Google will stop account sign-in for users running these old Android versions

 

Google is ending sign-in support for devices running on very old versions of Android. The tech giant is sending emails to users saying sign-in will not be supported on Android version 2.3.7 and lower. In order to continue using Google apps on their phones, they must upgrade to Android version 3.0 or higher.

“Signing in to your account on Google apps will no longer be supported on phones with Android version 2.3.7 or lower starting Sep. 27” reads the email received by some Google users. This means that starting September 27, those running Android version 2.3.7 or lower will not be able to sign into their accounts. These include Android 1.0, 1.1 (unnamed), 1.5 Cupcake, 1.6 Donut, 2.0 Eclair, 2.2 Froyo, and 2.3 Gingerbread.

In the email, Google says that the move is aimed to “help protect your account’s security. Actions like system and an application-level sign will result in a “username or password error”.

According to a Google support page, the following cases will sing-in error:

Perform a factory reset of your device and try to sign in.

Change your password either on the device or on a different device, which then signs you out everywhere else. When you try to sign in again, you will receive an error message.

Remove your account from your device and re-add it.

Create an account on the device.

However, users will still be able to sign in to their account on the phone's browser. “If you cannot update your device to a newer Android version (3.0+), you can try to log into your Google account on your device’s web browser. You can still use some Google services when logged into Google on your device’s web browser” Google says.

Source:https://timesofindia.indiatimes.com

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Google swipes left on 'Sugar Dating' apps, will uninstall them from Play Store by Sept 1

 Google is enforcing a blanket ban on all such apps such as SDM, Spoiler, and Sugar Daddy. For those uninitiated, Sugar Dating apps allow elderly people to date younger people to overcome loneliness. 

New Delhi: Google is all set to remove ‘Super Dating’ apps from the Play Store to make the app downloading platform for Android phones a safer place. The tech giant said that Play Store will stop hosting ‘Sugar Dating' apps from September 1. 

On the support page, Google has mentioned that the dating apps under the scanner will be removed for hosting ‘sexual content’ on the app. Google is also updating several other new policies such as Device and Network Abuse Policy, Permission Policy, starting September 1. 

On the Play Console support website, Google has specified the upcoming changes coming to Google Play Store. “We’re updating the Inappropriate Content policy to institute new restrictions on sexual content, specifically prohibiting compensated sexual relationships (i.e., sugar dating),” Google said. 

Google is enforcing a blanket ban on all such apps such as SDM, Spoiler, and Sugar Daddy. For those uninitiated, Sugar Dating apps allow elderly people to date younger people to overcome loneliness, but usually for money. 

Besides the ban on Sugar Dating apps, Google Play Store will incorporate several other new policies, including a developer preview of App Set ID for analytics or fraud prevention. 

“We’re updating our Ads policy to indicate changes in the usage of Android advertising ID. When a user deletes the Android advertising ID on a newer device, the advertising identifier will be removed and replaced with a string of zeros, Google said, adding that this policy change will come into effect from October 4, 2021.

Meanwhile, from September 29, 2021, Google will be updating its Store Listing and Promotion policy to prohibit spam text and graphics in-app titles, icons, and developer names. 

source:/https://zeenews.india.com/

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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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Study reveals Covid-19 severity is affected by proportion of antibodies targeting crucial viral protein

 

A recent study has revealed that Covid-19 antibodies wane significantly within several months of infection and preferentially target a different part of the virus in mild cases of Covid-19 than in comparison to severe ones.The findings which were published in Science Immunology identifies new links between the course of the disease and a patient’s immune response to it. They also raise concerns about whether people can be re-infected, whether antibody tests to detect prior infection may underestimate the breadth of the pandemic and whether vaccinations may need to be repeated at regular intervals to maintain a protective immune response.This is one of the most comprehensive studies to date of the antibody immune response to SARS-CoV-2 in people across the entire spectrum of disease severity, from asymptomatic to fatal,” said Scott Boyd, MD, Ph.D., associate professor of pathology. “We assessed multiple time points and sample types, and also analyzed levels of viral RNA in patient nasopharyngeal swabs and blood samples. It’s one of the first big-picture looks at this illness.”The study found that people with severe Covid-19 have low proportions of antibodies targeting the spike protein used by the virus to enter human cells compared with the number of antibodies targeting proteins of the virus’s inner shell.

