quora discussion https://bit.ly/36am1or
and
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re the brand new (est July 2020) journal and one of its articles linked above
Coronavirus (COVID-19) Research
Re: Coronavirus (COVID-19) Research
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Re: Coronavirus (COVID-19) Research
Well, this is really no surprise...
The Most Influential Spreader of Coronavirus Misinformation Online
Researchers and regulators say Joseph Mercola, an osteopathic physician, creates and profits from misleading claims about Covid-19 vaccines.
https://www.nytimes.com/2021/07/24/tech ... nline.html
The article that appeared online on Feb. 9 began with a seemingly innocuous question about the legal definition of vaccines. Then over its next 3,400 words, it declared coronavirus vaccines were “a medical fraud” and said the injections did not prevent infections, provide immunity or stop transmission of the disease.
Instead, the article claimed, the shots “alter your genetic coding, turning you into a viral protein factory that has no off-switch.”
Its assertions were easily disprovable. No matter. Over the next few hours, the article was translated from English into Spanish and Polish. It appeared on dozens of blogs and was picked up by anti-vaccination activists, who repeated the false claims online. The article also made its way to Facebook, where it reached 400,000 people, according to data from CrowdTangle, a Facebook-owned tool.
The entire effort traced back to one person: Joseph Mercola.
Dr. Mercola, 67, an osteopathic physician in Cape Coral, Fla., has long been a subject of criticism and government regulatory actions for his promotion of unproven or unapproved treatments. But most recently, he has become the chief spreader of coronavirus misinformation online, according to researchers.
An internet-savvy entrepreneur who employs dozens, Dr. Mercola has published over 600 articles on Facebook that cast doubt on Covid-19 vaccines since the pandemic began, reaching a far larger audience than other vaccine skeptics, an analysis by The New York Times found. His claims have been widely echoed on Twitter, Instagram and YouTube.
The activity has earned Dr. Mercola, a natural health proponent with an Everyman demeanor, the dubious distinction of the top spot in the “Disinformation Dozen,” a list of 12 people responsible for sharing 65 percent of all anti-vaccine messaging on social media, said the nonprofit Center for Countering Digital Hate. Others on the list include Robert F. Kennedy Jr., a longtime anti-vaccine activist, and Erin Elizabeth, the founder of the website Health Nut News, who is also Dr. Mercola’s girlfriend.
“Mercola is the pioneer of the anti-vaccine movement,” said Kolina Koltai, a researcher at the University of Washington who studies online conspiracy theories. “He’s a master of capitalizing on periods of uncertainty, like the pandemic, to grow his movement.”
Some high-profile media figures have promoted skepticism of the vaccines, notably Tucker Carlson and Laura Ingraham of Fox News, though other Fox personalities have urged viewers to get the shots. Now, Dr. Mercola and others in the “Disinformation Dozen” are in the spotlight as vaccinations in the United States slow, just as the highly infectious Delta variant has fueled a resurgence in coronavirus cases. More than 97 percent of people hospitalized for Covid-19 are unvaccinated, according to the Centers for Disease Control and Prevention.
President Biden has blamed online falsehoods for causing people to refrain from getting the injections. But even as Mr. Biden has urged social media companies to “do something about the misinformation,” Dr. Mercola shows the difficulty of that task.
Over the last decade, Dr. Mercola has built a vast operation to push natural health cures, disseminate anti-vaccination content and profit from all of it, said researchers who have studied his network. In 2017, he filed an affidavit claiming his net worth was “in excess of $100 million.”
And rather than directly stating online that vaccines don’t work, Dr. Mercola’s posts often ask pointed questions about their safety and discuss studies that other doctors have refuted. Facebook and Twitter have allowed some of his posts to remain up with caution labels, and the companies have struggled to create rules to pull down posts that have nuance.
“He has been given new life by social media, which he exploits skillfully and ruthlessly to bring people into his thrall,” said Imran Ahmed, director of the Center for Countering Digital Hate, which studies misinformation and hate speech. Its “Disinformation Dozen” report has been cited in congressional hearings and by the White House.
[Continued]
The Most Influential Spreader of Coronavirus Misinformation Online
Researchers and regulators say Joseph Mercola, an osteopathic physician, creates and profits from misleading claims about Covid-19 vaccines.
https://www.nytimes.com/2021/07/24/tech ... nline.html
The article that appeared online on Feb. 9 began with a seemingly innocuous question about the legal definition of vaccines. Then over its next 3,400 words, it declared coronavirus vaccines were “a medical fraud” and said the injections did not prevent infections, provide immunity or stop transmission of the disease.
Instead, the article claimed, the shots “alter your genetic coding, turning you into a viral protein factory that has no off-switch.”
Its assertions were easily disprovable. No matter. Over the next few hours, the article was translated from English into Spanish and Polish. It appeared on dozens of blogs and was picked up by anti-vaccination activists, who repeated the false claims online. The article also made its way to Facebook, where it reached 400,000 people, according to data from CrowdTangle, a Facebook-owned tool.
The entire effort traced back to one person: Joseph Mercola.
Dr. Mercola, 67, an osteopathic physician in Cape Coral, Fla., has long been a subject of criticism and government regulatory actions for his promotion of unproven or unapproved treatments. But most recently, he has become the chief spreader of coronavirus misinformation online, according to researchers.
An internet-savvy entrepreneur who employs dozens, Dr. Mercola has published over 600 articles on Facebook that cast doubt on Covid-19 vaccines since the pandemic began, reaching a far larger audience than other vaccine skeptics, an analysis by The New York Times found. His claims have been widely echoed on Twitter, Instagram and YouTube.
The activity has earned Dr. Mercola, a natural health proponent with an Everyman demeanor, the dubious distinction of the top spot in the “Disinformation Dozen,” a list of 12 people responsible for sharing 65 percent of all anti-vaccine messaging on social media, said the nonprofit Center for Countering Digital Hate. Others on the list include Robert F. Kennedy Jr., a longtime anti-vaccine activist, and Erin Elizabeth, the founder of the website Health Nut News, who is also Dr. Mercola’s girlfriend.
