Passengers arrive at Heathrow Airport Britain
Passengers arrive at Heathrow Airport, as Britain launches its 14-day quarantine for international arrivals, following the outbreak of the coronavirus disease (COVID-19), London, Britain, June 8, 2020. Image Credit: Reuters

Like millions of others around the world, Gulf News Foreign Correspondent Mick O’Reilly is currently under COVID-19 lockdown. This is what life is like in social isolation in Ireland, where there are strict rules about who is allowed out, where, and under limited circumstances.

DAY 75: Friday June 12, 9am



So, four months into this pandemic and 75 days of my lockdown in Ireland, if you were to ask people “where did coronavirus come from?” – their answer is likely to be China. But now researchers have found evidence that in Britain at least, coronavirus was brought into the UK on at least 1,300 separate occasions. The researchers can say that by their analysis of the genetics of the virus.

The study, by the COVID-19 Genomics UK consortium (Cog-UK), completely quashes the idea that a single “patient zero” started the whole UK outbreak.

Significantly, the analysis also finds China, where the pandemic started, had a negligible impact on cases in the UK. Instead those initial cases came mostly from European countries.

The researchers analysed the genetic code of viral samples taken from more than 20,000 people infected with coronavirus in the UK. Then, like a gigantic version of a paternity test, the geneticists attempted to piece together the virus’ massive family tree.

This was combined with data on international travel to get to the origins of the UK epidemic.

They found the UK's coronavirus epidemic did not have one origin – but at least 1,356 origins. On each of those occasions somebody brought the infection into the UK from abroad and the virus began to spread as a result.

The first Irish infections have been traced to people who travelled to Northern Italy or Austria, or from those who entered from the UK having been in contact with someone carrying the virus.


“The surprising and exciting conclusion is that we found the UK epidemic has resulted from a very large number of separate importations,” said Prof Nick Loman, from Cog-UK and the University of Birmingham. “It wasn't a patient zero.”

The study showed that less than 0.1 per cent of those imported cases came directly from China. Instead the UK’s coronavirus epidemic was largely initiated by travel from Italy in late February, Spain in early-to-mid-March and then France in mid-to-late-March.

“The big surprise for us was how fluid the process was, the rate of and source of virus introduction shifted rapidly over the course of only a few weeks,” said Prof Oliver Pybus, from the University of Oxford.

“This happened later than perhaps we would have expected,” added Prof Loman.

The study estimates 80 per cent of those initial cases arrived in the country between February 28 and March 28 – the time the UK was debating whether to lockdown. After this point, the number of new imported cases diminished rapidly.


The earliest one could be traced back to the beginning of February, but it is possible there were cases even earlier that could not be picked up by the analysis.

The study also says the controversial football match between Liverpool and Atletico Madrid, on March 11, probably had very little impact on bringing the virus into the country.

An estimated 3,000 fans flew in from Spain to watch the game, but there were 20,000 people flying in from Spain every single day in mid-March.

“It shows that individual events such as football matches likely made a negligible contribution to the number of imports at that time,” the study says.

The imported cases each started off a chain of transmission where the virus is passed from one person, to the next, to the next and so on.

However, the study shows lockdown has massively disrupted the spread of the virus. “If there’s good news here, these chains of transmission were and are being suppressed and going extinct as a result of social distancing and we continue to see that now,” Prof Loman said.


One expert who had advised the UK government suggested that imposing the lockdown a week earlier in March could have halved the death toll.

Professor Neil Ferguson’s comments came as the number of deaths involving COVID-19 in the UK passed 52,000, according to analysis of the latest available data.

The Imperial College London academic told the Commons Science and Technology Committee: “The epidemic was doubling every three to four days before lockdown interventions were introduced.

“So, had we introduced lockdown measures a week earlier, we would have reduced the final death toll by at least a half.”

Professor Ferguson’s modelling of the infection was instrumental in the lockdown being introduced but he later quit the Scientific Advisory Group for Emergencies (Sage) panel advising ministers after flouting the restrictions.

Asked about Professor Ferguson’s claim, Johnson said “all such judgments will need to be examined in the fullness of time”.

Culture Secretary Oliver Dowden, when asked about the professor’s remarks on ITV’s Peston programme, said: “There will be a time when we need to look at the lessons.”


The World Health Organisation has said that the COVID-19 pandemic is “still evolving” and is “by no means over”.

Speaking at a press conference in Geneva this afternoon, Michael Ryan, the WHO’s emergencies director said the virus is “growing in many parts of the world” and putting pressure on health services globally.

