Covid: France and Poland increase lockdown measures as infections surge

 

France and Poland have reintroduced partial lockdowns as both countries battle a sharp rise in Covid infections in recent weeks.

Some 21 million people in 16 areas of France, including the capital Paris, are affected as the country fears a third wave.

In Poland, non-essential shops, hotels, cultural and sporting facilities are now closed for three weeks.

The country has the highest new daily rates of Covid cases since November.

Coronavirus cases are also rising exponentially in Germany, with Chancellor Angela Merkel warning it is likely that the country will now need to apply an "emergency brake" and re-impose lockdown measures.

Covid wave intensifies in Central Europe

Why is the EU having vaccine problems?

The vaccine rollout across the European Union has been hindered by delayed deliveries, as well as the suspension in several countries of the use of the Oxford-AstraZeneca Covid-19 vaccine, over fears of possible side effects.

What's the situation in France and Poland?

In France, the partial lockdown took effect from midnight on Friday.

Trains leaving Paris for parts of the country where lockdown restrictions do not apply, such as Brittany and Lyon, were reportedly fully booked hours before the measures were due to come into effect.

Traffic jams were reported on several roads leaving the capital.

The new restrictions are not be as strict as the previous lockdown, with people allowed to exercise outdoors.

Non-essential businesses are shut, but schools remain open, along with hairdressers if they follow a "particular sanitary protocol".

France has reported more than 4.2 million infections since the start of the outbreak, with nearly 92,000 Covid-related deaths, according to the data compiled by Johns Hopkins University in the US.

In Poland, the three-week lockdown began on Saturday.

Polish health officials earlier warned the nationwide restrictions were necessary because of a rampant British variant of Covid-19 in the country. The variant now makes up more than 60% of infections.

Poland has had more than two million confirmed infections, and nearly 49,000 deaths, according to Johns Hopkins University.

Germany said on Friday it was now classifying neighbouring Poland as high risk. This means that from Sunday anyone crossing the border from Poland must provide a negative coronavirus test.

What's the latest on the AstraZeneca vaccine?

Despite assurances from the European medicines regulator that the AstraZeneca vaccine is safe and effective, some countries remain reluctant to resume their campaigns using the jab.

Finland's health authority has announced a pause in its use of the vaccine that will last at least a week.

The move, which follows two reports of blood clots in patients who had received the jab in the country, was said to be a precautionary measure.

Is the Oxford-AstraZeneca vaccine safe?

Is Europe's AstraZeneca jab decision-making flawed?

Meanwhile, Sweden, Denmark and Norway said on Friday that they needed more time to determine whether they should resume AstraZeneca inoculations.

Germany, Italy, France, Spain and the Netherlands are among the countries that have restarted their AstraZeneca vaccination campaigns.

Health authorities in France have recommended that the vaccine be offered only to people aged 55 and over.

The European Medicines Agency (EMA) reviewed the jab after 13 European countries suspended use of the vaccine over fears of a link to blood clots.

It found the jab was "not associated" with a higher risk of clots.

The World Health Organization (WHO) has urged countries to continue using the AstraZeneca vaccine.

On Friday, experts at the WHO said the vaccine had "tremendous potential to prevent infections and reduce deaths across the world".

"The available data do not suggest any overall increase in clotting conditions such as deep venous thrombosis or pulmonary embolism following administration of Covid-19 vaccines," the WHO's Global Advisory Committee on Vaccine Safety said in a statement.

Other European leaders have sought to reassure citizens that the Oxford-AstraZeneca jab is safe.

Italy's Prime Minister Mario Draghi, 73, said he would happily have the vaccine, but that he had "not yet made a booking".

His French counterpart, 55-year-old Jean Castex, received an AstraZeneca dose on Friday.

source:https://www.bbc.com

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Australia warned of 'life-threatening' flash floods

 

Emergency authorities in Australia are warning of "life threatening" flash floods as torrential rains batter parts of the country's east coast.

Dozens of people have been rescued from floodwaters, and residents in many low-lying communities of New South Wales have been ordered to leave their homes.

Police say hundreds of people have flocked to evacuation centres in areas north of the city of Sydney.

Major roads have been shut. Footage has emerged of a house being swept away.