“Mercola is the pioneer of the anti-vaccine movement,” said Kolina Koltai, a researcher at the University of Washington who studies online conspiracy theories. “He’s a master of capitalizing on periods of uncertainty, like the pandemic, to grow his movement.”
Some high-profile media figures have promoted skepticism of the vaccines, notably Tucker Carlson and Laura Ingraham of Fox News, though other Fox personalities have urged viewers to get the shots. Now, Dr. Mercola and others in the “Disinformation Dozen” are in the spotlight as vaccinations in the United States slow, just as the highly infectious Delta variant has fueled a resurgence in coronavirus cases. More than 97 percent of people hospitalized for Covid-19 are unvaccinated, according to the Centers for Disease Control and Prevention.
President Biden has blamed online falsehoods for causing people to refrain from getting the injections. But even as Mr. Biden has urged social media companies to “do something about the misinformation,” Dr. Mercola shows the difficulty of that task.
Over the last decade, Dr. Mercola has built a vast operation to push natural health cures, disseminate anti-vaccination content and profit from all of it, said researchers who have studied his network. In 2017, he filed an affidavit claiming his net worth was “in excess of $100 million.”
And rather than directly stating online that vaccines don’t work, Dr. Mercola’s posts often ask pointed questions about their safety and discuss studies that other doctors have refuted. Facebook and Twitter have allowed some of his posts to remain up with caution labels, and the companies have struggled to create rules to pull down posts that have nuance.
“He has been given new life by social media, which he exploits skillfully and ruthlessly to bring people into his thrall,” said Imran Ahmed, director of the Center for Countering Digital Hate, which studies misinformation and hate speech. Its “Disinformation Dozen” report has been cited in congressional hearings and by the White House.
[Continued]
Re: Coronavirus (COVID-19) Research
Doctors Worry That Memory Problems After COVID-19 May Set The Stage For Alzheimer's
July 26, 20215:00 AM ET
https://www.npr.org/sections/health-sho ... alzheimers
Before she got COVID-19, Cassandra Hernandez, 38, was in great shape — both physically and mentally.
"I'm a nurse," she says. "I work with surgeons and my memory was sharp."
Then, in June 2020, COVID-19 struck Hernandez and several others in her unit at a large hospital in San Antonio.
"I went home after working a 12-hour shift and sat down to eat a pint of ice cream with my husband and I couldn't taste it," she says.
The loss of taste and smell can be an early sign that COVID-19 is affecting a brain area that helps us sense odors.
Hernandez would go on to spend two weeks in the hospital and months at home disabled by symptoms including tremors, extreme fatigue and problems with memory and thinking.
"I would literally fall asleep if I was having a conversation or doing anything that involved my brain," she says.
Alzheimer's researchers sharing findings on COVID-19
Now, researchers at UT Health San Antonio are studying patients like Hernandez, trying to understand why their cognitive problems persist and whether their brains have been changed in ways that elevate the risk of developing Alzheimer's disease.
The San Antonio researchers are among the teams of scientists from around the world who will present their findings on how COVID-19 affects the brain at the Alzheimer's Association International Conference, which begins Monday in Denver.
What scientists have found so far is concerning.
For example, PET scans taken before and after a person develops COVID-19 suggest that the infection can cause changes that overlap those seen in Alzheimer's. And genetic studies are finding that some of the same genes that increase a person's risk for getting severe COVID-19 also increase the risk of developing Alzheimer's.
Alzheimer's diagnoses also appear to be more common in patients in their 60s and 70s who have had severe COVID-19, says Dr. Gabriel de Erausquin, a professor of neurology at UT Health San Antonio. "It's downright scary," he says.
A loss of smell can signal trouble
And de Erausquin and his colleagues have noticed that mental problems seem to be more common in COVID-19 patients who lose their sense of smell, perhaps because the disease has affected a brain area called the olfactory bulb.
"Persistent lack of smell, it's associated with brain changes not just in the olfactory bulb but those places that are connected one way or another to the smell sense," he says.
Those places include areas involved in memory, thinking, planning and mood.
COVID-19's effects on the brain also seem to vary with age, de Erausquin says. People in their 30s seem more likely to develop anxiety and depression.
"In older people, people over 60, the foremost manifestation is forgetfulness," he says. "These folks tend to forget where they placed things, they tend to forget names, they tend to forget phone numbers. They also have trouble with language; they begin forgetting words."
The symptoms are similar to those of early Alzheimer's, and doctors sometimes describe these patients as having an Alzheimer's-like syndrome that can persist for many months.
"Those people look really bad right now," de Erausquin says. "And the expectation is that it may behave as Alzheimer's behaves, in a progressive fashion. But the true answer is we don't know."
Another scientist who will present research at the Alzheimer's conference is Dr. Sudha Seshadri, founding director of the Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases at UT Health San Antonio.
The possibility that COVID-19 might increase the risk of Alzheimer's is alarming, Seshadri says. "Even if the effect is small, it's something we're going to have to factor in because the population is quite large," she says.
In the U.S. alone, millions of people have developed persistent cognitive or mood problems after getting COVID-19. It may take a decade to know whether these people are more likely than uninfected people to develop Alzheimer's in their 60s and 70s, Seshadri says.
Studies of people who have had COVID-19 may help scientists understand the role infections play in Alzheimer's and other brain diseases. Previous research has suggested that exposure to certain viruses, including herpes, can trigger an immune response in the brain that may set the stage for Alzheimer's.
"If one understands how the immune response to this virus is accelerating [Alzheimer's] disease, we may learn about the impact of other viruses," Seshadri says.
A long road back from COVID-19
Meanwhile, people like Cassandra Hernandez, the nurse, are simply trying to get better. More than a year after getting sick, she says, her brain is still foggy.
"We were at dinner and I forgot how to use a fork," she says. "It was embarrassing."