“We see health facilities now in many, many countries coming under huge pressure and strain, maybe not in Europe, maybe not in North America, but certainly in Central and South America, certainly in other parts of the world,” he said.

“I think each and every country has a different combination of risks and opportunities at this point, and it’s really down to national authorities to carefully consider where they are in the pandemic.

This may be a pandemic, it may be affecting the world, but it’s affecting each and every country in a different way depending on when the disease came, how the initial responses were managed and depending on how the disease is evolving at this point.

“And by no means is this over, if we look at the numbers over the last number of weeks, this pandemic is still evolving. It is still growing in many parts of the world,” he added.

Ryan also said there is “no indication yet” if the virus will be seasonal, as is the case with the winter influenza season.


Speaking at the same press conference, WHO director general Tedros Adhanom said that political leaders should commit to making any COVID-19 vaccine “a global public good”.

Adhanom said that those who need a vaccine should be ensured of getting it.

“There should be a political commitment by political leaders to have consensus on making vaccines a global public good. If there is no political commitment and public political support to make it a global public good then we will have a problem,” he said. “So I would use this as an opportunity to call on leaders to add their voices. So when a vaccine is discovered that it should be a global public good and access to those who needs is ensured.”

UN Secretary General Antonio Guterres also last week backed the development of a “people’s vaccine” for the new coronavirus that is available to everyone globally.

Chinese President Xi Jinping has previously stated that any vaccine developed in China would be designated as a global public good. China says it has five potential vaccines already in clinical trials.

Speaking in response to a question from a South African journalist, Adhanom also said the WHO would ensure that African countries would not become a “testing ground” for COVID-19 vaccines.


The arrival of warmer weather in the Northern Hemisphere raises the question of whether summer could slow the spread of the coronavirus outbreak.

While warmer weather typically ends the annual flu season in temperate zones, climate alone has not stopped the COVID-19 pandemic from sweeping any part of the globe. In fact, outbreaks in hot and sunny Brazil and Egypt are growing.

Still, recent data about how sunlight, humidity and outdoor breezes affect the virus gives some reason for optimism that summer could slow the spread.

The virus has not been around long enough for experts to know if coronavirus will be affected by seasonal factors to be certain.

Respiratory infections like flu and the common cold follow seasonal patterns in temperate regions. Environmental conditions including cold weather, low indoor humidity, and spending more time indoors can all hasten the spread of an epidemic.

Real-world evidence about the effect of weather on the new virus is mixed. One study of 221 Chinese cities found that temperature, humidity and daylight did not affect speed of spread.

Two other studies did find an effect, including a look at new infections in 47 countries that linked higher temperatures to slower transmission in places like the Philippines, Australia and Brazil.

“The Northern hemisphere may see a decline in new COVID-19 cases during summer and a resurgence during winter,” concluded the authors of another study of 117 countries, which found that each 1-degree of latitude increase in distance from the Equator was associated with a 2.6 per cent increase in cases.

The WHO’s Ryan cautioned: “We cannot rely on an expectation that the season or the temperature will be the answer to the disease’s spread.”


“The reason why cold weather is presumed to cause spreading of coughs, colds and flu is that cold air causes irritation in the nasal passages and airways, which makes us more susceptible to viral infection,” said Simon Clarke, an expert in cellular microbiology at Britain’s University of Reading.

Winter weather tends to inspire people to spend more time indoors, although air conditioning may also bring people back inside in the summer.

In the lab, when temperatures and humidity rise, coronavirus particles on surfaces more quickly lose their ability to infect people - and they are inactivated especially fast when exposed to sunlight, U.S. government researchers found.

It is still a good idea for people to wash hands frequently, practice social distancing and wear a mask in summer, experts say. While virus particles coughed or exhaled by an infected person will disperse faster outdoors, one study found a gentle breeze could carry saliva droplets up to six metres.


Vitamin D: Researchers are investigating whether levels of immunity-regulating vitamin D in people’s blood affect how vulnerable they are to infection with the new coronavirus or how sick they become. The majority of vitamin D in the body comes from skin exposure to sunlight.

Pollen: A study in the Netherlands of all “flu-like” illness, including COVID-19, in recent years concludes that pollen concentrations are a better predictor than sunlight of respiratory disease trends. Clouds of pollen act as air filters, snagging virus particles, and pollen activates immune responses, even in people without overt allergies. The study found that flu-like illness started to drop when pollen in the air reached 610 grains per cubic metre, a typical level from early spring to October in most middle latitudes.


I came across this on Facebook and it reminded me of when I lived in Dubai and pretty much everyone had a maid a couple of times a week or more to clean their home

Image Credit:



Sitting in a window seat—and staying seated for the duration of the flight—may be your best bet for not getting sick from fellow passengers. That’s according to researchers at Emory and Georgia Tech in a study published in the Proceedings of the National Academy of Sciences.

