Five months on, what do we now know about COVID-19 and how the body reacts? What complications can happen? And how long does recovery take?

Reed ended up in hospital and, after a full day of testing, he says doctors told him he had a "new kind of pneumonia". Fortunately, he was fit and healthy: his life didn't appear to be in danger. Steroid inhalers helped reduce inflammation in his lungs and, more than a month after that first sniffle, Reed recovered. When he called the hospital in early January to ask more about his test results, they told him what was about to hit headlines around the world in just a matter of days – a new kind of coronavirus had been identified in humans. Reed was one of the earliest suspected cases.

"It was hard to breathe," Reed says. "Even walking to the bathroom, I felt like I was running out of air. My ears hurt from it, I lost my balance at times. It started to get scary, like the worst flu I've ever had."

At first, Reed seemed to just have a cold. A week on, then early December, he was already feeling better when a fever hit, and a cough. His whole body started to ache. Another week went by. He thought he was on the mend until the cough became deeper, seeming to settle at the bottom of his lungs. He felt weighed down too.

Connor Reed, 25, knows well the racking cough and spiking fever of the illness now called COVID-19. He says he came down with it late last year in the centre of the initial outbreak, Wuhan in China. He still lives just a 20-minute walk from the wet market where it's believed the strain jumped from wild animals into humans .

How it plays out depends on the two factors important to any invasion: the strength of your defences and the strength (or dose) of what you’ve been hit with.

A cough, a clammy forehead, shadows on the lungs. Most people infected in the viral pandemic now sweeping the globe will come down with only a mild case of the mystery illness. Some won’t know they’ve had it at all. But when it's bad, it can mount an attack on the whole body – and start a storm in the lungs.

Early studies suggest this virus might be better at hacking into that receptor than SARS, which is why it's more infectious, says Professor Sharon Lewin, director of the Peter Doherty Institute for Infection and Immunity.

All three attack the lungs as well as the sinuses, sometimes developing into viral pneumonia – and, because they're new, our immune system is caught unprepared, with no memory of the virus. The virus behind COVID-19 is about 75 per cent similar to the SARS strain, so alike it is even called SARS 2 or SARS-CoV-2, and thought to bind to the same cell receptors (ACE2), which, it turns out, are found in large quantities in the lungs.

The four main coronaviruses found in humans tend to colonise only the nose and throat. Collectively, they cause about one in four cases of the common cold and symptoms are mild: a runny nose, a sore throat, sometimes a cough or a fever. But since 2003, three dangerous coronavirus illnesses have emerged in humans: SARS (Severe Acute Respiratory Syndrome), which also spawned global panic when it exploded onto the scene 20 years ago, the more deadly but less common MERS (Middle East Respiratory Syndrome) and now the latest, COVID-19, which has already infected more than 3 million people and killed about 200,000.

You can’t see the virus with the naked eye – it’s just nanometres wide. But when someone is infected they can shed it, shooting viral particles at least a metre into the air in water droplets from their nose and mouth, usually through coughing or sneezing. Viruses infect a new host by harnessing our own cellular machinery to replicate. To get in, they need the key – a receptor within a cell they can bind to. Which cell a virus latches onto largely determines where it will spread throughout the body – and helps guide treatment.

Connor Reed, 25, in Wuhan, China. Having recovered from one of the earliest suspected cases of the coronavirus COVID-19, he is hoping to return to Brisbane, Australia. Credit:Facebook

Still, infectious disease physician and microbiologist Professor Peter Collignon says it’s not yet clear whether everyone gets the new virus in their lungs. “Finding it down there isn't a tipping point [for severity] by any means. Some children have it in their lungs but display no symptoms," he says. "But it might not have travelled all the way down from the upper respiratory area in every case."

"Early on, you had doctors in China diagnosing just off chest scans because you can see that lung inflammation, even if it's not severe," Professor Lewin says. Now, Sydney scientists have developed a fast training tool to help frontline healthcare workers spot the tell-tale signs of COVID-19 on lung scans .

But both methods of testing can return false negatives – a throat or nasal swab can miss the virus because it's actually replicating lower down in the lungs. A blood testcan be performed too early – some people will take up to nine days to produce antibodies to fight off a virus – or it could confuse the antibody response with another virus.

The new strain has already been found in the lungs, nose, throat, even in faeces, says infectious disease expert Professor Raina MacIntyre. It can hitch a ride in the bloodstream to other organs such as the kidneys, liver, intestines as well as the heart, brain and central nervous system, too.