Even so, Hernandez says she's improving — slowly.
"Before this I was working on my master's," she says. "Now I can do basic math, addition and subtraction, I can read at a fifth-grade level. I'm still working hard every day."
Hernandez has been working with Dr. Monica Verduzco-Gutierrez, chair of the department of physical medicine and rehabilitation at UT Health and director of the COVID-19 recovery clinic.
Verduzco-Gutierrez says her practice used to revolve around people recovering from strokes and traumatic brain injuries. Now she spends some days seeing only patients recovering from COVID-19.
The most common complaint is fatigue, Verduzco-Gutierrez says. But these patients also frequently experience migraine headaches, forgetfulness, dizziness and balance issues, she says.
Some of these patients may never recover fully, Verduzco-Gutierrez says. But she's hopeful for Hernandez.
"She's made so much improvement and I would love for her to go back to nursing," Verduzco-Gutierrez says. "But again, we don't know what happens with this disease."
July 26, 20215:00 AM ET
https://www.npr.org/sections/health-sho ... alzheimers
Before she got COVID-19, Cassandra Hernandez, 38, was in great shape — both physically and mentally.
"I'm a nurse," she says. "I work with surgeons and my memory was sharp."
Then, in June 2020, COVID-19 struck Hernandez and several others in her unit at a large hospital in San Antonio.
"I went home after working a 12-hour shift and sat down to eat a pint of ice cream with my husband and I couldn't taste it," she says.
The loss of taste and smell can be an early sign that COVID-19 is affecting a brain area that helps us sense odors.
Hernandez would go on to spend two weeks in the hospital and months at home disabled by symptoms including tremors, extreme fatigue and problems with memory and thinking.
"I would literally fall asleep if I was having a conversation or doing anything that involved my brain," she says.
Alzheimer's researchers sharing findings on COVID-19
Now, researchers at UT Health San Antonio are studying patients like Hernandez, trying to understand why their cognitive problems persist and whether their brains have been changed in ways that elevate the risk of developing Alzheimer's disease.
The San Antonio researchers are among the teams of scientists from around the world who will present their findings on how COVID-19 affects the brain at the Alzheimer's Association International Conference, which begins Monday in Denver.
What scientists have found so far is concerning.
For example, PET scans taken before and after a person develops COVID-19 suggest that the infection can cause changes that overlap those seen in Alzheimer's. And genetic studies are finding that some of the same genes that increase a person's risk for getting severe COVID-19 also increase the risk of developing Alzheimer's.
Alzheimer's diagnoses also appear to be more common in patients in their 60s and 70s who have had severe COVID-19, says Dr. Gabriel de Erausquin, a professor of neurology at UT Health San Antonio. "It's downright scary," he says.
A loss of smell can signal trouble
And de Erausquin and his colleagues have noticed that mental problems seem to be more common in COVID-19 patients who lose their sense of smell, perhaps because the disease has affected a brain area called the olfactory bulb.
"Persistent lack of smell, it's associated with brain changes not just in the olfactory bulb but those places that are connected one way or another to the smell sense," he says.
Those places include areas involved in memory, thinking, planning and mood.
COVID-19's effects on the brain also seem to vary with age, de Erausquin says. People in their 30s seem more likely to develop anxiety and depression.
"In older people, people over 60, the foremost manifestation is forgetfulness," he says. "These folks tend to forget where they placed things, they tend to forget names, they tend to forget phone numbers. They also have trouble with language; they begin forgetting words."
The symptoms are similar to those of early Alzheimer's, and doctors sometimes describe these patients as having an Alzheimer's-like syndrome that can persist for many months.
"Those people look really bad right now," de Erausquin says. "And the expectation is that it may behave as Alzheimer's behaves, in a progressive fashion. But the true answer is we don't know."
Another scientist who will present research at the Alzheimer's conference is Dr. Sudha Seshadri, founding director of the Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases at UT Health San Antonio.
The possibility that COVID-19 might increase the risk of Alzheimer's is alarming, Seshadri says. "Even if the effect is small, it's something we're going to have to factor in because the population is quite large," she says.
In the U.S. alone, millions of people have developed persistent cognitive or mood problems after getting COVID-19. It may take a decade to know whether these people are more likely than uninfected people to develop Alzheimer's in their 60s and 70s, Seshadri says.
Studies of people who have had COVID-19 may help scientists understand the role infections play in Alzheimer's and other brain diseases. Previous research has suggested that exposure to certain viruses, including herpes, can trigger an immune response in the brain that may set the stage for Alzheimer's.
"If one understands how the immune response to this virus is accelerating [Alzheimer's] disease, we may learn about the impact of other viruses," Seshadri says.
A long road back from COVID-19
Meanwhile, people like Cassandra Hernandez, the nurse, are simply trying to get better. More than a year after getting sick, she says, her brain is still foggy.
"We were at dinner and I forgot how to use a fork," she says. "It was embarrassing."
Even so, Hernandez says she's improving — slowly.
"Before this I was working on my master's," she says. "Now I can do basic math, addition and subtraction, I can read at a fifth-grade level. I'm still working hard every day."
Hernandez has been working with Dr. Monica Verduzco-Gutierrez, chair of the department of physical medicine and rehabilitation at UT Health and director of the COVID-19 recovery clinic.
Verduzco-Gutierrez says her practice used to revolve around people recovering from strokes and traumatic brain injuries. Now she spends some days seeing only patients recovering from COVID-19.
The most common complaint is fatigue, Verduzco-Gutierrez says. But these patients also frequently experience migraine headaches, forgetfulness, dizziness and balance issues, she says.
Some of these patients may never recover fully, Verduzco-Gutierrez says. But she's hopeful for Hernandez.
"She's made so much improvement and I would love for her to go back to nursing," Verduzco-Gutierrez says. "But again, we don't know what happens with this disease."
