Showing: 1 - 9 of 9 RESULTS

Trump says he’s ‘immune’ to COVID. His doctors won’t say when he last tested negative

President Donald Trump on Sunday said he may have the “protective glow” of immunity from COVID-19 although it remains unknown when he last tested negative for the disease.

In an extensive interview with Fox News’ Maria Bartiromo, Trump claimed he “beat” the novel coronavirus, passing the “highest standards” for proving so. Trump said he is also no longer taking any medications to combat the virus after being placed on a heavy steroid typically given to individuals with more severe cases.

“It looks like I’m immune for, I don’t know, maybe a long time, maybe a short time,” he said. “It could be a lifetime. Nobody really knows, but I’m immune. So the president is in very good shape to fight the battles.”

As the Associated Press reported, COVID-19 reinfection is unlikely for at least three months after acquiring the virus, but few diseases come with lifetime immunity. Researchers said in August that a Hong Kong man had been infected with the virus for a second time, suggesting that immunity may be short-lasting for at least some patients.

Trump spoke hours after his physician said in a letter Saturday that Trump is no longer considered a transmission risk and can now be around others safely.

“Now at day 10 from symptom onset, fever-free for well over 24 hours and all symptoms improved, the assortment of advanced diagnostic tests obtained reveal there is no longer evidence of actively replicating virus,” Dr. Sean Conley said in a memo. “Moving forward, I will continue to monitor him clinically as he returns to an active schedule.”

Conley added that Trump has “decreasing viral loads,” meaning a lessening of how much virus is present in any sample taken from a patient.

But Conley, who had earlier this month admitted he was providing a rosier outlook on the president’s condition to convey an “upbeat” picture, did not say whether Trump has recently tested negative for the virus, nor did he indicate when Trump’s last negative test was.

Trump, his staff and medical team have repeatedly refused to provide specifics about his testing regime. Pressed by reporters last week, Conley said, “I don’t want to go backwards.”

Saturday’s letter also did not address Trump’s treatment protocol.

Centers for Disease Control and Prevention guidelines stipulate that those stricken with the virus isolate themselves for at least 10 days following the onset of symptoms — with those suffering from more severe cases needing to isolate for up to 20 days. Trump first reported symptoms 10 days ago.

The president’s treatment included a strong steroid, dexamethasone, as well as an antibody cocktail produced by Regeneron. He required supplemental oxygen on two occasions after experiencing symptoms, according to his medical team.

Trump is set to return to the campaign trail Monday for a Florida rally before visiting Pennsylvania and Iowa later in the week. On Saturday, the president held his first public event at the White House since his diagnosis.

“It is disappearing,” Trump said of the coronavirus as cases

Trump declares himself ‘immune’ to Covid-19. His doctors won’t say when he last tested negative.

President Donald Trump on Sunday said he may have the “protective glow” of immunity from Covid-19 although it remains unknown when he last tested negative for the disease.

In an extensive interview with Fox News’ Maria Bartiromo, Trump claimed he “beat” the novel coronavirus, passing the “highest standards” for proving so. Trump said he is also no longer taking any medications to combat the virus after being placed on a heavy steroid typically given to individuals with more severe cases.

“It looks like I’m immune for, I don’t know, maybe a long time, maybe a short time,” he said. “It could be a lifetime. Nobody really knows, but I’m immune. So the president is in very good shape to fight the battles.”

As the Associated Press reported, Covid-19 reinfection is unlikely for at least three months after acquiring the virus, but few diseases come with lifetime immunity. Researchers said in August that a Hong Kong man had been infected with the virus for a second time, suggesting that immunity may be short-lasting for at least some patients.

Trump spoke hours after his physician said in a letter Saturday that Trump is no longer considered a transmission risk and can now be around others safely.