Dams around Sydney are expected to overflow over the weekend, WaterNSW warns.

Up to 100mm (four inches) of rain is forecast for Sydney, and as much as 300mm for the lower Blue Mountains, west of the city.

Agata Imielska from the Bureau of Meteorology warned of localised intense rainfall and damaging winds, saying the public should be aware of "dangerous conditions" that can change quite quickly.

"If you don't need to travel, if you don't need to head out today, this is the day to stay at home," Ms Imielska was quoted as saying by the Sydney Morning Herald.

More storms are forecast in the coming days, and parts of eastern Australia could receive up to a metre of rain in the space of just a week, the BBC's Phil Mercer in Sydney reports.

source:https://www.bbc.com

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Friendly Fire: How Autoantibodies Could Drive Severe COVID-19

 

Some people get very sick with COVID-19; some die. Some have symptoms that last for months.

Yet others have only mild illness, or don’t even notice they’re infected. Last spring, as the pandemic got going, many immunologists began hunting, in patients’ blood samples, for the reason behind this broad variation. Perhaps, some surmised, the sickest patients wouldn’t have enough antibodies.

In fact, they found the opposite: People who were hospitalized with severe COVID-19 had plenty of antibodies against the SARS-CoV-2 virus, but also a diverse set of antibodies against their own body’s tissues and molecules.

Some of the autoantibodies attack organs or tissues in a pattern that looks an awful lot like autoimmune diseases such as lupus. Others attack the immune system itself, stifling the body’s ability to fight the infection. In some cases, people have autoantibodies before they’re ever infected with SARS-CoV-2; in others, the rogue antibodies arise as the body attempts to fight the virus.

And though there’s little direct evidence so far, some immunologists speculate that autoantibodies could contribute to the lingering symptoms experienced by long-haulers, who have symptoms for weeks and months after infection.

If autoantibodies are a problem in a subset of patients with COVID-19, identifying them and treating them for that issue could help. Here’s what scientists know so far.

What are autoantibodies?

Antibodies are Y-shaped molecules produced by B cells in the immune system. On the two top tips of the Y, they have regions that vary from antibody to antibody, allowing them to recognize different molecules. When they stick to their targets, they trigger elimination of those molecules or the cells that contain them.

The body has a large reservoir of B cells, each of which makes its own type of antibody. If one of those B cells finds its target, it starts copying itself, creating more B cells, plus effector cells that spew the antibodies into the bloodstream and memory B cells that will store the antibody for use against future infections.

But it takes up to a couple of weeks for B cells to get to that active state, says Matthew Woodruff, an immunologist at Emory University in Atlanta. That’s because there’s a “careful weeding out” of B cells that would also target — and harm — the body’s own tissues and molecules. The immune system has a variety of ways to kill or silence B cells with these dangerous autoantibodies.

At least, that’s what should happen in a perfectly balanced immune system, says Alexis Combes, an immunologist at the University of California, San Francisco. “It’s just that, at the end of the day, the system is not perfect,” he says. There are lots of possible routes for autoantibodies to sneak through the quality control process, especially in an immune system knocked off balance by a virus like SARS-CoV-2.

Imagine, Combes says, a B cell with an antibody that binds a foreign invader, but also sticks, just slightly, to some tissue, cell or molecule in the human body. It might sneak through the quality control process.

There are other, faster ways for B cells to get activated in an emergency situation such as severe infection, says Woodruff. He studies a process by which the B cells skip some of the quality control steps to make tons of antibodies right away. Woodruff and his colleagues have seen this fast-acting process at work in people with lupus, in which the autoantibodies circulating in the blood attack bodily tissues, causing pain, swelling and damage. The most common autoantibody in lupus attacks the cells’ own DNA.

Woodruff and others have also seen a similar process in patients with severe COVID-19, hinting that their bodies could be primed to let autoantibodies into the bloodstream.

What do autoantibodies have to do with severe COVID-19?

Researchers at Yale University in New Haven, Connecticut, checked the blood of 194 people with COVID-19 for 2,770 different autoantibodies, and found way more than the usual amount, according to a preprint that has not yet been reviewed by other scientists. People with severe COVID-19 had the most. Moreover, when the researchers administered similar autoantibodies to mice before infecting them with COVID-19, the mice got sicker than animals that received only the virus.