To find the virus, doctors need to catch it in the act , either by swabbing a sample directly from the nose and throat or in lung phlegm or by singling out the body’s immune response to the infection in a blood test.

With early symptoms deceptively similar to the common cold or flu, one sign of infection may be a loss of smell (and an accompanying reduction in taste), as the virus attacks that part of the respiratory system. Sometimes people infected with the virus who otherwise feel fine will find they cannot smell as usual – although experts say the effects are likely not permanent and the sudden loss of the sense is far from a "test" for the virus. (Not all patients report losing smell and the symptom is also associated with some other viruses).

A patient might also complain of chills, headaches or a sore throat, and nausea or diarrhoea have also been reported, though not in the numbers seen during SARS. Less than five per cent of cases so far involve a blocked nose.

Based on data given to the WHO in China, most patients seem to have:

Hollywood actor Tom Hanks offered an early public glimpse into life as a COVID-19 patient on March 11 when he revealed he and his wife, Rita Wilson, had both tested positive while in Australia shooting his latest film From hospital isolation on the Gold Coast, Hanks wrote of the illness's onset: "We felt a bit tired, like we had colds, and some body aches. Rita had some chills that came and went. Slight fevers too."

Much of what we know about COVID-19 comes from data of the first 55,000-odd cases in China given to the World Health Organisation , which found more than 80 per cent of people could fight off the illness without serious complications, though many still developed pneumonia. Lungs cleared, coughs eased and fevers broke. Anecdotally, some people have likened the infection to "three weeks in hell", racked by chills and struggling to breathe, while others have reported only a sore throat, a small cough, even no symptoms at all.

As the immune system ramps up its defences, blood vessels start to leak and the lungs can be flooded with cellular debris, making it harder for them to pump oxygen to the rest of the body – and harder for patients to draw breath. "They start to drown," Professor Collignon says.

On scans, they call it ground glass – a white mist over the usual empty black of the lungs. In some cases, there are bright spots, eerily similar to the “honeycomb-shaped” lesions left by SARS but mostly COVID-19 makes a finer and more-even pattern across both lungs. This inflammation is a sign the body is fighting back against the virus – in that battle, the lungs are ground zero. But Professor Collignon warns sometimes the collateral damage can be worse than the bug itself.

CT scans from a 77-year-old man with COVID-19 in China over 10 days, showing ground-glass opacity of the lungs and lesions. The man died 10 days after the final scan. Credit:The Lancet medical journal

Recently, doctors have also begun to report more cases of patients hit by "silent hypoxia" - seemingly mild cases, recovering at home, suddenly crashing. The reason? Their oxygen levels were dangerously low but they weren't getting the usual warning signs such as difficulty breathing.

At the WHO, assistant director-general Bruce Aylward warns when danger strikes, it's often fast-moving. Doctors report patients can go downhill quickly during those "critical" second and third weeks and urge people with or suspected to have the virus to monitor their symptoms, particularly their breathing and fever. Infectious diseases physician Sanjaya Senanayake says he's seen patients develop "bad shortness of breath" around the second week of symptoms. "Then if they're going to get very sick, about two-and-a-half days later, they [usually] start to develop fluid in their lungs."

In the case of COVID-19, Professor Collignon says patients generally appear to have mild symptoms for the first week or so. In severe cases, they can intensify into bad pneumonia during the second and, in rarer cases, the infection will turn unexpectedly deadly.

Falling blood oxygen levels put pressure on other organs, in particular the heart. More systems can start to fail, and blood pressure too, which, if it falls low enough can tip the body into septic shock, a whole-body infection.

"Even if the virus spreads to the heart or the kidneys and damages them, the real cause of death is still probably going to be oxygen levels falling and setting everything else off," Professor Collignon says. "If you're an older person or already unwell and those organs are weaker, it can be the straw that breaks the camel's back."

While there is a theory that people with already compromised immune systems might escape this effect and so cope with an infection better than expected, Professor Collignon warns they are especially vulnerable to the other big killer – co-infection.

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Usually being hit with two bugs at once is rare, though not impossible. But as the virus chews through cells, it leaves the lungs less able to filter out germs picked up from the nose and throat – and wide open to a case of the flu or even a bout of bacterial pneumonia. (The first man to die from COVID-19 in Thailand was reportedly also sick with dengue fever.) During the deadly 1918 Spanish Flu pandemic, most victims died not from the original virus but due to these second-wave bacterial pneumonia infections. Fortunately, medicine has advanced a lot since then (and discovered antibiotics), making such complications much easier to treat.