“Now at day 10 from symptom onset, fever-free for well over 24 hours and all symptoms improved, the assortment of advanced diagnostic tests obtained reveal there is no longer evidence of actively replicating virus,” Dr. Sean Conley said in a memo. “Moving forward, I will continue to monitor him clinically as he returns to an active schedule.”

Conley added that Trump has “decreasing viral loads,” meaning a lessening of how much virus is present in any sample taken from a patient.

But Conley, who had earlier this month admitted he was providing a rosier outlook on the president’s condition to convey an “upbeat” picture, did not say whether Trump has recently tested negative for the virus, nor did he indicate when Trump’s last negative test was.

Trump, his staff and medical team have repeatedly refused to provide specifics about his testing regime. Pressed by reporters last week, Conley said, “I don’t want to go backwards.”

Saturday’s letter also did not address Trump’s treatment protocol.

Centers for Disease Control and Prevention guidelines stipulate that those stricken with the virus isolate themselves for at least 10 days following the onset of symptoms — with those suffering from more severe cases needing to isolate for up to 20 days. Trump first reported symptoms 10 days ago.

The president’s treatment included a strong steroid, dexamethasone, as well as an antibody cocktail produced by Regeneron. He required supplemental oxygen on two occasions after experiencing symptoms, according to his medical team.

Trump is set to return to the campaign trail Monday for a Florida rally before visiting Pennsylvania and Iowa later in the week. On Saturday, the president held his first public event at the White House since his diagnosis.

“It is disappearing,” Trump said of the coronavirus as cases

Trump falsely dismisses virus danger: ‘You catch it, you get better, and you’re immune’

The president’s continued effort to minimize the danger comes as more than 211,000 American lives have died from the virus that continues to spread in many parts of the U.S., including inside the White House and within the ranks of his own administration.

PHOTO: President Donald Trump pulls off his protective face mask as he poses atop the Truman Balcony of the White House after returning from being hospitalized at Walter Reed Medical Center for coronavirus disease (COVID-19) treatment, Oct. 5, 2020.

President Donald Trump pulls off his protective face mask as he poses atop the Truman Balcony of the White House after returning from being hospitalized at Walter Reed Medical Center for coronavirus disease (COVID-19) treatment, Oct. 5, 2020.

President Donald Trump pulls off his protective face mask as he poses atop the Truman Balcony of the White House after returning from being hospitalized at Walter Reed Medical Center for coronavirus disease (COVID-19) treatment, Oct. 5, 2020.

Even as he touted the Regeneron antibody treatment he’s taken as a “cure,” without evidence, he portrayed his hospitalization as having been unnecessary and suggested he could have “would have done it fine without drugs.”

“I didn’t have to go in frankly, I think it would have gone away by itself,” Trump said.

The president’s confidence in his condition comes after he was twice administered oxygen in recent days as he has fought the virus and seemed to confirm he is still being treated with a steroid, even as he said he is off all other medications.

“I think I’m taking almost nothing,” Trump said. “I think you go a little bit longer on, they have steroid, it’s not heavy steroid, they have that go a little bit longer, but I am not taking, I am almost not taking anything. I feel great.”

The White House and the president’s doctors have refused to answer basic questions about Trump’s illness and treatments, such as when he last tested negative for COVID-19 before he received a positive test and what impact the virus has had on his lungs.

“I will be tested very soon, but I am essentially very clean, they say it’s over a period of six, seven days, and I was — you know amazing thing happened to me I just went in, I didn’t feel good. And that’s OK, I expected that at some point,” Trump said, likening the virus to a “microscopic piece of dust.”

Despite not having been tested, the president said he doesn’t think he is contagious “at all anymore” and said he is feeling so well that he would like to do a rally tonight and felt he could have done one last night.

The president said whether or not he is contagious, if he were at a rally

Charting a Covid-19 Immune Response

Amid a flurry of press conferences delivering upbeat news, President Trump’s doctors have administered an array of experimental therapies that are typically reserved for the most severe cases of Covid-19. Outside observers were left to puzzle through conflicting messages to determine the seriousness of his condition and how it might inform his treatment plan.