Re: Coronavirus (COVID-19) Research
I finally got the Pfizer/BioNTech mRNA vaccine last month. It was no big deal. The first shot was uneventful. I felt a little cruddy after the second shot, but that only lasted for a day.
Re: Coronavirus (COVID-19) Research
Humoral and T-Cell Response to SARS-CoV-2 Vaccination in Patients With Multiple Sclerosis Treated With Ocrelizumab
JAMA Neurol. 2021 Sep 23;e213599.
Importance: B-cell-depleting therapies may affect the development of a protective immune response following vaccination. Understanding the ability to develop vaccine-specific immunity to COVID-19 in patients with multiple sclerosis (MS) treated with B-cell-depleting therapy is of importance for clinical decisions.
Objective: To assess SARS-CoV-2 vaccine-specific humoral and cellular responses in patients treated with ocrelizumab compared with healthy controls.
Design, setting, and participants: This single-center study performed at Hadassah Medical Center in Jerusalem, Israel, included patients with MS treated with ocrelizumab, healthy controls, and untreated patients with MS. Vaccination occurred between December 2020 and April 2021. Participants donated blood 2 to 4 and 2 to 8 weeks after the second vaccine dose for antibody and T-cell assessments, respectively.
Exposures: All participants received 2 doses of BNT162b2 vaccine (Pfizer/BioNTech) and completed the study.
Main outcomes and measures: Proportion of patients treated with ocrelizumab with SARS-CoV-2-specific serology and/or T-cell responses following vaccination. All participants underwent SARS-CoV-2 antibody testing; 29 patients treated with ocrelizumab and 15 healthy controls had evaluation of SARS-CoV-2-specific T-cell responses.
Results: Of 112 participants, 49 (43.8%) had MS and were treated with ocrelizumab (33 [67.3%] female; mean [SD] age, 47.9 [13.3] years), 23 (20.5%) had MS and were not treated with disease-modifying therapies (18 [78.3%] female; mean [SD] age, 49 [13.4] years), and 40 (35.7%) were healthy controls (25 [62.5%] female; mean [SD] age, 45.3 [16] years). Twenty-six of 29 patients (89.7%) treated with ocrelizumab and 15 of 15 healthy controls (100%) had SARS-CoV-2-specific T cells following vaccination at similar levels (mean [SD], 15.4 [7.6] and 14.3 [6.3] spot-forming cells, respectively). Mean antibody titers and positive serology rate were lower in the group of patients treated with ocrelizumab (mean [SD] antibody titers and positive serology rate, 26.2 [49.2] and 376.5 [907.6] AU/mL; 10 of 40 [25%] and 20 of 49 [40.8%] for S1/S2 and receptor-binding domain, respectively) compared with healthy controls (mean [SD] antibody titers and positive serology rate, 283 [100] and 12 712 [9114] AU/mL; 100% S1/S2 and receptor-binding domain) and untreated patients (mean [SD] antibody titers and positive serology rate, 288.3 [113.8] and 10 877 [9476] AU/mL; 100% S1/S2 and receptor-binding domain), with positive association to time from ocrelizumab infusion (S1/S2: r = 0.7, P < .001; receptor-binding domain: r = 0.4, P = .04).
Conclusion and relevance: In this study, patients with MS who were treated with ocrelizumab generated comparable SARS-CoV-2-specific T-cell responses with healthy controls and had lower antibody response following vaccination. Given the potential role of T cells in protection from severe disease, this is reassuring and will help physicians develop consensus guidelines regarding MS treatment in the era of the COVID-19 pandemic.
Comment: It would be interesting to know about memory B cells as well.
JAMA Neurol. 2021 Sep 23;e213599.
Importance: B-cell-depleting therapies may affect the development of a protective immune response following vaccination. Understanding the ability to develop vaccine-specific immunity to COVID-19 in patients with multiple sclerosis (MS) treated with B-cell-depleting therapy is of importance for clinical decisions.
Objective: To assess SARS-CoV-2 vaccine-specific humoral and cellular responses in patients treated with ocrelizumab compared with healthy controls.
Design, setting, and participants: This single-center study performed at Hadassah Medical Center in Jerusalem, Israel, included patients with MS treated with ocrelizumab, healthy controls, and untreated patients with MS. Vaccination occurred between December 2020 and April 2021. Participants donated blood 2 to 4 and 2 to 8 weeks after the second vaccine dose for antibody and T-cell assessments, respectively.
Exposures: All participants received 2 doses of BNT162b2 vaccine (Pfizer/BioNTech) and completed the study.
Main outcomes and measures: Proportion of patients treated with ocrelizumab with SARS-CoV-2-specific serology and/or T-cell responses following vaccination. All participants underwent SARS-CoV-2 antibody testing; 29 patients treated with ocrelizumab and 15 healthy controls had evaluation of SARS-CoV-2-specific T-cell responses.
Results: Of 112 participants, 49 (43.8%) had MS and were treated with ocrelizumab (33 [67.3%] female; mean [SD] age, 47.9 [13.3] years), 23 (20.5%) had MS and were not treated with disease-modifying therapies (18 [78.3%] female; mean [SD] age, 49 [13.4] years), and 40 (35.7%) were healthy controls (25 [62.5%] female; mean [SD] age, 45.3 [16] years). Twenty-six of 29 patients (89.7%) treated with ocrelizumab and 15 of 15 healthy controls (100%) had SARS-CoV-2-specific T cells following vaccination at similar levels (mean [SD], 15.4 [7.6] and 14.3 [6.3] spot-forming cells, respectively). Mean antibody titers and positive serology rate were lower in the group of patients treated with ocrelizumab (mean [SD] antibody titers and positive serology rate, 26.2 [49.2] and 376.5 [907.6] AU/mL; 10 of 40 [25%] and 20 of 49 [40.8%] for S1/S2 and receptor-binding domain, respectively) compared with healthy controls (mean [SD] antibody titers and positive serology rate, 283 [100] and 12 712 [9114] AU/mL; 100% S1/S2 and receptor-binding domain) and untreated patients (mean [SD] antibody titers and positive serology rate, 288.3 [113.8] and 10 877 [9476] AU/mL; 100% S1/S2 and receptor-binding domain), with positive association to time from ocrelizumab infusion (S1/S2: r = 0.7, P < .001; receptor-binding domain: r = 0.4, P = .04).
