

In the months after January, researchers rapidly tested new therapies against COVID-19, identifying dexamethasone, and have developed many safe and highly effective vaccines against COVID-19 that are now in use.

Future questions

Although we are learning daily about COVID-19, several important scientific questions remain that will shape the future of SARS-CoV-2, and humanity, for decades. The first is how will SARS-CoV-2 evolve, adapt and change over the next year in the face of natural or acquired immunity through vaccination?

A second, less academic point would be whether this is important. Our treatments and public health measures will still work, but what about our vaccines?


We continue to track, predict and understand SARS-CoV-2 evolution with regards to vaccine ‘escape’, and all our available evidence suggests it is minimal at best and that our current vaccine platforms are robust enough to withstand any changes if needed.

We must also remain alert to the chance of SARS-CoV-2 establishing itself in another species, such as mink.

Then there is the question of how SARS-CoV-2 will interact with the other viruses that circulate in humans. The human respiratory tract is home to several viruses that circulate together – often in a single person.

These viruses promote or impede the infection of other viruses. We now know that thanks to social distancing, the spread of most of our respiratory viruses, such as influenza and RSV, has been severely restricted.

How will they “react” when mitigation measures, such as social distancing, end?

Finally, we must identify the origin of SARS-CoV-2 to prevent the continued spill-over of SARS-CoV-2-like (or indeed other pathogenic coronaviruses) into humans.

We know that SARS-CoV-2 probably emerged recently in south-east Asia and that ultimately the virus was in a horseshoe bat. But the biological and ecological steps it took to reach humans remain obscure.


Solving this puzzle will help safeguard our health for decades to come, in the same way as has been achieved for swine and avian flu infections.

As I said in my article a year ago, these epidemics “are a constant reminder of the need to invest in research into emerging virus biology and evolution, and ultimately to identify safe and effective drugs to treat – or vaccines to prevent – serious disease”.

The COVID-19 pandemic has demonstrated that science and scientists can and will deliver results, given the right financial and societal support. How then we will apply the lessons of COVID-19 to other serious problems, such as emerging infections, antimicrobial resistance and climate change?The Conversation

Connor Bamford, Research Fellow, Virology, Queen’s University Belfast.

This article is republished from The Conversation under a Creative Commons license. Read the original article.


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First Confirmed Case of COVID-19 Transmission to Great Apes

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At least two gorillas at California’s San Diego Zoo have caught the coronavirus, the first known instance of natural transmission to great apes, officials said Monday.

Two primates began coughing last week and have since tested positive for COVID-19, while a third is showing symptoms, Governor Gavin Newsom said.


They are thought to have contracted the virus from an asymptomatic zoo worker, though this has yet to be confirmed.

“Aside from some congestion and coughing, the gorillas are doing well,” the world-famous zoo’s executive director Lisa Peterson said in a statement.

“The troop remains quarantined together and are eating and drinking. We are hopeful for a full recovery.”

Gorillas share up to 98 percent of their DNA with humans, and studies have found that some non-human primates are susceptible to COVID-19 infection.

It is not yet known if the gorillas will have a serious reaction to the disease that has killed 1.94 million humans, or if other troop members have also been infected.

The San Diego Zoo Safari Park, where the gorillas are kept, has been closed to visitors since early December as record cases began surging through Southern California.

Workers are all required to wear personal protective equipment such as masks when near the gorillas, the zoo said.

© Agence France-Presse


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Few Vaccines Actually Prevent Infection – Here’s Why That’s Not Actually a Problem

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Vaccines are a marvel of medicine. Few interventions can claim to have saved as many lives. But it may surprise you to know that not all vaccines provide the same level of protection. Some vaccines stop you getting symptomatic disease, but others stop you getting infected too.


The latter is known as “sterilising immunity”. With sterilising immunity, the virus can’t even gain a toehold in the body because the immune system stops the virus entering cells and replicating.

There is a subtle yet important difference between preventing disease and preventing infection. A vaccine that “just” prevents disease might not stop you from transmitting the disease to others – even if you feel fine. But a vaccine that provides sterilising immunity stops the virus in its tracks.

In an ideal world, all vaccines would induce sterilising immunity. In reality, it is actually extremely difficult to produce vaccines that stop virus infection altogether. Most vaccines that are in routine use today do not achieve this.

For example, vaccines targeting rotavirus, a common cause of diarrhoea in infants, are only capable of preventing severe disease. But this has still proven invaluable in controlling the virus. In the US, there has been almost 90 percent fewer cases of rotavirus-associated hospital visits since the vaccine was introduced in 2006. A similar situation occurs with the current poliovirus vaccines, yet there is hope this virus could be eradicated globally.


The first SARS-CoV-2 vaccines to be licensed have been shown to be highly effective at reducing disease. Despite this, we don’t yet know whether these vaccines can induce sterilising immunity.

It is expected that data addressing this question will be available from the ongoing vaccine clinical trials soon. Although even if sterilising immunity is induced initially, this may change over time as immune responses wane and viral evolution occurs.