Sick passengers will most likely not transmit droplet-spread infections to passengers seated farther than two seats beside them, and one row in front or in back.

Vicki Hertzberg, an Emory nursing professor, and Howard Weiss, a Georgia Tech mathematics professor, assessed rates and routes of possible germ transmission during flights. Team members monitored specific areas of the passenger cabin during five round trips from the East to West Coast of the United States recording movements of passengers and crew. They collected air samples and surface samples from areas most likely to harbour microbes. The study, funded in partnership with Boeing, used the data to create thousands of simulated flight scenarios.

“Respiratory diseases are often spread through close contact,” says Hertzberg. “We now know a lot about how passengers move around on flights.” Around 40 percent of passengers never leave their seats, another 40 per cent get up once during the flight, and 20 per cent get up two or more times. Also, people closer to the aisle moved around more: About 80 per cent of those in aisle seats got up during the flight, 60 per cent in middle seats, and 40 per cent in window seats.

Passengers who leave their seats are up for an average of five minutes.

Another way germs are spread, researchers found, was through exposure to viruses that remain on surfaces such as tray tables, seat belts, and handles. Fliers “can eliminate this risk of indirect transmission through hand hygiene and keeping their hands away from their nose and eyes,” the study says.


I came across and interesting element on NBC where those under lockdown posted their one line confessions from lockdown. What they thought, what they did, their fears and other worries or concerns. The comments show that we’re pretty much the same the world over.. You can always share yours to and mark it for the Going Viral blog.

Here are today’s 25 confessions:

1: No more wearing makeup since I have to wear a mask at the office. It’s the little things that count.

2: Friends widening circles, socialising without masks or distancing. COVID-19’s not over! Pre-existing conditions here.

3: My hospital is asking employees to self-monitor their symptoms for COVID-19. If you’re sick stay home. No screening by employer.

4: My manager took a poll asking if we felt safe and were being paid enough. After hours and salaries were cut. I lied and said yes.

5: I want this pandemic to end so I can finally get a hug again or spend time with my family and friends. I miss people!

6: I haven't been allowed to see my husband in months as our marriage is "nonessential."

7: At this point, I feel more concerned about the selfish, dangerous behavior of my “fellow citizens” than I do about the virus.

8: My father just passed away from battling a heart condition for years and I can't see any of my friends or family for support.

9: I worry about my nine years with asthma and the resident I care for. I can barely sleep at night. God help me.

10: Only "essential" employees are currently onsite at my workplace. Next week, they are due back. I'm nervous to be around them.

11: I am overwhelmed.

12: I don't social distance. I see my boyfriend three times a week.

13: I’ve gained weight since quarantine started. Glad there’s not the possibility of running into my ex in public, I can’t go anywhere.

14: I'm a law enforcement officer who has tested positive for the COVID-19. Here's to 2020 being quarantined away from society.

15: My job can be done from home but here I am at the office! Someone has to train the new people if I’m to die.

16: My daughter’s graduation is at the end of May and I’m probably going to have a nervous breakdown about going. 500 plus in her class.

17: I have friends who don’t talk to me anymore due to my concerns about the virus and their wellbeing. I’m told I’m overreacting.

18: I am tired of watching my neighbours have parties in their backyard while our family is social distancing.

19: My brother admitted himself for suicidal thoughts, and it killed me that I couldn't be at the hospital while he waited.

20: Never realised how much I hate my job and the people I work with until now.

21: I feel guilty that I hate my brother because he is in a strong happy relationship and mine is on the rocks.

22: The school told me to consider dropping their programme if I am having a hard time with it while taking care of my eight-month-old child.

23: It doesn’t help when my mom says to stay positive. In fact it angers me. I have a right to feel upset with this situation.

24: Had to tell a guy to back up while checking out. He asked why and I told him social distancing. He said, “you’re one of those!”

25: Recently divorced. Those complaining about spending "too much time" with their spouse are selfish, ungrateful, and stupid.


Surgeons have performed a double lung transplant on a COVID-19 patient in Chicago, the hospital that carried out the procedure said Thursday, in what is thought to be a first in the United States.

The patient is a young Hispanic woman in her twenties, and had spent six weeks on a life support machine in the intensive care unit of Northwestern Memorial Hospital in Chicago.

By early June, her lungs had become so badly damaged that it was decided that a transplant was her only option.

“A lung transplant was her only chance for survival,” said Ankit Bharat, chief of thoracic surgery and surgical director of the Northwestern Medicine Lung Transplant Programme.