The antibodies in people with severe COVID-19 included ones against several parts of the immune system, such as signaling molecules called cytokines and proteins on the surface of immune cells. Antibodies against a class of cytokine called interferons, for example, were present in more than 5% of the hospitalized COVID-19 patients. These interferons are an “alarm signal” that tells cells to fight back against viruses, says Jean-Laurent Casanova, a pediatric immunologist at the Rockefeller University in New York. So if interferons are inactivated by the autoantibodies, that alarm signal could be blunted.

Casanova and colleagues found evidence of just that in their own study. Ten percent of 987 patients with life-threatening COVID-19 — 101 total — had the anti-interferon antibodies, and those patients had little or no interferon in their blood. That likely compromised their ability to fight off the virus; more than one-third of that 10% died.

The findings suggest that it could be helpful to give more interferon, of a type less likely to raise autoimmunity, to people who have this particular COVID-19 complication. (In fact, Casanova says he tried that recently in a woman with high levels of autoantibodies. “She’s done great,” he says.)

Casanova says that these patients had autoantibodies before they ever contracted COVID-19. He also suspects that these antibodies may be more prevalent in older adults, who have higher risk for severe COVID-19 infections. The autoantibodies also were much more common in men: 95 of the 101 subjects with anti-interferon were male. That might help explain why men are at higher risk for severe COVID-19 disease, speculates Casanova, who wrote about genetic factors that can compromise the immune system and predispose people to infections for the Annual Review of Pathology: Mechanisms of Disease.

In addition to anti-interferons, the Yale team observed autoantibodies against other body parts, such as the nervous system and blood vessels, in their study. That might mean autoantibodies are wreaking havoc around the body in certain COVID-19 patients, causing organ and tissue damage the way they do in autoimmune conditions like lupus and rheumatoid arthritis.

If so, that might contribute to some of the diverse symptoms, like brain fog and muscle pain, associated with the disease in different people. The Yale researchers did see that people who had autoantibodies against part of the brain were more likely to go into a coma-like state. But a direct link between autoantibodies and specific symptoms is “far from proven at this time,” says Iñaki Sanz, another immunologist and rheumatologist on the Emory team.

Sanz, Woodruff and colleagues at Emory are investigating the link between COVID-19 antibodies and other autoimmune diseases. In an as-yet-unreviewed preprint, they’ve reported autoantibody profiles in people with severe COVID-19 that are similar to those of lupus.

Theoretically, this suggests that treatments for autoimmune conditions, such as those that suppress B cells, might be useful for autoantibody-producing COVID-19 patients, says Sanz. But there aren’t enough data for him to recommend it yet.

It’s not unusual for autoantibodies to result from a viral infection, when the immune system is amped up. It happens in mononucleosis, dengue and rubella, to name a few diseases, but seems particularly intense in COVID-19. “In normal situations, this is self-limited,” Sanz says: The immune system manages to turn off the autoantibodies within a few weeks.

Might autoantibodies be involved in “long” cases of COVID-19?

So far, evidence pointing one way or the other is scarce, but there are a few hints that this might be the case. For example, a Boston University study — another preprint that is still to be peer reviewed, with a very small sample size — found autoantibodies in five COVID-19 patients with persistent symptoms, compared with two of four patients who recovered fully. And scientists in Europe found autoantibodies in children who developed multi-system inflammatory syndrome, a condition that can emerge a month or more after COVID-19 infections. Targets of those autoantibodies included molecules involved in the activation of immune cells, biochemical signalling and heart development.

Researchers at Emory and elsewhere now are collecting samples from people with ongoing symptoms to check out the autoantibody theory. But even if they’re right, autoantibodies might explain just a subset of long COVID-19 cases, says F. Eun-Hyung Lee, also an immunologist at Emory. “I think there’s lots of mechanisms of why somebody may have this long-hauler syndrome.”

And for anyone who may wonder: There’s no reason to expect that someone would develop autoantibodies after receiving a COVID-19 vaccine. In fact, because people with autoimmune diseases may be at higher risk for COVID-19 complications, it’s especially important for them to get vaccinated.

source:https://science.thewire.in/

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