Immunity in individuals

What would a lack of sterilising immunity mean for those vaccinated with the new COVID vaccines? Quite simply it means that if you encounter the virus after vaccination, you may get infected but show no symptoms. This is because your vaccine-induced immune response is not able to stop every virus particle from replicating.

It is generally understood that a particular type of antibody known as a “neutralising antibody” is needed for sterilising immunity. These antibodies block virus entry into cells and prevent all replication.

However, the infecting virus may have to be identical to the vaccine virus in order to induce the perfect antibody.


Thankfully, our immune responses to vaccines involve many different cells and components of the immune system. Even if the antibody response isn’t optimal, other aspects of immune memory can kick in when the virus invades. These include cytotoxic T cells and non-neutralising antibodies. Viral replication will be slowed and consequently disease reduced.

We know this from years of study on influenza vaccines. These vaccines typically induce protection from disease, but not necessarily protection from infection. This is largely due to the different strains of influenza that circulate – a situation that may also occur with SARS-CoV-2.

It is reassuring to note that flu vaccines, despite being unable to induce sterilising immunity, are still extremely valuable at controlling the virus.

file 20210104 13 1xbf603The inverse relationship between coronavirus infection severity and protective immunity. (Sarah L Caddy)

Immunity in a population

In the absence of sterilising immunity, what effect might SARS-CoV-2 vaccines have on the spread of a virus through a population? If asymptomatic infections are possible after vaccination, there has been concern that SARS-CoV-2 will simply continue to infect as many people as before. Is this possible?

Asymptomatically infected people typically produce virus at lower levels. Though there is not a perfect relationship, usually more virus equals more disease. Therefore, vaccinated people are less likely to transmit enough virus to cause severe disease.

This in turn means that the people getting infected in this situation are going to transmit less virus to the next susceptible person. This has been neatly shown experimentally using a vaccine targeting a different virus in chickens; when only part of a flock was vaccinated, unvaccinated birds still showed milder disease and produced less virus.

So, while sterilising immunity is often the ultimate goal of vaccine design, it is rarely achieved. Fortunately, this hasn’t stopped many different vaccines substantially reducing the number of cases of virus infections in the past.

By reducing disease levels in individuals, this also reduces virus spread through populations, and this will hopefully bring the current pandemic under control.The Conversation

Sarah L Caddy, Clinical Research Fellow in Viral Immunology and Veterinary Surgeon, University of Cambridge.

This article is republished from The Conversation under a Creative Commons license. Read the original article.


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Herd Immunity Won’t Happen in 2021, WHO Warns

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Scientists at the World Health Organization warned Monday that mass vaccinations would not bring about herd immunity to the coronavirus this year, even as one leading producer boosted its production forecast.


England meanwhile launched the first of its mass-inoculation sites in major cities, racing to get ahead of the rapid spread of a new strain of the disease there.

The pandemic has infected more than 90 million people and the death toll has passed 1.94 million since China confirmed the first death in the central city of Wuhan a year ago.

China has largely brought the virus under control, but is tackling a number of local infections.

More than half a million people were placed under lockdown in Beijing on Monday as the government imposed strict measures to stamp out a handful of cases.

Infection numbers were, however, surging across Europe, particularly as Britain coped with a new strain of the disease that could see hospitals being overwhelmed.

Russia on Sunday confirmed its first case of the new UK coronavirus strain, which scientists fear is significantly more contagious.

The virus has also exploded across the United States, the hardest-hit country, where US President-elect Joe Biden publicly received his second dose of the vaccine.

‘Worst weeks’ to come

German company BioNTech said it could produce millions more doses of its coronavirus doses than originally expected this year, boosting production forecast from 1.3 to two billion.

The announcement by BioNTech, which partnered with US firm Pfizer to produce the first vaccine approved in the West, was a boost to countries struggling to deliver the jabs.


But the company also warned that COVID-19 would “likely become an endemic disease”, and said vaccines would need to fight against the emergence of new viral variants and a “naturally waning immune response”.

Later Monday, the WHO’s chief scientist Soumya Swaminathan warned it would take time to produce and administer enough vaccine doses to halt the spread of the virus.

“We are not going to achieve any levels of population immunity or herd immunity in 2021,” she said, stressing the need to maintain physical distancing, hand-washing and mask-wearing to rein in the pandemic.

Britain, the first country to approve the Pfizer/BioNTech jab, opened seven mass vaccination sites across England on Monday.

But England’s chief medical officer Chris Whitty told BBC television: “The next few weeks are going to be the worst weeks of this pandemic in terms of numbers into the NHS (National Health Service).”

“What we need to do, before the vaccines have had their effect… is we need to really double down” on observing lockdown measures, he added.

India – with the world’s second-biggest virus caseload – will begin giving shots to its 1.3 billion people from Saturday in a colossal and complex undertaking.

Russian officials said Monday they would trial a one-dose version of the country’s Sputnik V vaccine, part of efforts to provide a stopgap solution for badly hit countries.


Safest city

South Africa meanwhile shut land borders for a month to counter an unprecedented resurge in cases fuelled by a new virus strain.