Conclusion and relevance: In this study, patients with MS who were treated with ocrelizumab generated comparable SARS-CoV-2-specific T-cell responses with healthy controls and had lower antibody response following vaccination. Given the potential role of T cells in protection from severe disease, this is reassuring and will help physicians develop consensus guidelines regarding MS treatment in the era of the COVID-19 pandemic.
Comment: It would be interesting to know about memory B cells as well.
Re: Coronavirus (COVID-19) Research
Those unvaccinated may find that life is about to become much more difficult.
Vaccine verification starts Monday in King County: What to expect
https://www.kiro7.com/news/local/vaccin ... I6MN7U2AQ/
Other regions will likely enact similar policies.
Vaccine verification starts Monday in King County: What to expect
https://www.kiro7.com/news/local/vaccin ... I6MN7U2AQ/
Other regions will likely enact similar policies.
Re: Coronavirus (COVID-19) Research
Beware the New Delta Plus Variant | A New Vaccine to the Rescue?
https://www.peoplespharmacy.com/article ... he-rescue/
The Delta Variant of COVID-19 ravaged India. Now there's the Delta Plus variant. Is it more contagious than the already nasty Delta variant?
A new variant of SARS-CoV-2 is starting to spread around the US. Scientists have named it AY.4.2. The popular press, on the other hand, has dubbed it the Delta plus variant. This subvariant of the Delta coronavirus is spreading in the UK, making up over 11% of cases there. It has also been isolated in dozens of other countries.
Now, the Delta plus variant is spreading in the US. At least eight states are reporting cases and it is expected to spread even faster than the original Delta variant. How worrisome is this variant of a variant? British public health authorities suggest it may be more transmissible than Delta, but the available vaccines still protect people from this new version.
At the moment, people who have caught the Delta plus variant do not appear to be sicker than those with COVID infections attributed to earlier forms of the coronavirus. Needless to say, the CDC is tracking the emergence of the Delta+ subvariant very closely to make sure it doesn’t develop into something more worrisome.
–•–•–•–•–•–•–•–•–•–•–•– The Delta Plus Variant Has Emerged:
This new mutant form of the SARS-CoV-2 is the Delta plus variant. It arose in India. That’s hardly a surprise. India has been slammed for weeks. Vineeta Bal is an immunologist at the Indian Institute of Science Education and Research in Pune, India.
She told NPR (June 23, 2021):
“The fear in everybody’s mind is that now there is a further mutation and it might again take us towards another wave.”
[continued]
https://www.peoplespharmacy.com/article ... he-rescue/
The Delta Variant of COVID-19 ravaged India. Now there's the Delta Plus variant. Is it more contagious than the already nasty Delta variant?
A new variant of SARS-CoV-2 is starting to spread around the US. Scientists have named it AY.4.2. The popular press, on the other hand, has dubbed it the Delta plus variant. This subvariant of the Delta coronavirus is spreading in the UK, making up over 11% of cases there. It has also been isolated in dozens of other countries.
Now, the Delta plus variant is spreading in the US. At least eight states are reporting cases and it is expected to spread even faster than the original Delta variant. How worrisome is this variant of a variant? British public health authorities suggest it may be more transmissible than Delta, but the available vaccines still protect people from this new version.
At the moment, people who have caught the Delta plus variant do not appear to be sicker than those with COVID infections attributed to earlier forms of the coronavirus. Needless to say, the CDC is tracking the emergence of the Delta+ subvariant very closely to make sure it doesn’t develop into something more worrisome.
–•–•–•–•–•–•–•–•–•–•–•– The Delta Plus Variant Has Emerged:
This new mutant form of the SARS-CoV-2 is the Delta plus variant. It arose in India. That’s hardly a surprise. India has been slammed for weeks. Vineeta Bal is an immunologist at the Indian Institute of Science Education and Research in Pune, India.
She told NPR (June 23, 2021):
“The fear in everybody’s mind is that now there is a further mutation and it might again take us towards another wave.”
[continued]
Re: Coronavirus (COVID-19) Research
Unvaccinated Oregon man spends 102 days in hospital, now has a message for Americans
Howard Breidenbach used to think COVID wasn’t a serious threat to his health, so didn’t get vaccinated when he had the opportunity. But now after spending a grueling 102 days in the hospital he wishes he had got the vaccination.
Howard Breidenbach used to think COVID wasn’t a serious threat to his health, so didn’t get vaccinated when he had the opportunity. But now after spending a grueling 102 days in the hospital he wishes he had got the vaccination.
Re: Coronavirus (COVID-19) Research
Kids Are Coming Down with Diabetes After Getting Over COVID
https://www.peoplespharmacy.com/article ... ver-covid/
Insurance data show that youngsters under 18 have been coming down with diabetes after they recover from COVID-19 infections.
The researchers used two large insurance databases to compare the health of youngsters under 18 who had contracted COVID to those who had avoided the infection. In one of the databases, health care providers diagnosed more than 80,000 kids with COVID-19 between March 2020 and February 2021. The other database included nearly 440,000 youngsters diagnosed between March 2020 and June 2021.
Scientists compared rates of newly diagnosed diabetes within each dataset. Kids were matched for all variables except the diabetes diagnosis. In both datasets, children recovering from infection were significantly more likely to develop diabetes. In the database from IQVIA, the rate of diabetes was 316 per 100,000 person-years among kids diagnosed with COVID-19. By comparison, the rate for children who did not have COVID-19 was 118 per 100,000 person-years.