Boyd is a senior author of the study, which was published December 7 in Science Immunology. Other senior authors are Benjamin Pinsky, MD, Ph.D., associate professor of pathology, and Peter Kim, Ph.D., the Virginia and D. K. Ludwig Professor of Biochemistry. The lead authors are research scientist Katharina Roltgen, Ph.D.; postdoctoral scholars Abigail Powell, Ph.D., and Oliver Wirz, Ph.D.; and clinical instructor Bryan Stevens, MD.

The virus binds to the ACE2 receptor

The researchers studied 254 people with asymptomatic, mild, or severe Covid-19 who were identified either through routine testing or occupational health screening at Stanford Health Care or who came to a Stanford Health Care clinic with symptoms of Covid-19. Of the people with symptoms, 25 were treated as outpatients, 42 were hospitalized outside the intensive care unit and 37 were treated in the intensive care unit. Twenty-five people in the study died of the disease.SARS-CoV-2 binds to human cells via a structure on its surface called the spike protein. This protein binds to a receptor on human cells called ACE2. The binding allows the virus to enter and infect the cell. Once inside, the virus sheds its outer coat to reveal an inner shell encasing its genetic material. Soon, the virus co-opts the cell’s protein-making machinery to churn out more viral particles, which are then released to infect other cells.

Antibodies that recognize and bind to the spike protein block its ability to bind to ACE2, preventing the virus from infecting the cells, whereas antibodies that recognize other viral components are unlikely to prevent viral spread. Current vaccine candidates use portions of the spike protein to stimulate an immune response.Boyd and his colleagues analyzed the levels of three types of antibodies -- IgG, IgM, and IgA -- and the proportions that targeted the viral spike protein or the virus’s inner shell as the disease progressed and patients either recovered or grew sicker. They also measured the levels of viral genetic material in nasopharyngeal samples and blood from the patients. Finally, they assessed the effectiveness of the antibodies in preventing the spike protein from binding to ACE2 in a laboratory dish.

“Although previous studies have assessed the overall antibody response to infection, we compared the viral proteins targeted by these antibodies,” Boyd said. “We found that the severity of the illness correlates with the ratio of antibodies recognizing domains of the spike protein compared with other nonprotective viral targets. Those people with mild illness tended to have a higher proportion of anti-spike antibodies, and those who died from their disease had more antibodies that recognized other parts of the virus.”

Substantial variability in the immune response

The researchers caution, however, that although the study identified trends among a group of patients, there is still substantial variability in the immune response mounted by individual patients, particularly those with severe disease.

“Antibody responses are not likely to be the sole determinant of someone’s outcome,” Boyd said. “Among people with severe disease, some die, and some recover. Some of these patients mount a vigorous immune response, and others have a more moderate response. So, there are a lot of other things going on. There are also other branches of the immune system involved. It’s important to note that our results identify correlations but don’t prove causation.”

As in other studies, the researchers found that people with asymptomatic and mild illness had lower levels of antibodies overall than did those with severe disease. After recovery, the levels of IgM and IgA decreased steadily to low or undetectable levels in most patients over a period of about one to four months after symptom onset or estimated infection date, and IgG levels dropped significantly.“This is quite consistent with what has been seen with other coronaviruses that regularly circulate in our communities to cause the common cold,” Boyd said. “It’s not uncommon for someone to get re-infected within a year or sometimes sooner. It remains to be seen whether the immune response to SARS-CoV-2 vaccination is stronger, or persists longer than that caused by natural infection. It’s quite possible it could be better. But there are a lot of questions that still need to be answered.”

Boyd is a co-chair of the National Cancer Institute’s SeroNet Serological Sciences Network, one of the nation’s largest coordinated research efforts to study the immune response to Covid-19. He is the principal investigator of the Centre of Excellence in SeroNet at Stanford, which is tackling critical questions about the mechanisms and duration of immunity to SARS-CoV-2.“For example, if someone has already been infected, should they get the vaccine? If so, how should they be prioritized?” Boyd said. “How can we adapt seroprevalence studies in vaccinated populations? How will immunity from vaccination differ from that caused by a natural infection? And how long might a vaccine be protective? These are all very interesting, important questions.”

source:https://www.hindustantimes.com

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