He added that while the procedure itself was “technically challenging,” it can be performed safely and thus “offers the terminally ill COVID-19 patients another option for survival”.

It is believed to be the first time a double-lung transplant for a COVID-19 patient has taken place in the US. China previously announced a similar operation on a 66-year-old woman, in March in eastern Zhejiang province.


Before the US patient could receive the transplant, she had to test negative for the SARS-CoV-2 virus and needed her other organ systems working well enough to give her a realistic chance of surviving.

“For many days, she was the sickest person in the Covid ICU – and possibly the entire hospital,” said Beth Malsin, a critical care doctor.

“There were so many times, day and night, our team had to react quickly to help her oxygenation and support her other organs to make sure they were healthy enough to support a transplant if and when the opportunity came.”

It was this combined effort – keeping her alive on life support long enough for her body to clear the virus and test negative – that paved the way for the successful outcome.

It is very unusual for a young woman to have suffered such extensive lung damage from the coronavirus, and doctors hope to study her closely to learn more about why this happened.

For now, they are hopeful she will go on to make a full recovery despite having almost succumbed to multi-organ failure.



This is a week that I’d rather forget – with four days of trading wiping more than £1,000 off my portfolio. Thankfully, it’s just pretend!

A reminder that this is all pretend, I started out in lockdown with £10,000 – about Dh45,000 to invest on the London Stock Exchange, I don’t pay for trades and I can only buy or sell when the market is closed. There’s no minimum on the amount of stocks I can buy, just as long as I can afford them.

Markets in Asia, Europe and North America were all down on Thursday – in part because of the US Federal Reserve Bank issuing a bleak forecast for the US economy moving out of the coronavirus pandemic. I am not alone in feeling pain.

This is how things stand:

Net worth £13,045.88

Ocado, 100 shares: £1960.00

Diageo, 100 shares: £2774.00

PowerHouse, 1200 shares: £4200.00

Ryanair, 350 shares: £3878.00

Cash in hand: £233.88

£ loss on last trading day: £505.80

% gain overall: 30.4 per cent

£ Gain overall: £3,045.88


Researchers have been looking at why do some people infected with the coronavirus suffer only mild symptoms, while others become deathly ill?

Geneticists have been scouring our DNA for clues. Now, a study by European scientists is the first to document a strong statistical link between genetic variations and COVID-19, the illness caused by the coronavirus.

Variations at two spots in the human genome are associated with an increased risk of respiratory failure in patients with COVID-19, the researchers found. One of these spots includes the gene that determines blood types.

Having Type A blood was linked to a 50 per cent increase in the likelihood that a patient would need to get oxygen or to go on a ventilator, according to the new study.

The study was equally striking for the genes that failed to turn up. The coronavirus attaches to a protein called ACE2 on the surface of human cells in order to enter them, for example. But genetic variants in ACE2 did not appear to make a difference in the risk of severe COVID-19.

The findings suggest that relatively unexplored factors may be playing a large role who develops life-threatening COVID-19. “There are new kids on the block now,” said Andre Franke, a molecular geneticist at the University of Kiel in Germany and a co-author of the new study, which is currently going through peer review.


Scientists have already determined that factors like age and underlying disease put people at extra risk of developing a severe case of COVID-19. But geneticists are hoping that a DNA test might help identify patients who will need aggressive treatment.

Figuring out the reason that certain genes may raise the odds of severe disease could also lead to new targets for drug designers.

As the pandemic gained momentum in February, Dr. Franke and his colleagues set up a collaboration with doctors in Spain and Italy who were struggling with a rising wave of COVID-19.

The doctors took blood samples from 1,610 patients who needed an oxygen supply or had to go on a ventilator. Dr. Franke and his colleagues extracted DNA from the samples and scanned it using a rapid technique called genotyping.

The researchers did not sequence all three billion genetic letters in the genome of each patient. Instead, they looked at nine million letters. Then the researchers carried out the same genetic survey on 2,205 blood donors with no evidence of COVID-19.

The scientists were looking for spots in the genome, called loci, where an unusually high number of the severely ill patients shared the same variants, compared with those who were not ill.

Two loci turned up. In one of these sites is the gene that determines our blood type. That gene directs production of a protein that places molecules on the surface of blood cells.


It’s not the first time Type A blood has turned up as a possible risk. Chinese scientists who examined patient blood types also found that those with Type A were more likely to develop a serious case of COVID-19.

No one knows why. While Dr. Franke was comforted by the support from the Chinese study, he could only speculate how blood types might affect the disease. “That is haunting me, quite honestly,” he said.