Restrictions already in place, such as a ban on alcohol sales and large gatherings, and an overnight curfew, remain.

Portugal’s Prime Minister Antonio Costa said Monday a new lockdown was unavoidable as the country suffered record numbers of virus deaths and infections.

“We are certainly facing a third wave” of the virus, Costa told journalists.

Lebanon tightened its virus restrictions with an 11-day total lockdown and fresh travel restrictions.

A team of 10 scientists from the WHO were preparing for a mission to China on Thursday to investigate the origins of the disease.

It will “conduct joint research cooperation on the origins of COVID-19 with Chinese scientists”, Beijing’s National Health Commission said in a statement that provided no further details.

The visit, comes more than a year after the pandemic began amid accusations that Beijing tried to thwart the investigation into the virus.

The United States and Australia have led international calls for an independent inquiry, enraging China.

The anniversary of the first reported death passed by unmarked on Monday in Wuhan, where commuters moved freely to work, and parks and riverside promenades buzzed with visitors.

“Wuhan is the safest city in China now, even the whole world,” 66-year-old resident Xiong Liansheng told AFP.

© Agence France-Presse


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Here’s What We Know About The New COVID-19 Mutations So Far

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The emergence in Britain and South Africa of two new variants of Sars-CoV-2, which are potentially far more infectious versions of the virus, has prompted widespread concern. Here is what we know – and what we don’t – about the mutations.


What are they?

All viruses mutate when they replicate in order to adapt to their environment.

Scientists have tracked multiple mutations of Sars-CoV-2, the virus that causes COVID-19, since it appeared in China in late 2019.

The vast majority of mutations did not materially alter either the virus’s virulence or transmissibility.​

However, one mutation – variant B117, which likely emerged in southeastern England in September, according to Imperial College London – has now been detected in countries across the world, including the United States, France, and India.​

Another variant, 501.V2, was detected in South Africa in October, and has since spread to several nations, including Britain and France.​

Both have multiple mutations to the virus, most notably on its spike protein – the part of the virus that latches on to human cells and helps it spread.

Specifically, the mutated versions have an altered receptor binding domain known as N501Y, which is situated on the virus’ protein spike and which allows easier access to the ACE2 receptor in human cells.

This makes the mutated versions potentially more infectious than other strains.

The European Centre for Disease Control (ECDC) says that while there is “no clear relationship” between enhanced ACE2 binding and increased transmissibility, “it is plausible that such a relationship exists”.


Are they more contagious?

Indeed, several recent studies – yet to be peer-reviewed – have concluded that the British variant of Sars-CoV-2 is likely to be far more transmissible than other strains.

​The NERVTAG expert committee which advises the British government on disease control has estimated the new mutation is between 50 percent and 70 percent more transmissible.​

A team at the London School of Hygiene and Tropical Medicine (LSHTM) concurs, with experts putting increased transmissibility in the 50-74 percent range.

Last week, researchers at Imperial College London released the results of a study into thousands of genetic sequences of Sars-CoV-2 found in Britain between October and December.

They found that the new variant had a “substantial transmission advantage”, with a reproduction rate between 0.4 and 0.7 higher than the unmutated virus.​

Preliminary studies on the South African variant have also concluded it is more contagious than regular Sars-CoV-2.

Although initial data seems to confirm that the two new versions are more contagious, experts have urged caution.

Bruno Coignard, head of infectious diseases at France’s health authority Sante Publique France, told AFP that the British variant’s spread was due to “a combination of factors”.

“These concern the virus’ characteristics but also prevention and control measures put in place,” he said.


Are they more dangerous?

There is currently no evidence to suggest that the mutated viruses are any stronger than normal.

But increased transmissibility alone poses an enormous problem, given that a small but consistent percentage of COVID-19 patients require hospital care.

“Increased transmissibility eventually translates to a far higher incidence rate, and even with the same mortality, this means significant pressure on health systems,” said Coignard.

Adam Kucharski, an epidemiologist at LSHTM, said that a virus that is 50 percent more contagious would be a “much bigger problem” than one that is 50 percent more deadly.

​In a Twitter thread, he explained how a disease such as COVID-19, with a reproduction (R) rate of 1.1 – where each patient on average infects 1.1 others – and a mortality rate of 0.8 percent would be expected to produce 129 deaths within a month.​

If the mortality rate increased 50 percent, the number of deaths would rise to 193.

But due to the exponential growth in cases with a more contagious variant, a disease with a 50 percent higher transmission rate would see the death toll hit 978.​

Arnaud Fontanet, an epidemiologist with France’s science council, admitted on Monday that the new British variant was “extremely concerning right now”.


Initial studies also concluded that the British variant was significantly more contagious among young people, which raises the issue of whether or not to keep schools open.​

The LSHTM study concluded that lockdowns similar to those seen across Britain in November would be insufficient to stem the new variant’s spread “unless primary schools, secondary schools, and universities are also closed”.

Will vaccines still work?