So who is at risk of serious complications?

Based off that first big data set out of China, the WHO estimated about 20 per cent of cases became severe, requiring medical intervention for serious breathing difficulties and falling blood oxygen levels. Of those, 6 per cent were pushed into critical care – as multiple organs began to fail alongside the lungs or septic shock set in. About 3.4 per cent died. But experts expect the real death rate is actually much lower, given so many mild cases will likely go undiagnosed.

Still, as the virus has spread across the world, taking hold in Europe and the US with particular ferocity, WHO spokeswoman Dr Margaret Harris says that the number of people requiring medical intervention (such as ventilation) is actually more like 30 per cent than 20. "And even if you don't need to go to hospital, it's [usually] not mild, it's still pneumonia. I've had colleagues absolutely slammed by it, struggling to breathe and exhausted for weeks."

Older people and those with other conditions such as diabetes or heart disease are most at risk of fatal complications. ("Over the age of 50, the immune system starts to fall apart," Professor MacIntyre explains). But in Italy, where the virus gained a particularly deadly foothold, doctors have also warned that younger patients (in their 30s, 40s and 50s) have arrived at overwhelmed emergency departments needing help to breathe.

Data since compiled from elsewhere in Europe and North America also reflects a concerning number of hospitalisations among people under 55, prompting warnings for younger adults to take COVID-19 more seriously. In Australia, Deputy Chief Medical Officer Paul Kelly has said many of those in ICU with the illness have been younger without other risk factors. "This is not just an old person's disease," he said. Australians in their 20s have seen the highest number of coronavirus infections of any age bracket.

Fortunately, very few children have been diagnosed or suffered serious cases globally – a phenomenon also observed during SARS. Still, they are not immune and some have died from the illness, including the heartbreaking case of a six-week-old baby in the United States.

Smokers are considered more at risk, as early studies show the same cell receptors (ACE2) the virus hijacks in the lungs increase with cigarette smoke. But pregnant women and breastfeeding mothers so far do not appear in any heightened danger, as they were during the last pandemic, the 2009 swine flu. Still, they should take precautions as they are known to be more susceptible to other common respiratory viruses.

Whatever your personal vulnerability, the dose of virus you first receive – say, from touching a contaminated door knob versus caring for an infected person over several days – also plays a big part in how your body copes. "The higher the dose the faster you will get sick, and the harder it will be on you," Professor MacIntyre says.

That could explain why otherwise young and healthy medical workers have died from the disease. Li Wenliang, the 34-year-old doctor who blew the whistle on early cases of COVID-19 in China, went through a gamut of treatments after falling ill himself, including antivirals, antibiotics, even having his blood pumped through an artificial lung, but he died weeks later. As with SARS, clusters of severe infection are emerging in hospitals and households as people come into sustained close contact.

What other complications are emerging?

In hospitals from China to Italy to New York overrun with COVID-19, doctors have reported other mysterious complications in patients, though at much lower numbers. What starts as a respiratory problem suddenly morphs into a seizure or a heart attack. Others are hit with strokes or blood clots, even down in their toes. Some go into kidney failure.

Australian neurologist Dr Thomas Oxley recalls operating on a COVID-19 patient in New York in April - the man had been doing fine at first, he was 44, healthy, at home during the city's lockdown. Then suddenly he was in Oxley's hospital with a giant clot in his brain - he had had a stroke.

Oxley, who has just published clinical data on a cluster of strokes among young COVID-19 patients, says the virus is not just behaving like your typical respiratory illness. Doctors are finding it is spreading in the heart, kidneys, gut, blood vessels, even the brain itself. As he sucked out the clot from inside the skull of that 44-year-old man, Oxley says another began to form even before his eyes.

"This isn't like anything else we've seen before. There was a few reports of strokes and clotting with SARS in Singapore, but this looks pretty unusual," Oxley says. "We know the virus latches onto ACE2 and that's in a lot of places. If you follow it around the body, you can hunt down the virus."

When Australian opera singer Helena Dix was rushed to hospital with COVID-19 complications late last month, doctors told her she was famous.

"Not for my high notes, unfortunately – it was for the size of the blood clot in my lungs," she says. "They said it was one of the biggest they had ever seen. They couldn’t believe I was still breathing."