Though Mr. Trump may leave Walter Reed National Military Medical Center tonight to continue his recovery in the White House, the future of his health status is unclear. Physicians have warned that the president remains at a precarious point in his disease course. The coronavirus can be a tricky adversary — and for many people whose cases of Covid-19 are severe, the greatest threat to survival might not be the pathogen itself, but the deadly forces that the body marshals to fight it.

To quash the virus, the immune system unleashes an arsenal of powerful weapons. Sometimes these turn inward and destroy healthy tissues. Combatting this friendly fire has become as crucial a part of the Covid-19 treatment strategy as subduing the virus itself.

Mild and Severe Cases

From the moment the coronavirus enters the body, the immune system mounts a defense, launching a battalion of cells and molecules against the invader.

Most people who are infected with the coronavirus recover, sometimes without ever experiencing symptoms, and do not progress to severe Covid-19. In some cases, the virus may even be brought under control before it has the chance to become established in the body.

Should the virus gain a foothold, it will swiftly infiltrate cells and repeatedly copy itself until levels of the virus, or the viral load, build up. The viral load may even peak before symptoms appear, if they appear at all.


Still, symptoms like fever, cough, congestion and fatigue — all of which have been reported in Mr. Trump — signal that an immune response is underway in the body and may be driving the viral load down. Once the immune system has finished the job, symptoms may abate without medical intervention.

In severe cases, however, the clash between the virus and the immune system rages much longer. Other parts of the body, including those not directly affected by the virus, become collateral damage, prompting serious and potentially life-threatening symptoms.

[For more details on the progression of a typical Covid-19 case, see Charting a Coronavirus Infection.]

Triggering the Immune System

A typical immune response launches its defense in two phases. First, a cadre of fast-acting fighters rushes to the site of infection and attempts to corral the invader. This so-called innate response buys the rest of the immune system time to mount a second, more tailored attack, called the adaptive response, which kicks in about a week later, around the time the first wave begins to wane.


In people with severe disease, however, the immune system appears to botch the timing. The first wave mobilizes too late and must play a frantic game of catch-up that persists even after reinforcements

Immune Cells Show the Way in This Medical Mystery

A 54-year-old man presents to a foot and ankle clinic in Maryland with a diffuse, hard lesion in the middle of the arch of his left foot; it is tender to the touch and painful to walk on.

He explains that it began developing gradually about 3 years earlier as a dry, scaly spot, and that the skin later cracked but there was no pain. He says he had not been concerned, since he had a history of having severe eczema and dry patches of skin in the same spot on his foot.

However, his efforts to treat the eczema with topical cortisone cream and “over-the-counter acid” have been ineffective, he said, adding that he became concerned when the lesion slowly grew thicker and harder.

The patient’s surgical and medical histories include thyroidectomy (for thyroid cancer) at age 28, a diagnosis of bipolar disorder, headaches/migraines, and high blood pressure. His family history is unremarkable, and clinical assessment reveals no major abnormalities.

Dermatological Examination

Dermatological assessment shows a 3.0-cm, scaly, keratotic patch with slight erythema in the plantar central region of the left arch, which is notably tender to palpation. There is no evidence of skin atrophy or lymphadenopathy. Laboratory test results are within normal limits.

Clinicians perform a skin punch biopsy and send the sample for histological evaluation.

The report notes infiltration of atypical lymphocytes in the upper dermis. Most of the atypical lymphocytes are round or ovoid with a cerebriform nuclear contour but with no clear nuclear membrane or nucleoli.