As vaccination campaigns get underway across the world, is there any reason to fear that the new mutations may not respond to the host of vaccines already on the market?​

After all, the messenger RNA vaccines developed by Pfizer and Moderna trick the body into reproducing the virus’s spike protein – the precise part of the pathogen that has mutated in the new versions.​

The ECDC said it was too soon to know if the mutations will impact vaccine efficacy.

Last week, Henry Walke from the American Centers for Disease Control told reporters that “experts believe our current vaccines will be effective against these strains”.

On Monday however, Francois Balloux, professor of Computational Systems Biology and Director at University College London’s Genetics Institute said that the South African variant’s spike protein mutation “helps the virus to bypass immune protection provided by prior infection or vaccination”.

German vaccine developer BioNTech said Friday its vaccine appeared to be effective at neutralising a variant of the coronavirus that shared a key spike protein mutation with the British variant.​

In unreviewed research, scientists in the US took blood samples from 20 people who had received two doses of the Pfizer/BioNTech vaccine and exposed them to virus molecules with the N501Y mutation.

They found “no reduction in neutralisation activity against the virus bearing the (mutated) spike”.

What can we do about them?

Coignard said it was impossible to eradicate the new viral variants entirely, although the goal from policymakers should be “maximum delay” of their spread.

The ECDC says that in countries currently unaffected by the new mutations, “efforts to delay the spread should mirror those made during the earlier stage of the pandemic“.

These include tests and quarantining of new arrivals, contact tracing, and limited travel, it said.

By sheer luck, certain existing PCR tests can detect the British variant.

Fontanet, therefore, advocated “extremely aggressive surveillance” through widespread testing.

“We need to be even more vigilant in our prevention measures to slow the spread of COVID-19 by wearing masks, staying at least six feet apart from people we don’t live with, avoiding crowds, ventilating indoor spaces, and washing our hands,” said Walke.​

© Agence France-Presse


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Research Says Alzheimer’s Is Actually 3 Distinct Disease Subtypes

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Alzheimer’s Disease (AD) is probably more diverse than our traditional models suggest.

Postmortem, RNA sequencing has revealed three major molecular subtypes of the disease, each of which presents differently in the brain and which holds a unique genetic risk. 


Such knowledge could help us predict who is most vulnerable to each subtype, how their disease might progress and what treatments might suit them best, potentially leading to better outcomes. 

It could also help explain why effective treatments for AD have proved so challenging to find thus far.

The mouse models we currently have for pharmaceutical research match a particular subset of AD, the authors found, but not all subtypes simultaneously.

This may “partially explain why a vast majority of drugs that succeeded in specific mouse models do not align with generalised human trials across all AD subtypes,” they say.

“Therefore,” the authors conclude, “subtyping patients with AD is a critical step toward precision medicine for this devastating disease.”

Traditionally, AD is thought to be marked by clumps of amyloid-beta plaques (Aβ), as well as tangles of tau proteins (NFTs) found in postmortem biopsies of the brain.

Both of these markers have become synonymous with the disease, but in recent years our leading hypotheses about what they actually do to our brains have come under question.


Typically, accumulations of Aβ and NFT are thought to drive neuronal and synaptic loss, predominantly within the cerebral cortex and hippocampus. Further degeneration then follows, including inflammation and degeneration of nerve cells’ protective coating, which causes signals in our brains to slow down. 

Strangely enough, however, recent evidence has shown up to a third of patients with a confirmed, clinical diagnosis have no Aβ plaques in postmortem biopsies. What’s more, many of those found with plaques at death did not show cognitive impairment in life.

Instead of being an early trigger of AD, setting off neurodegeneration and driving memory loss and confusion, in some people, Aβ plaques appear to be latecomers.

On the other hand, recent evidence suggests tau proteins are there from the very earliest stages.

In light of all this research, it’s highly likely there are specific subtypes of AD that we simply haven’t teased apart yet. The new research has helped unbraid three major strands. 

To do this, researchers analysed 1,543 transcriptomes – the genetic processes being express in the cell – across five brain regions, which were collected post mortem from two AD cohorts.


Using RNA sequencing to profile these transcriptomes, the authors identified three major molecular subtypes of AD, which correspond to different dysregulated pathways.

These include: susceptibility to tau-mediated neurodegeneration; amyloid-β neuroinflammation; synaptic signaling; immune activity; mitochondria organisation; and myelination. 

All of the subtypes were both independent of age and disease severity. Their molecular signatures were also present in all brain regions, but especially so in the hippocampus, which is largely associated with forming new memories.

What’s more, Aβ and tau proteins could not fully explain the different subtypes, which suggests cognitive impairment “is neither dependent on nor fully assured by” by their accumulation in the brain.

In fact, only about a third of AD cases carried these consistent hallmarks of a ‘typical’ AD presentation. The rest of the cases showed opposite forms of gene regulation within molecules, which caused complex changes in multiple brain pathways and cell types.

“It is more likely that Aβ and tau accumulation are often mediators or the end effects of neurodegeneration and inflammation, independent of hippocampal load,” the authors write.

In other words, the mere presence of Aβ and tau clumps might not be as important as the way they interact with each other and other cell processes.


