Article:

Now we know how COVID attacks your heart Even patients with mild COVID symptoms could face a higher risk of developing heart disease and stroke

By Sanjay Mishra

Nov 07, 2023 04:08 PM5 min. readView original Scientists have noticed that COVID-19 can trigger serious cardiovascular problems, especially among older people who have a buildup of fatty material in their blood vessels. But now a new study has revealed why and shown that SARS-CoV-2, the virus that causes COVID-19, directly infects the arteries of the heart.

The study also found that the virus can survive and grow inside the cells that form plaque—the buildup of fat-filled cells that narrow and stiffen the arteries leading to atherosclerosis. If the plaque breaks, it can block blood flow and cause a heart attack or a stroke. The SARS-CoV-2 infection makes the situation worse by inflaming the plaque and increasing the chance that it breaks free.

This can explain long-term cardiovascular effects seen in some, if not all, COVID-19 patients.

SARS-CoV-2 virus has already been found to infect many organs outside the respiratory system. But until now it hadn't been shown to attack the arteries.

"No one was really looking if there was a direct effect of the virus on the arterial wall," says Chiara Giannarelli, a cardiologist at NYU Langone Health, in New York, who led the study. Giannarelli noted that her team detected viral RNA—the genetic material in the virus—in the coronary arteries. “You would not expect to see [this] several months after recovering from COVID.”

Mounting evidence now shows that SARS-CoV-2 is not only a respiratory virus, but it can also affect the heart and many other organ systems, says Ziyad Al-Aly, a clinical epidemiologist at Washington University in St. Louis. Al-Aly's research has shown that the risk of developing heart and cardiovascular diseases, including heart failure, stroke, irregular heart rhythms, cardiac arrest, and blood clots increases two to five times within a year of COVID-19, even when the person wasn't hospitalized.

"This important study links, for the first time, directly the SARS-CoV-2 virus with atherosclerotic plaque inflammation," says Charalambos Antoniades, chair of cardiovascular medicine at the University of Oxford, United Kingdom.

Virus triggers the inflammation in plaque

A recent study of more than 800,000 people led by Fabio Angeli, a cardiologist at University of Insubria in Varese, Italy, has shown that COVID-19 patients develop high blood pressure twice as often as others. More worrying is that the risk of cardiac diseases can also rise for patients who suffered only mild COVID symptoms.

"I saw a patient who now has a defibrillator, and she didn't even have a severe [COVID] illness," says Bernard Gersh, a cardiologist at Mayo Clinic, Rochester, Minnesota.

Wondering whether the cardiovascular damage during COVID was due to the virus directly attacking the blood vessels, the NYU team analyzed autopsied tissue from the coronary arteries and plaque of older people who had died from COVID-19. They found the virus was present in the arteries regardless of whether the fatty plaques were big or small.

"The original finding in this study is that the virus was convincingly found in the plaque in the coronary artery," says Juan Carlos Kaski, a cardiovascular specialist at St George's, University of London, who was not involved in the study.

The NYU team found that in the arteries, the virus predominantly colonized the white blood cells called macrophages. Macrophages are immune cells that are mobilized to fight off an infection, but these same cells also absorb excess fats—including cholesterol from blood. When microphages load too much fat, they change into foam cells, which can increase plaque formation.

To confirm that the virus was indeed infecting and growing in the cells of the blood vessels, scientists obtained arterial and plaque cells—including macrophages and foam cells—from healthy volunteers. Then they grew these cells in the lab in petri dishes and infected them with SARS-CoV-2.

Giannarelli found that although virus infected macrophages at a higher rate than other arterial cells, it did not replicate in them to form new infectious particles. But when the macrophages had become loaded with cholesterol and transformed into foam cells, the virus could grow, replicate, and survive longer.

"We found that the virus tended to persist longer in foam cells," says Giannarelli. That suggests that foam cells might act as a reservoir of SARS-CoV-2. Since more fatty buildup would mean a greater number of foam cells, plaque can increase the persistence of the virus or the severity of COVID-19.

Scientists found that when macrophages and foam cells were infected with SARS-CoV-2 they released a surge of small proteins known as cytokines, which signal the immune system to mount a response against a bacterial or viral infection. In arteries, however, cytokines boost inflammation and formation of even more plaque.