Australian opera singer Helena Dix, performing in Norma for Melbourne Opera last year (left), and in a British hospital (right) after developing a large blood clot in her lungs. Credit:Robin Halls

But Dix had been training for just such an emergency all her life without realising it - performing all around the world as a talented soprano.

"Singers are the Olympic athletes of breathing," says Dix, who is now recovering at her home in Britain. "What was so terrifying about this was I had to use all my exercises, everything I knew about breath, and it still ... took it away."

So why is this happening? One theory is that inflammation, likely caused by the body's same over-zealous immune response, disrupts the natural clotting mechanism of the blood vessels.

"Of course, ACE2 is found in the walls of blood vessels too so our working theory is that it attacks the vessels and starts an inflammation cascade," Oxley says. "Our hospital [Mount Sinai] has now updated its guidelines so every COVID-19 patient sick enough to be in ICU is now being put on powerful blood thinners right away."

Senanayake agrees clotting is now one of the main mysteries facing doctors treating COVID-19, though the cases still appear to be low and mostly among severe patients. In Australia, where total infections are relatively few, health authorities say they are yet to see patients suffering from strokes or clotting. Both Senanayake and Deputy Chief Medical Officer, Nick Coatsworth, say it's unclear what is causing it – it could well be part of the usual stress of a serious infection on the body and long stays in ICU.

"We're seeing other strange [complications] and neurological symptoms too," Oxley says. "Seizures and confusion, really bad fatigue, kind of a haziness."

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How do doctors treat COVID-19?

Despite the breakneck speed of global research, a safe and effective vaccine for COVID-19 is still not a guarantee and is likely at least a year away. And, while antivirals and therapies that block diseases such as malaria, Ebola and HIV are being trialled against the new disease in some parts of the world, including Australia, treatment right now is largely about managing complications – providing oxygen, keeping up fluids and monitoring how the body is coping. Antibiotics don't work on the virus as it is not caused by bacteria but they can be deployed against secondary infections. If breathing starts to fall, respirators and other measures will kick in to keep the lungs going.

As Professor Lewin explains, doctors have a key choice when treating any new virus: is it better to block it directly with antiviral therapies that stop it replicating in our cells or should they instead help the body recover, dampening down the body's immune response using drugs such as Interferon, to minimise the fall-out damage?

"Sometimes that can help but sometimes it means the infection overwhelms," Professor Lewin says. "It didn't work with SARS but there's been some success with MERS. Already for this, there's been candidate [therapies] that look good in test tubes, but we need [results] from our trials.

No vaccine exists for either SARS or MERS – the former died out within about nine months so an inoculation never hit the market while the less common MERS has struggled to attract research funding since it emerged in 2012. After the big Ebola outbreak of 2014, a global group formed to speed up research into vaccines and MERS was recently identified as a priority. "Then this new one hit," Professor Lewin says. Nobel-prize-winning immunologist Professor Peter Doherty sighs a similiar accelerator program for drug therapies should have been set up too.

The Doherty Institute has now launched a major international trial with New Zealand, meaning most COVID-19 patients in the region will be able to opt in for an experimental drug. During the last pandemic, swine flu, experts say two anti-virals that already worked on the illness helped keep the death toll relatively low, even though it spread to about 20 per cent of the world's population. Finding a treatment could be a gamechanger this time too.

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But Professor Collignon warns against rushing the science - without large, well run-trials, small studies can miss big problems on roll-out.

Experts have also been wary of increased pressure on hospitals if severe coronavirus cases hit wards all at once. While Australia's healthcare system is strong compared to other countries, its population is also older, Professor MacIntyre notes, meaning more demand for intensive care. To slow the spread of the virus and avoid a "pinch" around flu season, Australia has followed other countries in rolling out stricter containment measures such as quarantining suspected cases, shutting down gatherings and ordering people to stay home except for essential reasons. So far it's working - a surge in new infections in mid-March has now dramatically flattened. But the world is still holding its breath for a second wave, even as it slowly wakes back up from lockdown.

What happens if I have to go to intensive care?

On March 27, Prime Minister Boris Johnson revealed he had himself tested positive for coronavirus. At first, his symptoms were mild, a fever and a cough. But when his temperature remained high more than 10 days later, he was moved to hospital, and from there into intensive care.