Comparing the results to current mouse models, the authors found a serious mismatch. Most mouse models used in clinical research are based on ‘typical’ presentations of AD, which would only cover a third of the cases in this study.

This means treatments tested on mice may not work for all patients. To develop a more personalised approach to treatment, scientists have been trying to identify and verify molecular biomarkers just like these.

“As we have shown, AD subtypes have very different transcriptomic signatures and therefore will likely require specialised treatments,” the authors conclude.

“Given that many subtype-specific key regulators have opposite directions in some AD subtypes, it is also possible that drugs that reduce AD symptoms in one subtype may exacerbate symptoms in another subtype.”

Further research is needed to confirm this idea, but that’s just the sort of information we really need to know.

The study was published in the Science Advances.


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A Day-by-Day Breakdown of Coronavirus Symptoms Shows How The Disease Progresses

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As doctors observe a growing number of coronavirus patients, they have identified a few patterns in how typical symptoms progress.

As many as 40 percent of coronavirus cases are asymptomatic, according to the Centres for Disease Control and Prevention. And 20 percent of symptomatic cases become severe or critical.


Among patients who develop symptoms, a fever and cough are usually the first to arrive. They’re often followed by a sore throat, headache, muscle aches and pains, nausea, or diarrhoea (though in severe cases, gastrointestinal issues can appear earlier in the course of an infection).

Patients with severe infections tend to develop difficulty breathing – one of the virus‘ hallmark symptoms – around five days after symptoms start.

But symptoms generally don’t appear right after a person has been infected. The virus’ median incubation period is about four to five days, according to the Centres for Disease Control and Prevention.

During that time, an infected person likely won’t yet know they’re sick, but evidence shows they could transmit the virus during the presymptomatic phase.

A day-by-day breakdown

After observing thousands of patients during China’s outbreak earlier this year, hospitals there identified a pattern of symptoms among COVID-19 patients:


  • Day 1: Symptoms start off mild. Patients usually experience a fever, followed by a cough. A minority may have had diarrhoea or nausea one or two days before this, which could be a sign of a more severe infection.
  • Day 3: This is how long it took, on average, before patients in Wenzhou were admitted to the hospital after their symptoms started. A study of more than 550 hospitals across China also found that hospitalized patients developed pneumonia on the third day of their illness.
  • Day 5: In severe cases, symptoms could start to worsen. Patients may have difficulty breathing, especially if they are older or have a preexisting health condition.
  • Day 7: This is how long it took, on average, for some patients in Wuhan to be admitted to the hospital after their symptoms started. Other Wuhan patients developed shortness of breath on this day.
  • Day 8: By this point, patients with severe cases will have most likely developed shortness of breath, pneumonia, or acute respiratory distress syndrome (ARDS), an illness that may require intubation. ARDS is often fatal.
  • Day 9: Some Wuhan patients developed sepsis, an infection caused by an aggressive immune response, on this day.
  • Days 10-11: If patients have worsening symptoms, this is the time in the disease’s progression when they’re likely to be admitted to the ICU. These patients probably have more abdominal pain and appetite loss than patients with milder cases.
  • Day 12: In some cases, patients don’t develop ARDS until nearly two weeks after their illness started. One Wuhan study found that it took 12 days, on average, before patients were admitted to the ICU. Recovered patients may see their fevers resolve after 12 days.
  • Day 16: Patients may see their coughs resolve on this day, according to a Wuhan study.
  • Day 17-21: On average, people in Wuhan either recovered from the virus and were discharged from the hospital or passed away after 2.5 to 3 weeks.
  • Day 19: Patients may see their shortness of breath resolve on this day, according to a Wuhan study.
  • Day 27: Some patients stay in the hospital for longer. The average stay for Wenzhou patients was 27 days.

5f7dee2b94fce90018f7ba8d(Shayanne Gal/Insider)

Just because patients leave the hospital, though, doesn’t mean their symptoms are fully gone. Some coronavirus patients report having symptoms for months, including chest pain, shortness of breath, nausea, heart palpitations, and loss of taste and smell.

People who got sick and were never hospitalized can have lingering symptoms, too.


July report from CDC researchers found that among nearly 300 symptomatic patients, 35 percent had not returned to their usual state of health two to three weeks after testing positive.

Patients who felt better after a few weeks said their symptoms typically resolved four to eight days after getting tested. Loss of taste and smell usually took the longest to get back to normal, they said: around eight days, on average.

COVID-19 may be a vascular disease more than a respiratory one

Though the coronavirus attacks the lungs first, it can infect the heart, kidneys, liver, brain, and intestines as well. Some research has suggested that COVID-19 is a vascular disease instead of a respiratory one, meaning it can travel through the blood vessels. This is the reason for additional complications like heart damage or stroke.

Scientists have a few theories about why some coronavirus patients take a rapid turn for the worse. One is that immune systems overreact by producing a “cytokine storm” – a release of chemical signals that instruct the body to attack its own cells.