Other respiratory infections did not increase the likelihood of children coming down with diabetes. As the authors conclude, this increased risk underscores the importance of measures to prevent COVID-19 infections among young people.
https://www.peoplespharmacy.com/article ... ver-covid/
Insurance data show that youngsters under 18 have been coming down with diabetes after they recover from COVID-19 infections.
The researchers used two large insurance databases to compare the health of youngsters under 18 who had contracted COVID to those who had avoided the infection. In one of the databases, health care providers diagnosed more than 80,000 kids with COVID-19 between March 2020 and February 2021. The other database included nearly 440,000 youngsters diagnosed between March 2020 and June 2021.
Scientists compared rates of newly diagnosed diabetes within each dataset. Kids were matched for all variables except the diabetes diagnosis. In both datasets, children recovering from infection were significantly more likely to develop diabetes. In the database from IQVIA, the rate of diabetes was 316 per 100,000 person-years among kids diagnosed with COVID-19. By comparison, the rate for children who did not have COVID-19 was 118 per 100,000 person-years.
Other respiratory infections did not increase the likelihood of children coming down with diabetes. As the authors conclude, this increased risk underscores the importance of measures to prevent COVID-19 infections among young people.
Re: Coronavirus (COVID-19) Research
Covid vaccine response was significantly lower in MS patients taking Ocrevus, fingolimod and cladribine.
Humoral- and T-Cell-Specific Immune Responses to SARS-CoV-2 mRNA Vaccination in Patients With MS Using Different Disease-Modifying Therapies
https://pubmed.ncbi.nlm.nih.gov/34810244/
Humoral- and T-Cell-Specific Immune Responses to SARS-CoV-2 mRNA Vaccination in Patients With MS Using Different Disease-Modifying Therapies
https://pubmed.ncbi.nlm.nih.gov/34810244/
Re: Coronavirus (COVID-19) Research
Could COVID-19 Infection Harm Your Gut Microbiota?
A study shows that COVID-19 infection can harm your gut microbiota, reducing diversity and beneficial bacteria. Will probiotics help?
https://www.peoplespharmacy.com/article ... icrobiota/
Over the past decade, scientists have learned a lot about the importance of the gut microbiota. This is the collection of bacteria, fungi and viruses that hang out mostly in the large intestine. All these microbes form a sort of ecological system. A healthy system is diverse and thriving, and helps keep its host healthy as well. But certain drugs and infections can harm your gut microbiota.
COVID-19 Infection Can Harm Your Gut Microbiota:
New research indicates that COVID-19 infection alters the gut microbiota. A study of elderly French patients hospitalized with COVID-19 examined how the bacteria in their digestive tracts differed from uninfected healthcare workers who served as controls (medRxiv, Feb. 8, 2022).
Researchers analyzed stool samples and recorded clinical outcomes among the patients. Bacterial diversity of the gut microbiome was far lower among the COVID patients.
Unfortunately, some of the types of bacteria that were reduced or went missing are known to be beneficial. They secrete butyrate, which improves the intestinal barrier and calms inflammation. In addition, COVID patients were less likely to have normal levels of Bifidobacteria, which are beneficial bacterial strains.
[continued]
A study shows that COVID-19 infection can harm your gut microbiota, reducing diversity and beneficial bacteria. Will probiotics help?
https://www.peoplespharmacy.com/article ... icrobiota/
Over the past decade, scientists have learned a lot about the importance of the gut microbiota. This is the collection of bacteria, fungi and viruses that hang out mostly in the large intestine. All these microbes form a sort of ecological system. A healthy system is diverse and thriving, and helps keep its host healthy as well. But certain drugs and infections can harm your gut microbiota.
COVID-19 Infection Can Harm Your Gut Microbiota:
New research indicates that COVID-19 infection alters the gut microbiota. A study of elderly French patients hospitalized with COVID-19 examined how the bacteria in their digestive tracts differed from uninfected healthcare workers who served as controls (medRxiv, Feb. 8, 2022).
Researchers analyzed stool samples and recorded clinical outcomes among the patients. Bacterial diversity of the gut microbiome was far lower among the COVID patients.
Unfortunately, some of the types of bacteria that were reduced or went missing are known to be beneficial. They secrete butyrate, which improves the intestinal barrier and calms inflammation. In addition, COVID patients were less likely to have normal levels of Bifidobacteria, which are beneficial bacterial strains.
[continued]
Re: One variant to rule them all
Omicron keeps finding new evolutionary tricks to outsmart our immunity
https://www.knkx.org/2022-10-25/omicron ... r-immunity
Throughout the pandemic, the virus that causes COVID-19 has been evolving fast, blindsiding the world with one variant after another.
But the World Health Organization hasn't given a SARS-CoV-2 variant a Greek name in almost a year, a move that's reserved for new variants that do or could have significant public health impacts, such as being more transmissible or causing more severe disease.
That raises the question: Has the evolution of the virus finally started to ebb, possibly making it more predictable?
The answer — according to a dozen evolutionary biologists, virologists and immunologists interviewed by NPR — is no.
"SARS-CoV-2 is continuing to evolve extremely rapidly," says Trevor Bedford, a computational biologist who studies the evolution of viruses at the Fred Hutchinson Cancer Center in Seattle. "There's no evidence that the evolution is slowing down."
Instead, the most consequential evolutionary changes have stayed confined to the omicron family, rather than appearing in entirely new variants.
Whereas alpha, beta, gamma and the other named variants sprouted new branches on the SARS-CoV-2 family tree, those limbs were dwarfed by the omicron bough, which is now studded with a plethora of subvariant stems.
[continued]
https://www.knkx.org/2022-10-25/omicron ... r-immunity
Throughout the pandemic, the virus that causes COVID-19 has been evolving fast, blindsiding the world with one variant after another.
But the World Health Organization hasn't given a SARS-CoV-2 variant a Greek name in almost a year, a move that's reserved for new variants that do or could have significant public health impacts, such as being more transmissible or causing more severe disease.
That raises the question: Has the evolution of the virus finally started to ebb, possibly making it more predictable?