Single units or small clusters of these have infiltrated up into the epithelial layers (epidermotropism), down into the eccrine sweat glands (syringotropism) and the walls of the blood vessels in the dermis.

image

Histopathology and immunostaining profiles of mycosis fungoides palmaris et plantaris: (A) An infiltrate of the atypical lymphocytes in the upper dermis (hematoxylin and eosin [H&E], 40×1). (B) Round or ovoid atypical lymphocytes with cerebriform nuclear contour and no clear nuclear membrane or nucleoli (HE, 400×1). (C) Atypical lymphocytes infiltrating into the epidermis (epidermotropism) (HE, 100×1). (D) Atypical lymphocytes infiltrating into eccrine sweat glands (syringotropism) (HE, 100×1). (E) Perivascular infiltration of the atypical lymphocytes in the dermis (HE, 100×1). (F) Strong CD4 expression in atypical lymphocytes (3, 3 -diaminobenzidine [DAB], 100×1). (G) Reduced CD7 expression in atypical lymphocytes (DAB, 100×1). (H) Reduced CD8 expression in atypical lymphocytes (DAB, 100×1).

Immunostaining of the atypical lymphocytes shows almost uniformly strong positive staining for CD3, CD4 antibodies and about 30% positivity for CD7 and CD8; staining for CD20 was negative.

Clinicians note an approximately 3:1 ratio of CD4- to CD8-positive cells. Results of periodic acid-Schiff staining for fungal elements are negative for both spores and hyphae; yet the histomorphology and immunostaining profiles are judged to be consistent with mycosis fungoides palmaris et plantaris (MFPP).

The team discusses the treatment options with the patient, and he is referred to a dermatologist. The patient receives topical psoralen plus ultraviolet A (PUVA) photochemotherapy, which results in complete remission.

At 5-year follow-up, the

Elderly hit so hard by COVID-19 because of lower levels of certain immune cells

Elderly people who get COVID-19 have lower levels of important immune cells, which may explain why they are more likely than younger patients to have severe symptoms or die, new research suggests.

For the study, the researchers analyzed blood samples from 30 people with mild COVID-19, ranging in age from the mid-20s to late-90s. Compared with healthy people, all of the COVID-19 patients had lower numbers of T cells — which target virus-infected cells — in their blood.

But COVID-19 patients over 80 years of age had fewer T cells than those who were younger, and so-called “killer” T cells in older patients produced lower amounts of cytotoxic molecules that find and kill infected cells, the investigators found.

This age-related difference in immune response may partially explain why older COVID-19 patients have more severe illness, according to the authors of the study published this month in the journal mBio.

“Elderly people have more severe diseases compared to young people, and we found that the cytotoxic part of immune control is not as efficient to respond to the virus in older people,” said study leader Gennadiy Zelinskyy, a virologist at University Hospital Essen, in Germany.

The lower levels of T cells in COVID-19 patients is among the many unwelcome surprises of the pandemic, he noted in a news release from the American Society for Microbiology.

Once inside the body, most viruses trigger a boost in T cells, including cytotoxic-producing killer T cells that play a critical role in destroying virus-infected cells. If a person’s immune system produces fewer of these T cells, it has greater difficulty combating a viral infection.

The findings suggest that cytotoxic T cells play a key role in control of early infections, but Zelinskyy said it’s too soon to know if these cells can be used to create an immunotherapy against the new coronavirus.

More study is needed to understand the potential risks and benefits of interfering with T cells as a way to control the new coronavirus and other viruses, he concluded.

More information
The U.S. Centers for Disease Control and Prevention has more on COVID-19.

Copyright 2020 HealthDay. All rights reserved.

Source Article

Immune system holds clues to virus reaction

One of COVID-19’s scariest mysteries is why some people are mildly ill or have no symptoms and others rapidly die — and scientists are starting to unravel why.

An international team of researchers found that in some people with severe COVID-19, the body goes rogue and attacks one of its own key immune defenses instead of fighting the coronavirus. Most were men, helping to explain why the virus is hitting men harder than women.

And separate research suggests that children fare better than adults thanks to robust “first responder” immune cells that wane with age.