Dr. Panagis Galiatsatos, a pulmonary physician at Johns Hopkins Bayview Medical Centre, compared that process to an earthquake – generally, it’s the falling buildings that kill someone, not the quake itself.

“Your infection is a rattling of your immune system,” he said. “If your immune system is just not well structured, it’s just going to collapse.”

The most concerning symptom: shortness of breath

Once symptoms appear, some early signs should be treated with more caution than others.

“I would of course always ask about shortness of breath before anything, because that’s somebody who has to be immediately helped,” Megan Coffee, an infectious-disease clinician who analysed the Wenzhou data, told Business Insider.

Patients who develop ARDS may need to be put on a ventilator in ICU. Coffee estimated that one in four hospitalized COVID-19 patients wind up on the ICU track. Those who are ultimately discharged, she added, should expect another month of rest, rehabilitation, and recovery.

But viewing coronavirus infections based on averages can hide the fact that the disease often doesn’t progress in a linear fashion.

“Courses can step by step worsen progressively. They can wax and wane, doing well one day, worse the next,” Coffee said.

“An 80-year-old man with medical issues can do quite well. Sometimes a 40-year-old woman with no medical issues doesn’t.”

This story was originally published February 21, 2020. It has been updated over time with additional research findings.

This article was originally published by Business Insider.

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On The Eve of Thanksgiving, The US Recorded Its Highest COVID-19 Death Toll Since May

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Thanksgiving could not be better designed to be a coronavirus superspreading event.

Already, COVID-19 cases, deaths, and hospitalizations are skyrocketing around the US, approaching a new peak. Thanksgiving will likely accelerate that uptick, allowing the virus to enter millions of densely-packed and insufficiently-ventilated homes.


As of Thursday, at least 12.8 million Americans have tested positive for coronavirus, according to Johns Hopkins University

The COVID Tracking Project reported that nearly 90,000 people in the US were hospitalized with COVID-19 as of Wednesday, with hospitalizations breaking national records daily for the past 16 days.

More than 262,400 Americans have died of COVID-19, and more than 2,300 of them died on Wednesday alone. This week marks the first time the US has surpassed 2,000 daily deaths since early May, per The New York Times.

It’s been more than 10 months since the first coronavirus case was detected in the US, but these grim milestones are becoming more frequent.

Still, President Donald Trump, who tested positive in October, has repeatedly downplayed the threat of the virus, insisting that the country is “rounding the turn” and that COVID-19 will “just disappear”

The White House is even planning indoor holiday parties over Christmas and Hanukkah, officials told Axios.

The opportunity to ‘translocate disease’ across the US

Health experts have urged Americans to reimagine Thanksgiving and the 2020 holiday season and avoid situations where they can contract or transmit the virus. The Centres for Disease Control and Prevention has asked people to avoid mixing households and to hold small, brief, and masked gatherings that are outdoors, if possible.

Travel has been a major point of concern with the CDC categorising medium-sized events with people travelling from outside the area as “higher-risk”.

“Right now, as we’re seeing exponential growth in cases and the opportunity to translocate disease or infection from one part of the country to another leads to our recommendation to avoid travel at this time,” Dr. Henry Walke, the COVID-19 incident manager at the CDC, told reporters on November 19.


One in 3 Americans aren’t changing their plans

Dr. Anthony Fauci, the nation’s top infectious disease expert, made a “final plea before the holiday” while speaking to ABC News chief anchor George Stephanopoulos on Wednesday.

“We all know how difficult that is because this is such a beautiful, traditional holiday. But by making that sacrifice, you’re going to prevent people from getting infected,” said Fauci, whose own daughters declined to travel home for Thanksgiving in a bid to protect their 79-year-old father.

He added: “If we can just hang in there a bit longer and continue to do the simple mitigation things that we’re talking about all the time – the masks, the distancing, the avoiding crowds, particularly indoors. If we do those things, we’re going to get through it.”

Still, not everyone has heeded this advice. An Insider poll of 1,110 people in the US revealed that nearly one in three people surveyed – or 37 percent – are not doing things differently this year. And 57 percent of respondents said they plan to bring different households together around their dinner tables in the absence of masks and open windows.

Airports are also seeing a surge in travellers. The Transportation Security Administration reported screening more than 1 million passengers last Friday and then again on Sunday and on Wednesday. These have been the biggest days for air travel since March 16, per the agency’s logs.


Daily COVID-19 deaths could double in the next 10 days

Meanwhile, the CDC published a forecast on Wednesday projecting an increase in coronavirus deaths over the next four weeks, with between 10,600 and 21,400 new deaths likely to be reported the week of December 19.

“The national ensemble predicts that a total of 294,000 to 321,000 COVID-19 deaths will be reported by this date,” the CDC said.

Dr. Jonathan Reiner, a professor of medicine at George Washington University, predicted to CNN that daily recorded deaths will not simply jump but double in the coming 10 days.

5fbfe16d037cbd0018612804Daily new COVID-19 deaths in the US. (Worldometers)

There’s about a two-week lag between people getting infected and winding up in hospitals, with symptoms showing up around five to seven days in.