The answer — according to a dozen evolutionary biologists, virologists and immunologists interviewed by NPR — is no.
"SARS-CoV-2 is continuing to evolve extremely rapidly," says Trevor Bedford, a computational biologist who studies the evolution of viruses at the Fred Hutchinson Cancer Center in Seattle. "There's no evidence that the evolution is slowing down."
Instead, the most consequential evolutionary changes have stayed confined to the omicron family, rather than appearing in entirely new variants.
Whereas alpha, beta, gamma and the other named variants sprouted new branches on the SARS-CoV-2 family tree, those limbs were dwarfed by the omicron bough, which is now studded with a plethora of subvariant stems.
[continued]
Re: Coronavirus (COVID-19) Research
Severe COVID-19 induces molecular signatures of aging in the human brain
medRxiv. 2021 Nov 24;2021.11.24.21266779.
Coronavirus disease 2019 (COVID-19) is predominantly an acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and remains a significant threat to public health. COVID-19 is accompanied by neurological symptoms and cognitive decline, but the molecular mechanisms underlying this effect remain unclear. As aging induces distinct molecular signatures in the brain associated with cognitive decline in healthy populations, we hypothesized that COVID-19 may induce molecular signatures of aging. Here, we performed whole transcriptomic analysis of human frontal cortex, a critical area for cognitive function, in 12 COVID-19 cases and age- and sex-matched uninfected controls. COVID-19 induces profound changes in gene expression, despite the absence of detectable virus in brain tissue. Pathway analysis shows downregulation of genes involved in synaptic function and cognition and upregulation of genes involved in immune processes. Comparison with five independent transcriptomic datasets of aging human frontal cortex reveals striking similarities between aged individuals and severe COVID-19 patients. Critically, individuals below 65 years of age exhibit profound transcriptomic changes not observed among older individuals in our patient cohort. Our data indicate that severe COVID-19 induces molecular signatures of aging in the human brain and emphasize the value of neurological follow-up in recovered individuals.
Free full text.
medRxiv. 2021 Nov 24;2021.11.24.21266779.
Coronavirus disease 2019 (COVID-19) is predominantly an acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and remains a significant threat to public health. COVID-19 is accompanied by neurological symptoms and cognitive decline, but the molecular mechanisms underlying this effect remain unclear. As aging induces distinct molecular signatures in the brain associated with cognitive decline in healthy populations, we hypothesized that COVID-19 may induce molecular signatures of aging. Here, we performed whole transcriptomic analysis of human frontal cortex, a critical area for cognitive function, in 12 COVID-19 cases and age- and sex-matched uninfected controls. COVID-19 induces profound changes in gene expression, despite the absence of detectable virus in brain tissue. Pathway analysis shows downregulation of genes involved in synaptic function and cognition and upregulation of genes involved in immune processes. Comparison with five independent transcriptomic datasets of aging human frontal cortex reveals striking similarities between aged individuals and severe COVID-19 patients. Critically, individuals below 65 years of age exhibit profound transcriptomic changes not observed among older individuals in our patient cohort. Our data indicate that severe COVID-19 induces molecular signatures of aging in the human brain and emphasize the value of neurological follow-up in recovered individuals.
Free full text.
Re: Coronavirus (COVID-19) Research
SARS-CoV-2 infection and persistence in the human body and brain at autopsy
Nature. 2022 Dec;612(7941):758-763.
Coronavirus disease 2019 (COVID-19) is known to cause multi-organ dysfunction1-3 during acute infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some patients experiencing prolonged symptoms, termed post-acute sequelae of SARS-CoV-2 (refs. 4,5). However, the burden of infection outside the respiratory tract and time to viral clearance are not well characterized, particularly in the brain3,6-14. Here we carried out complete autopsies on 44 patients who died with COVID-19, with extensive sampling of the central nervous system in 11 of these patients, to map and quantify the distribution, replication and cell-type specificity of SARS-CoV-2 across the human body, including the brain, from acute infection to more than seven months following symptom onset. We show that SARS-CoV-2 is widely distributed, predominantly among patients who died with severe COVID-19, and that virus replication is present in multiple respiratory and non-respiratory tissues, including the brain, early in infection. Further, we detected persistent SARS-CoV-2 RNA in multiple anatomic sites, including throughout the brain, as late as 230 days following symptom onset in one case. Despite extensive distribution of SARS-CoV-2 RNA throughout the body, we observed little evidence of inflammation or direct viral cytopathology outside the respiratory tract. Our data indicate that in some patients SARS-CoV-2 can cause systemic infection and persist in the body for months.
Free full text.
Nature. 2022 Dec;612(7941):758-763.
Coronavirus disease 2019 (COVID-19) is known to cause multi-organ dysfunction1-3 during acute infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some patients experiencing prolonged symptoms, termed post-acute sequelae of SARS-CoV-2 (refs. 4,5). However, the burden of infection outside the respiratory tract and time to viral clearance are not well characterized, particularly in the brain3,6-14. Here we carried out complete autopsies on 44 patients who died with COVID-19, with extensive sampling of the central nervous system in 11 of these patients, to map and quantify the distribution, replication and cell-type specificity of SARS-CoV-2 across the human body, including the brain, from acute infection to more than seven months following symptom onset. We show that SARS-CoV-2 is widely distributed, predominantly among patients who died with severe COVID-19, and that virus replication is present in multiple respiratory and non-respiratory tissues, including the brain, early in infection. Further, we detected persistent SARS-CoV-2 RNA in multiple anatomic sites, including throughout the brain, as late as 230 days following symptom onset in one case. Despite extensive distribution of SARS-CoV-2 RNA throughout the body, we observed little evidence of inflammation or direct viral cytopathology outside the respiratory tract. Our data indicate that in some patients SARS-CoV-2 can cause systemic infection and persist in the body for months.
Free full text.
The new Omicron variant, Kraken XBB.1.5
Will the Kraken XBB.1.5 COVID Subvariant Get You?