They’re the latest in a list of studies uncovering multiple features of the immune system’s intricate cascade that can tip the scales between a good or bad outcome. Next up: Figuring out if all these new clues might offer much-needed ways to intervene.

“We have the knowledge and capability of really boosting many aspects of the immune system. But we need to not use the sledge hammer,” cautioned Dr. Betsy Herold of New York’s Albert Einstein College of Medicine, who co-authored the child study.

Adding to the complexity, people’s wildly varying reactions also reflect other factors, such as how healthy they were to begin with and how much of the virus — the “dose” — they were exposed to.

“Infection and what happens after infection is a very dynamic thing,” said Alessandro Sette, a researcher at the La Jolla Institute for Immunology in San Diego, who is studying yet another piece of the immune response.

IMMUNE PRIMER

There are two main arms of the immune system. Innate immunity is the body’s first line of defense. As soon as the body detects a foreign intruder, key molecules, such as interferons and inflammation-causing cytokines, launch a wide-ranging attack.

Innate immune cells also alert the slower-acting “adaptive” arm of the immune system, the germ-specific sharpshooters, to gear up. B cells start producing virus-fighting antibodies, the proteins getting so much attention in the vaccine hunt.

But antibodies aren’t the whole story. Adaptive immunity’s many other ingredients include “killer” T cells that destroy virus-infected cells — and “memory” T and B cells that remember an infection so they spring into action quicker if they encounter that germ again.

A MISSING PIECE

Usually when a virus invades a cell, proteins called Type I interferons spring into action, defending the cell by interfering with viral growth. But new research shows those crucial molecules were essentially absent in a subset of people with severe COVID-19.

An international project uncovered two reasons. In blood from nearly 1,000 severe COVID-19 patients, researchers found 1 in 10 had what are called auto-antibodies — antibodies that mistakenly attack those needed virus fighters. Especially surprising, autoimmune disorders tend to be more common in women — but 95% of these COVID-19 patients were men.

The researchers didn’t find the damaging molecules in patients with mild or asymptomatic COVID-19.

In another 660 severely ill patients, the same team found 3.5% had gene mutations that didn’t produce Type I interferons.

Each

Moderna says coronavirus vaccine boosts immune system response in older adults

Biotech company Moderna announced on Tuesday that its coronavirus vaccine candidate elicited immune responses in older adults from a Phase 1 study in levels comparable to those seen in younger adults. The findings were published Tuesday in the New England Journal of Medicine.

The vaccine candidate, dubbed mRNA-1273, “induced consistently high levels” of neutralizing antibody levels in 40 healthy participants across two age cohorts – 56-70 and 71 and over – per the company announcement.

CLICK HERE FOR FULL CORONAVIRUS COVERAGE

Biotech company Moderna announced on Tuesday that its coronavirus vaccine candidate elicited immune responses in older adults from a Phase 1 study in levels comparable to those seen in younger adults. (iStock)

Biotech company Moderna announced on Tuesday that its coronavirus vaccine candidate elicited immune responses in older adults from a Phase 1 study in levels comparable to those seen in younger adults. (iStock)

“These interim Phase 1 data suggests that mRNA-1273, our vaccine candidate for the prevention of COVID-19, can generate neutralizing antibodies in older and elderly adults at levels comparable to those in younger adults,” Dr. Tal Zaks, chief medical officer of Moderna, said in the announcement. “Given the increased morbidity and mortality of COVID-19 in older and elderly adults, these data give us optimism in demonstrating mRNA-1273’s protection in this population, which is being evaluated in the Phase 3 COVE study.”

MODERNA SEES ‘POSITIVE’ PHASE I DATA FOR POTENTIAL CORONAVIRUS VACCINE

The data stemmed from a second interim analysis which assessed a two-dose vaccination administered 28 days apart in two dose levels, 25 micrograms (µg) and 100 micrograms, reporting findings one month after the second dose.

“This analysis found that both the 25 µg and 100 µg dose levels were generally well-tolerated in both age cohorts,” per the announcement.