"We saw that there was a degree of inflammation [caused] by the virus that could aggravate atherosclerosis and cardiovascular events," says Giannarelli.

These findings also confirm previous reports that measuring inflammation in the blood vessel wall can diagnose the extent of long-term cardiovascular complications after COVID-19, says Antoniades.

"What this study has found is that plaque rupture can be accelerated and magnified by the presence of the virus," says Kaski.

Understanding heart diseases after COVID

While this new research clearly shows that SARS-CoV-2 can infect, grow, and persist in the macrophages of plaques and arterial cells, more studies are needed to fully understand the many ways COVID-19 can alter cardiac health.

"The NYU study identifies one potential mechanism, especially the viral reservoir, to explain the possible effects" says Gersh. "But It's not going to be the only mechanism."

This study only analyzed 27 samples from eight elderly deceased patients, all of whom already had coronary artery disease and were infected with the original strains of virus. So, the results of this study do not necessarily apply to younger people without coronary artery disease; or to new variants of the virus, which cause somewhat milder disease, says Angeli.

"We do not know if this will happen in people who have been vaccinated," says Kaski. "There are lots of unknowns."

It is also not clear whether and to what extent the high inflammatory reaction observed in the arteries of patients within six months after the infection, as shown in the new study, will last long-enough to trigger new plaque formation. "New studies are needed to show the time-course of the resolution of vascular inflammation after the infection," says Antoniades.

COVID patients should watch for any new incidence of shortness of breath with exertion, chest discomfort, usually with exertion, palpitations, loss of consciousness; and talk to their physician about possible heart disease.

Thank you to Reddit user u/spacelambhat for providing article content. https://www.reddit.com/r/Coronavirus/comments/17qher4/comment/k8c8ila/

Edited to update title and info accordingly

Novavax’s updated Covid vaccine won the backing of the FDA and CDC.

Evolving peak SARS-CoV-2 loads relative to symptom onset may influence home-test timing

News brief

September 28, 2023

Mary Van Beusekom, MS

Topics COVID-19

In a group of adults in the state of Georgia tested for both COVID-19 and influenza A, most of whom were vaccinated and/or previously infected, median SARS-CoV-2 viral loads peaked on the fourth day of symptoms, while flu loads peaked soon after symptom onset.

The authors of the study, published today in Clinical Infectious Diseases, say the findings have implications for the use of rapid antigen tests for COVID-19 and flu.

The Emory University-led team evaluated SARS-CoV-2 and influenza A viral loads relative to symptom duration in symptomatic patients aged 16 years and older tested for COVID-19 from April 2022 to April 2023, a period of Omicron variant predominance.

Median age among the 348 COVID-positive patients was 39.2 years, 65.5% were women, and 91.1% were vaccinated, previously infected, or both. Among the 74 influenza A-positive patients, the median age was 35.0 years, and 55.4% were women.

The researchers noted that early in the pandemic, viral loads peaked at the same time as symptom onset and then steadily decreased. At that time, the Food and Drug Administration approved rapid antigen test instructions directing symptomatic people to test only once in the first week of symptoms. In November 2022, the FDA amended the instructions, recommending repeat testing within 48 hours of an initial negative result. Peak viral loads now peak days later

Median SARS-CoV-2 viral loads, as measured by polymerase chain reaction cycle threshold (Ct) and antigen concentrations, rose from symptom onset, peaking on the fourth or fifth day of symptoms. Estimated rapid antigen test sensitivity was 30.0% to 60.0% on the first day, 59.2% to 74.8% on the third, and 80.0% to 93.3% on the fourth.

Median influenza viral loads among the 74 flu-positive patients peaked on the second day of symptoms.

"Our data suggest that the relationship between SARS-CoV-2 Ct value distributions (as a well-established proxy for viral load distributions) and the timing of symptom onset in a highly immune population is very different than the relationship between these parameters observed early in the pandemic—a finding with major implications for testing practice going forward," the researchers wrote.

TUCSON, Ariz. (KVOA) - In a groundbreaking development, Arizonans can now apply for worker's compensation if they contract COVID-19 while on the job. This landmark decision stems from a widow's determined fight to secure worker's compensation following her husband's tragic demise due to COVID-19.

Gabrielle Parish has all of the details after an Arizona woman won a lawsuit to receive workers comp benefits after her husband died after getting Covid-19 at work.