Most people with COVID-19 end up in hospital because they're having trouble breathing, says the head of the Alfred Hospital’s intensive care unit, Associate Professor Steve Mcgloughin. Once admitted and getting oxygen via a mask, a person’s condition may improve – but others will need ventilators or other machines to keep their lungs and organs working.

Anyone who’s had a general anaesthetic will have relied on a breathing machine known as a ventilator, whether they know it or not. But Dr Suzi Nou at the Australian Society of Anaesthetists says that while a patient having routine surgery will need a ventilator for minutes or hours – perhaps a few days in ICU – a patient with COVID-19 might need one for as long as 10 days. Around the world the machines are now worth their weight in gold.

Opera singer Helena Dix used singing in hospital to help test her breathing and keep her spirits up.

On April 12, Johnson left hospital, crediting its staff with saving his life as "it could have gone either way". He recalled how two ICU nurses watched over him around the clock, adjusting his oxygen. “The reason, in the end, my body did start to get enough oxygen was because for every second of the night they were watching and they were thinking and they were caring.”

For some, oxygen is not the only concern, as the complications outlined above take hold.

How long does recovery take and is damage permanent?

Symptoms tend to clear up within a fortnight in mild cases or six weeks for more serious cases, Senanayake says.

Australian researchers have now mapped the body's immune response, identifying the antibodies it recruits to defeat the new virus, in some people starting the fight within just three days of the initial infection.

University of Sydney infectious diseases expert Robert Booy says there's "no doubt" the virus particularly affects the lungs in the days and weeks following a case. Scarring, even in the heart, might be detected for months or years in certain patients, he says. But it's too early to know for sure how often the illness will lead to this kind of permanent damage – such as the lung tissue scarring seen in some severe SARS and MERS patients.

Doctors studying the virus expect the small subset of patients with neurological symptoms including confusion, stroke and seizures could experience more long-term impairment. But University of NSW senior medical virologist Professor Bill Rawlinson says that, while it's still guesswork right now, most of the evidence points to a majority of patients making a full recovery.

Is a person immune after catching the virus?

Our immune system has a memory but it's not perfect. Successfully fighting off a virus generally leaves us armed with antibodies ready for round two should it comes back, which usually gives us at least a period of immunity (if not always a lifelong shield).

But with COVID-19, there are still questions about how many antibodies patients produce and how long they might last – some early studies have found disappointingly low numbers. Common coronaviruses such as the ones that give you a cold tend to go away for at a few months or a year before we become susceptible again. Studies of MERS-CoV has found antibodies still present in survivors more than 18 months after recovery, and some survivors of SARS retained antibodies for many years though actual immunity time is not clear.

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For COVID-19, there have already been cases of people cleared of the virus, only to test positive again days later or, in the case of one woman, more than a month down the line. But while experts say it's possible to be reinfected, it's more likely the virus was still in their system. Some studies have even suggested it can lie dormant in other parts of the body for weeks, with the longest period of infectiousness so far recorded as 37 days. "But in some cases, when people are returning persistently positive tests after getting better, they might be finding dead virus," Senanayake says.

Amid a shortage of testing kits worldwide, Australia has so far only been retesting frontline staff in health and aged care to confirm their recovery. That means official recovery data remains patchy. Most patients are instead told to wait 72 hours after symptoms disappear (provided they have already isolated for 10 days from illness onset).

A federal government spokesman said a patient who keeps testing positive after symptoms vanish is not necessarily still infectious. "There have been case reports of patients testing positive for a couple of weeks post-symptom resolution, but are viral culture negative – meaning they are unlikely infectious for very long after symptoms resolve," he said.

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Back in Wuhan, Reed was cleared to leave his own home quarantine months ago but, along with tens of millions of people in China, he'd spent the first three months of 2020 under lockdown. On April 8, the streets finally reopened. Residents waved flags and sang songs as they left their homes for the first time in 11 weeks. While the local government did not appear to pick up early cases of the virus, Reed says China took the right step, however extreme, in shutting down parts of the country. The government's data says new infections have all but stopped within its borders, even as new frontiers of the virus rage in the US and Europe.

"In Italy, it seems to be a similar thing to Wuhan," Reed says. "The virus was there but people didn't notice; it was brewing quietly for a while and then it suddenly exploded. Now they've followed China with lockdowns. Australians need to take this seriously."

If you suspect you or a family member has coronavirus you should call (not visit) your GP or ring the national Coronavirus Health Information Hotline on 1800 020 080.

With Felicity Lewis

This article was originally published on March 13 and has been updated to include new research.