“We’ll be seeing close to 4,000 deaths a day,” he said on Thursday.

And as it gets colder and people move indoors, experts are concerned about a “humanitarian crisis,” Dr. John Brownstein from Boston Children’s Hospital, told ABC News.

“If we layer in travel and large indoor gatherings which we know are drivers of transmission, we expect to see a massive surge on top of an already dire situation,” he said.


Michael Osterholm, the director of the Centre for Infectious Disease Research and Policy at the University of Minnesota, echoed that sentiment.

“I worry that the Thanksgiving Day surge will then just add into what will become the Christmas surge, which will then make this one seem as if it wasn’t so bad,” he told CNN, adding, “We have to understand we’re in a very dangerous place. People have to stop swapping air. It’s just that simple.”

Already, medical resources across the country are being stretched thin, with nurses and doctors working around the clock and risking exposure to the coronavirus themselves.

Dr. Joseph Varon, chief of staff at United Memorial Medical Centre in Houston, Texas, told CNN that the pandemic has forced him to work 251 days in a row. His hospital is at maximum capacity, and scrambling to open two new wings in preparation for an influx of patients after Thanksgiving.

Varon described treating people amid the pandemic as “a never-ending story,” and warned of a rapidly deteriorating situation nationwide, without proper precautions.

“My concerns for the next six to 12 weeks is that if we don’t do things right, America is going to see the darkest days in modern American medical history,” he said.

This article was originally published by Business Insider.

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Superspreader Events Played a Key Role in Igniting The Current Pandemic Globally

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At churches, on cruise ships, and even in the White House, superspreading events that can sicken dozens, even hundreds, of people have illustrated the potential for the coronavirus to infect in dramatic bursts.​


Experts say these large clusters are more than just extreme outliers, but rather the pandemic‘s likely main engine of transmission.

And understanding where, when, and why they happen could help us tame the spread of the virus in the period before a vaccine may be widely available.

Research increasingly suggests that the coronavirus SARS-CoV-2 does not fan out evenly across the population, but spreads at the extremes in an almost “all or nothing” pattern.

Many studies now suggest the majority of people with COVID-19 barely pass it on to anyone else, but when infections happen, they can be explosive and supercharge an outbreak.

Then the virus can infect “10, 20, 50, or even more people”, said Benjamin Althouse, research scientist at the Institute for Disease Modeling.

This corresponds to the “80/20 rule” of epidemiology, where 80 percent of cases come from only 20 percent of those infected, but Althouse said this coronavirus may be even more extreme, with 90 percent of cases coming from potentially just 10 percent of carriers.

This transmission pattern is like “throwing matches on a pile of kindling”, he told AFP.


“You throw one match, it doesn’t ignite. You throw another match, it doesn’t ignite. You throw yet another match, and this time you see flames blaze up,” he said.​

“For SARS-CoV-2, this means that while it is difficult to establish in new places, once established, it can spread rapidly and far.”

Virus ‘hallmark’

Superspreading events have grabbed headlines, looming large in the narrative of the unfolding pandemic.​

In February, the Diamond Princess and its 4,000 passengers spent weeks in quarantine at port in Japan as the number of infections on board climbed, reaching 700.​

The same month a 61-year-old woman, known as “Patient 31”, attended several church services of the Shincheonji Church of Jesus in the South Korean city of Daegu.​

The Korea Centers for Disease Control and Prevention has since linked more than 5,000 infections to Shincheonji.

More recently the virus managed to infiltrate the White House despite a host of measures to keep it out.

Political gatherings, business conferences, and sports tournaments have all acted as infection incubators, but these high profile events could just be the tip of the iceberg.


A study by US researchers, based on one of the world’s largest contact tracing operations and published in Science in September, found that “superspreading predominated” in transmission.

Analysing data from the first four months of the pandemic in the states of Tamil Nadu and Andhra Pradesh in India, the authors found that just eight percent of infected individuals accounted for 60 percent of new cases, while 71 percent of people with the virus did not pass it on to any of their contacts.

Perhaps this should not be a surprise.

Maria Van Kerkhove, an infectious disease epidemiologist at the heart of the World Health Organization‘s pandemic response, tweeted in October that “superspreading is a hallmark” of coronaviruses.

Indeed, it has been observed in many infectious diseases.

One of the most famous superspreaders was Mary Mallon, a cook working in New York in the early 1900s who was the first documented healthy carrier of typhoid bacteria in the US.

Blamed for giving the illness to dozens of people, she was given the unsympathetic label “Typhoid Mary” and forcibly confined for years.

Measles, smallpox and Ebola also see clustering patterns, as did the other coronaviruses, SARS and MERS.


K factor

Early in the pandemic, much attention was focused on the basic reproduction number (R0) of SARS-CoV-2.

This helps calculate the speed a disease can spread by looking at the average number of others a person with the virus infects.

But looking at transmission through this metric alone often “fails to tell the whole story”, said Althouse, who co-authored a paper on the limitations of R0 in the Journal of the Royal Society Interface this month.

For instance, he said Ebola, SARS-CoV-2, and influenza, all have an R0 value of around two to three.