He also noted that the locus where the blood-type gene is situated also contains a stretch of DNA that acts as an on-off switch for a gene producing a protein that triggers strong immune responses.

The coronavirus triggers an overreaction of the immune system in some people, leading to massive inflammation and lung damage — the so-called cytokine storm. It is theoretically possible that genetic variations influence that response.

A second locus, on Chromosome 3, shows an even stronger link to COVID-19, Dr. Franke and his colleagues found. But that spot is home to six genes, and it is not yet possible to say which of them influences the course of COVID-19.

One of those gene candidates encodes a protein known to interact with ACE2, the cellular receptor needed by the coronavirus to enter host cells. But another gene nearby encodes a potent immune-signaling molecule. It is possible that this immune gene also triggers an overreaction that leads to respiratory failure.


Dr. Franke and his colleagues are part of an international effort called the COVID-19 Host Genetics Initiative. A thousand researchers in 46 countries are collecting DNA samples from people with the disease. They are now beginning to post data on the initiative’s website.

Andrea Ganna, a genetic epidemiologist at the University of Helsinki, said that initiative’s collected data were beginning to point to a single spot on Chromosome 3 as a potentially important player.

It’s not common for genetic variants to emerge out of studies of so few people, said Jonathan Sebat, a geneticist at the University of California, San Diego, who was not involved in the new study.

“We were all hoping optimistically this was one of those situations,” Dr. Sebat said.

Previous attempts to find any genetic loci that varied significantly between sick people and healthy ones have failed. Dr. Sebat speculated that the new study succeeded because the researchers focused only on people who had respiratory failure and were clearly vulnerable to serious forms of COVID-19.

“They had the ideal cohort,” he said.

New studies, such as the one Dr. Sebat is running in California, will allow scientists to see if the two loci really do matter as much as they seem to now.

The geneticists may be able to zero in on exactly which gene in each locus affects the disease, he said. And researchers will most likely find many other genes with subtler influences on the course of COVID-19.


A regular reminder that covidiocy is passed at surface level….


Tottenham midfielder Dele Alli has been suspended for one match by the English Football Association over a post on social media about coronavirus.

Alli, 24, put a video on Snapchat in February in which he joked about the outbreak and appeared to mock an Asian man. The England international has also been fined £50,000 and ordered to undertake an education course. He will miss Spurs' match at home to Manchester United on 19 June.

The video posted by Alli showed him wearing a face mask in an airport lounge, before moving the camera to show a man of Asian appearance, and then zooming in on a bottle of antiseptic hand wash.

In his hearing, Alli said that he had “very quickly” realised the video may have the “potential to cause upset” and deleted it before catching his flight. However, he said he had been “betrayed” by a friend who sold the video on his private account to the media.

In a statement, Alli said: “In response to the FA decision, I would like to apologise again for any offence caused by my behaviour. It was an extremely poorly judged joke about a virus that has now affected us more than we could ever have imagined. I’m grateful that the FA has confirmed that my actions were not racist because I despise racism of any kind. We all need to be mindful of the words and actions we use and how they can be perceived by others.”


Spain has fined Belgium’s Prince Joachim €10,400 euros (Dh43,500) for breaking quarantine rules last month during a trip to the country, where he tested positive for the coronavirus, a Spanish government official said.

The prince, 28, who is the nephew of Belgium’s King Philippe, travelled to the southern Spanish region of Andalusia from Belgium on May 24 for an internship.

He has been penalised for failing to quarantine himself for 14 days on arrival, a requirement for anyone entering the country, the government official in Andalusia told Reuters.

Prince Joachim admitted breaching quarantine rules, and has 15 days to respond to the fine, the official said.

The prince’s lawyer could not immediately be reached for comment.

Prince Joachim, who is tenth in line to the Belgian throne, tested positive after attending a party in the city of Cordoba on May 26.

The official said the prince is now quarantined in Spain.

Spanish authorities are investigating the party, which Spain’s El Pais newspaper reported last month was attended by 27 people. This would have breached lockdown rules in Cordoba, where restrictions capped gatherings at a maximum of 15 people.

However, a source close to the Belgian Royal Palace said that the prince had attended two separate gatherings, with 12 people at one and 15 at the other.


I’m not an expert, but I might be able to help you make a bit of sense of this. And we can all get through it together. Isn’t this what this is all about.

Send your questions for me to

That’s it for now. Let’s check in with each other tomorrow. I have used files from Reuters, AP, DW, Sky News, Twitter and other European and North American media outlets in today’s blog. And remember to stay safe.

Mick O’Reilly is the Gulf News Foreign Correspondent based in Europe