Court documents unequivocally state that if someone contracts COVID-19 at their workplace, they are entitled to file for worker's compensation. An essential detail to note is that if a worker succumbs to the virus, their next of kin will receive financial support.

We had the opportunity to speak with Attorney Dennis Kurth, who played a crucial role in this case. He shed light on how it all began: "She filed a work comp complaint with the Industrial Commission of Arizona to secure widow's benefits, and that claim was denied," Kurth explained.

This denial prompted the widow to take legal action against the company, marking the inception of this historic case. Kurth noted, "This is apparently the first case where an insurance company lost and then decided to take it to the court of appeals. They are arguing that COVID-19 should never be covered by workers' comp as a matter of law."

However, there is a catch. If an employee chooses to accept the compensation, they relinquish their right to sue the company, even if they can prove they contracted the virus on the job. Additionally, there's a time frame to keep in mind: workers must file their claims within a year after contracting COVID-19.

Kurth added, "Now that the court of appeals has published an opinion stating that COVID-19 is compensable if you meet the statutory and case law requirements, people may start looking back and thinking, 'Oh, I should have filed a claim.'"

It's essential to emphasize that the person filing for worker's compensation must have contracted the disease at work for this ruling to apply. Otherwise, these provisions do not come into play.

Posted at the top of the article: "We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply. "

Sorry about the sensationalist title; I just copy/pasted the original.

Original study this article is based on: "A computationally designed antigen eliciting broad humoral responses against SARS-CoV-2 and related sarbecoviruses" https://www.nature.com/articles/s41551-023-01094-2

YouTube starts censoring medical information and content. And only content that "meets WHO guidelines" appears on YouTube. No other medical data.

I found this very dangerous, because people should be able to judge themselves what they want to read or hear about. It's our body and your health. I would like to make my own decisions.

More info: https://support.google.com/youtube/answer/13813322

U.S. Investigating Veterans Nursing Homes in New Jersey for Possibly Understating Covid Deaths https://www.wsj.com/articles/u-s-investigating-veterans-nursing-homes-in-new-jersey-for-possibly-understating-covid-deaths-11603900994 The U.S. Department of Justice has opened a civil-rights investigation into New Jersey veterans homes’ handling of deadly coronavirus outbreaks earlier this year, according to a letter from the department to the state’s governor, Phil Murphy.

Four preliminary laboratory studies released over the weekend found that antibodies from previous infections and vaccinations appear capable of neutralizing the variant, known as BA.2.86.

"It is reassuring," says Dr. Dan Barouch, who conducted one of the studies at the Beth Israel Deaconess Medical Center in Boston.

When it was first spotted, BA.2.86 set off alarm bells. It contains more than 30 mutations on the spike protein the virus uses to infect cells. That's a level of mutation on par with the original Omicron variant, which caused a massive surge.

The concern was BA.2.86, while still rare, could sneak around the immunity people had built up and cause another huge, deadly wave.

TLDR:

As the number of problems that require mask wearing (including air pollution and COVID-19) grows, masks are increasingly important. Now that masks are all but required, the harmful chemicals that can be released from them must be evaluated. In this study, VOCs generated from various types of masks, including commonly used KF94 disposable masks, were assessed. The types and concentrations of VOCs that humans are likely to be exposed to from these masks under various conditions (i.e., emission time, temperature, and mask types) were calculated and compared. This study demonstrated that disposable masks (KF94) released higher concentrations of TVOCs in comparison to cotton masks, with values of 3730 ± 1331 µg m–3 for KF94 and 268 ± 51.6 µg m–3 for cotton masks. The concentrations of TVOCs in KF94 masks are high enough to pose a concern based on indoor air quality guidelines established by the German Federal Environment Agency. However, when KF94 masks were opened and left undisturbed for 30 min at room temperature, TVOC concentrations significantly decreased to 724 ± 5.86 µg m–3 (a 78.2 ± 9.45% reduction from levels measured immediately upon opening). It is clear that particular attention must be paid to the VOCs associated with the use of KF94 masks their effects on human health. Based on our findings, we suggest that prior to wearing a KF94 mask, each product should be opened and not worn for at least 30 min, thereby reducing TVOC concentrations to levels that will not impair human health.