The 100 microgram dose elicited higher antibody levels, “supporting the selection of the 100 µg dose for further study in the Phase 3 trial.” Moderna previously announced plans to use the 100 microgram dose in its late-stage trial, which will enroll up to 30,000 volunteers in the U.S. As of Sept. 25, there were 27,232 participants enrolled, 30% of which were from diverse communities.

CORONAVIRUS WAS EVEN MORE CONTAGIOUS AT BEGINNING OF PANDEMIC THAN EXPERTS THOUGHT, STUDY FINDS

Company officials said the majority of adverse events were mild to moderate, like headache, fatigue and chills, among others.

After the second vaccination, one patient in the 56-70 cohort with the 25 microgram dose experienced a fever, and a second patient in the older cohort and higher dose had fatigue, but officials said “clinical laboratory values of Grade 2 or higher revealed no pattern of concern” and that the patients would be followed through 13 months for a longer assessment.

The findings were said to be confirmed through three live virus assays, and “robust neutralizing activity was observed in all participants 14 days after the second vaccination.”

The U.S. government already struck a deal with Moderna for 100 million doses of the vaccine, with an option to buy an additional 400 million doses.

CLICK HERE FOR THE FOX NEWS APP

Source Article

One in Seven Dire COVID Cases May Result from a Faulty Immune Response

Perhaps the most unnerving aspect of COVID-19 is its startling range of severity: from completely asymptomatic to deadly. Starting early in the pandemic, researchers identified factors that put people at risk of a serious case of the disease, such as advanced age, having certain chronic diseases and being male. But these demographic trends do not get at the biological mechanisms that actually cause a life-threatening infection. Nor do they explain why some young, fit, healthy people become mortally ill from the SARS-CoV-2 virus.

Two related papers published in Science onSeptember 24 begin to address these mysteries. They may also partially account for men’s greater vulnerability to the virus and point the way to possible treatments and protective measures. Both studies highlight the critical role of a class of immune system proteins called interferons, so named because they interfere with the replication of viruses.

The new papers were produced by the COVID Human Genetic Effort, a huge international consortium of researchers hunting for genetic mutations that either make individuals unusually susceptible to SARS-CoV-2 or confer exceptional resistance. The consortium is co-led by Jean-Laurent Casanova of the Rockefeller University and Helen Su of the National Institute of Allergy and Infectious Diseases, who are co-senior authors of both of the studies.

In their first paper, the researchers compared DNA from 659 gravely ill COVID-19 patients from around the world with DNA from a control group of 534 infected people who were only mildly affected by the novel coronavirus or did not have symptoms. The scientists specifically looked for mutations that would impair the production of type I interferons—a set of proteins made by every cell in the body that comprise a first-line defense against viruses. Previous work by Casanova and others showed that such mutations left people extremely vulnerable to influenza and other viruses. As it turned out, some of the same mutations associated with life-threatening flu were also present in 3.5 percent of patients with life-threatening COVID-19. No one in the new study’s control group had these mutations.

The second paper focuses on another mechanism that disables interferon responses in patients with severe COVID-19. In this set of studies, researchers examined blood samples from 987 such individuals and discovered that 13.7 percent contained antibodies—dubbed “auto-antibodies”—to the patients’ own type I interferons. In 10.2 percent of the subjects, the auto-antibodies completely blocked the action of these critical virus fighters.

Lab experiments showed that when human cells were exposed to plasma (the liquid part of blood) taken from patients with these self-attacking antibodies, the cells could not defend themselves against SARS-CoV-2. The antibodies were found in 12.5 percent of the severely ill men but only 2.6 percent of similarly ill women—making them a possible factor in the higher COVID-19 mortality rate among men. They were also more common in patients older than 65.

Antibodies to the body’s own cytokines, cell-signaling proteins of the immune system that include interferons, have been known to exacerbate other types of infections. The effect is the same as having