Did you think we were done with COVID? The highly transmissible subvariant dubbed the Kraken XBB.1.5 is spreading fast. How can you avoid it?
https://www.peoplespharmacy.com/article ... nt-get-you
So many variants: Alpha (B.1.1.7), Beta (B.1.351), Delta (B.1.617.2) and Omicron (with lots of subvariants including BA.5, BQ.1 and BQ.1.1). Now we are faced with the Kraken XBB.1.5. It is spreading like wildfire. Why should you care?
Have You Given Up On COVID-19?
Most people seem to be fed up with the coronavirus. They have thrown away their masks and stopped worrying about catching COVID-19.
Those who have already caught the virus once figure they are now protected against future infections because their immunity is strong. Individuals who have been vaccinated and boosted believe that they have done everything possible to protect themselves. “Time to get on with life” is their mantra!
Why Is the Kraken XBB.1.5 Different?
We have all seen COVID variants come and go. Why should the Kraken XBB.1.5 be any different? What’s the big deal?
This subvariant is highly transmissible. It was first identified in the northeast US in October. The XBB.1.5 version of COVID-19 has rapidly raced through New York and New England. Now it has overtaken previous coronavirus variants throughout North America and Europe.
Why Are People Calling XBB.1.5 the Kraken?
Blame the name on Dr. Ryan Gregory. He is a biologist at the University of Guelph in Ontario, Canada. He got fed up with the alphabet soup of letters and numbers that virologists love to use. Who can remember mutations like E484K, K417N or B.1.1.529?
Dr. Gregory took note of a Tweet that referred to Omicron BA.2.75 as Centaurus. The name came from Greek mythology. Centaurus was the father of mythological beasts (Centaurs) that had the bodies of horses and the head and arms of humans.
That got him thinking of other names for COVID subvariants. He hit on Kraken, a mythical Nordic sea monster. This creature looks a bit like a giant squid and was reputed to attack ships with its long tentacles. The Kraken was purported to drag Scandinavian sailors down to their deaths. Kind of an apt image for the fast-spreading COVID XBB.1.5 subvariant.
Why Is the Kraken XBB.1.5 So Worrisome?
This variant is taking over fast! That means it is far more contagious than previous subvariants. Some infectious disease experts downplay the Kraken XBB.1.5 worry factor because it does not appear to cause more severe disease. But epidemiologists are concerned because it spreads so easily.
In addition, this subvariant appears to have developed the ability to evade our immune defenses (dubbed “immune evasive” by immunologists). People who have recovered from a previous COVID infection may be vulnerable to this new variant. And vaccination is less effective against the Kraken XBB.1.5.
Some public health experts insist that someone who is fully vaccinated and boosted will be protected against severe disease. We hope that is true, but we want to see more data before we draw any conclusions.
Even the bivalent booster wanes with time. Because of the unique mutations of the Kraken XBB.1.5, it is not clear how much extra protection the bivalent booster will provide. Some experts suggest that the answer is not very much.
[continued]
Did you think we were done with COVID? The highly transmissible subvariant dubbed the Kraken XBB.1.5 is spreading fast. How can you avoid it?
https://www.peoplespharmacy.com/article ... nt-get-you
So many variants: Alpha (B.1.1.7), Beta (B.1.351), Delta (B.1.617.2) and Omicron (with lots of subvariants including BA.5, BQ.1 and BQ.1.1). Now we are faced with the Kraken XBB.1.5. It is spreading like wildfire. Why should you care?
Have You Given Up On COVID-19?
Most people seem to be fed up with the coronavirus. They have thrown away their masks and stopped worrying about catching COVID-19.
Those who have already caught the virus once figure they are now protected against future infections because their immunity is strong. Individuals who have been vaccinated and boosted believe that they have done everything possible to protect themselves. “Time to get on with life” is their mantra!
Why Is the Kraken XBB.1.5 Different?
We have all seen COVID variants come and go. Why should the Kraken XBB.1.5 be any different? What’s the big deal?
This subvariant is highly transmissible. It was first identified in the northeast US in October. The XBB.1.5 version of COVID-19 has rapidly raced through New York and New England. Now it has overtaken previous coronavirus variants throughout North America and Europe.
Why Are People Calling XBB.1.5 the Kraken?
Blame the name on Dr. Ryan Gregory. He is a biologist at the University of Guelph in Ontario, Canada. He got fed up with the alphabet soup of letters and numbers that virologists love to use. Who can remember mutations like E484K, K417N or B.1.1.529?
Dr. Gregory took note of a Tweet that referred to Omicron BA.2.75 as Centaurus. The name came from Greek mythology. Centaurus was the father of mythological beasts (Centaurs) that had the bodies of horses and the head and arms of humans.
That got him thinking of other names for COVID subvariants. He hit on Kraken, a mythical Nordic sea monster. This creature looks a bit like a giant squid and was reputed to attack ships with its long tentacles. The Kraken was purported to drag Scandinavian sailors down to their deaths. Kind of an apt image for the fast-spreading COVID XBB.1.5 subvariant.
Why Is the Kraken XBB.1.5 So Worrisome?
This variant is taking over fast! That means it is far more contagious than previous subvariants. Some infectious disease experts downplay the Kraken XBB.1.5 worry factor because it does not appear to cause more severe disease. But epidemiologists are concerned because it spreads so easily.
In addition, this subvariant appears to have developed the ability to evade our immune defenses (dubbed “immune evasive” by immunologists). People who have recovered from a previous COVID infection may be vulnerable to this new variant. And vaccination is less effective against the Kraken XBB.1.5.
Some public health experts insist that someone who is fully vaccinated and boosted will be protected against severe disease. We hope that is true, but we want to see more data before we draw any conclusions.
Even the bivalent booster wanes with time. Because of the unique mutations of the Kraken XBB.1.5, it is not clear how much extra protection the bivalent booster will provide. Some experts suggest that the answer is not very much.
[continued]