But while people with the flu tend to infect two or three others “consistently”, the transmission pattern for those with Ebola and SARS-CoV-2 is overdispersed, meaning most will hardly spread it and some will give rise to tens of other cases.

A different metric – “k” – is used to capture this clustering behaviour, although it usually requires “more detailed data and methodology”, said Akira Endo, a research student at the London School of Hygiene and Tropical Medicine.

His modelling from the early international spread of the virus, published in Wellcome Open Research, suggested SARS-CoV-2 could be highly overdispersed.

A telltale clue, he said, was that some countries reported numerous imported cases but no signs of sustained transmission – like the match analogy – while others reported large local outbreaks with only a few imported cases.

But even k may not give the full picture, said Felix Wong, a postdoctoral fellow at the Massachusetts Institute of Technology.

His research analysing known COVID-19 superspreading events, published this month in the journal PNAS, found that they were happening even more frequently than predicted by traditional epidemiological models.

They are “extreme, yet probable occurrences”, Wong told AFP.

Biology vs opportunity

So why does superspreading occur?

We don’t know definitively whether biological factors, such as viral load, play much of a role.

But what we do know is people can spread SARS-CoV-2 without symptoms and given a poorly-ventilated, crowded space – particularly where people talk, shout, or sing – the virus can run rampant.​

This could be why a study in Nature this month found that restaurants, gyms, and cafes account for most COVID-19 infections in the United States.​

Using the mobile phone data of 98 million people, researchers found about 10 percent of venues accounted for over 80 percent of cases.

Given this, experts say the focus should be on these types of spaces – and reducing opportunities for the virus to access large numbers of people.

Wong said his modelling showed that if each individual was limited to ten transmissible contacts, “viral transmission would quickly die down”.

Tracking back

Overdispersed spread also means that most people testing positive for the virus are likely to be part of a cluster.

This opens up another way to trace infections: backwards.​

“The idea being that it could be more efficient to trace back, and isolate, superspreaders than it is to trace downstream and isolate individuals who, even if they were infected, might transmit the virus to very few people,” said Wong.

Both Japan and South Korea have used backwards contact tracing, which has been credited with helping them curb their epidemics, along with other control measures.

Masks, social distancing and reducing contacts are all ways to limit transmission opportunities, Althouse said, adding that even characterising people as “superspreaders” is misleading.

“There are vast differences in biology between individuals – I may have a million times more virus in my nose than you – but if I am a recluse, I can infect no one,” he said.

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Abandoning Big Cities Beats Closing Borders When Fighting Pandemics, Simulation Shows

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It’s been a year like no other for studying pandemics. Now, new research offers an intriguing suggestion for slowing the spread of infections: by getting people to relocate away from large cities, rather than sealing off borders.


Applying commonly used SIR (susceptible, infected, and recovered) dynamics, researchers ran some 10,000 simulations looking at one-way migration from a densely populated area to a lightly populated area while a disease is spreading.

The overall infection rate was reduced if the populations mixed, the stats showed, although the infection rate in the lightly populated area did go up. If movement was forced away from the densely populated area, the overall infection rate dropped further.

“Instead of taking mobility, or the lack of mobility, for granted, we decided to explore how an altered mobility would affect the spreading,” says data scientist Massimiliano Zanin, from the Institute for Cross-Disciplinary Physics and Complex Systems (IFISC) in Spain.

Assuming 90 percent of people begin in a densely populated area like a city, and 10 percent begin in a lightly populated area such as a village, the study showed overall infection rates could be reduced from around 35 percent of the population to around 23 percent if people were allowed to move freely.

And while the percentage of infected people in our hypothetical village would go up as a result, the drop in the percentage of infected people in our hypothetical city would go down by a greater amount, the researchers found.


The negative impact on the smaller community can be mitigated by health checks at the border, by only allowing healthy people to relocate, and by limiting the movement of relocated people, the researchers say.

If people are allowed to move back and forth between their old and new homes the benefits are reduced, the study shows.

“People always assume that closing borders is good,” says Zanin. “We found that it is almost always bad.”

As Zanin is keen to point out, this is just a model of movement, without the complexity and unpredictability of real life. A whole host of assumptions – including reinfection and immunity rates, behaviour patterns and so on – have been made to generate the numbers.

With that in mind, modelling studies like this can’t give definitive answers, but they can put forward some useful suggestions – and it would seem that keeping people confined in place could be worse for overall infection rates, even if it does allow some regions to stay relatively free from disease.

In the real world, allowing people to relocate from a main city home to a village holiday home might stop the spread of disease, the researchers say, as long as there was no going back until the pandemic was over.

Of course there are many other economic and social considerations to think about besides the infection rate – not least whether city dwellers would be keen to move out or whether village dwellers would be happy to have them – which highlights the difficult job that governments have in managing the spread of coronavirus.

“Collaboration between different governments and administrations is an essential ingredient towards controlling a pandemic, and one should consider the possibility of small-scale sacrifices to reach a global benefit,” says Zanin.

The research has been published in Chaos.


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