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/

I requested for "sidebar" to be placed in the pop-up menu after long pressing an instance name. I don't know when it was implemented and I don't know if it was in reaponse to my request, but I noticed it today and wanted to say "thank you"!

"The authors proposed three universal concepts of selection: the basic ability to endure; the enduring nature of active processes that may enable evolution; and the emergence of novel characteristics as an adaptation to an environment."

Rich, high-fat foods such as ice cream are loved not only for their taste, but also for the physical sensations they produce in the mouth — their ‘mouthfeel’. Now scientists have identified a brain area that both responds to the smooth texture of fatty foods and uses that information to rate the morsel’s allure, guiding eating behaviour1.

These findings, published on 16 October in The Journal of Neuroscience, “add a new dimension” of the eating experience to scientists’ understanding of what motivates people to choose certain foods, says Ivan de Araujo, a neuroscientist at the Max Planck Institute for Biological Cybernetics in Tübingen, Germany, who was not involved in the study.

A tongue for texture

To explore how food textures influence eating habits, Fabian Grabenhorst, a neuroscientist at the University of Oxford, UK, and his colleagues set out to quantify the mouthfeel of fatty foods. The authors prepared several milkshakes with varying fat and sugar contents and placed a sample of each between two pig tongues procured from a local butcher. The researchers then slid the tongues across each other and measured the amount of friction between the two surfaces, providing a numerical index of each shakes smoothness.

The researchers then gave 22 participants milkshakes with the same compositions as those tested on the pig tongues. After tasting each milkshake, participants placed bids on how much they would spend to drink a full glass of it after the experiment.

Accompanying brain scans showed that activity patterns in an area called the orbitofrontal cortex (OFC), which is involved in reward processing, reflected the shakes’ texture. The scans also identified OFC activity patterns that reflected participants’ bids, suggesting that this brain region links mouthfeel to the value placed on that food.

To find out whether this finding extends to food intake, the researchers invited the participants to return to the laboratory for a free lunch of several curry dishes with varying fat contents. Unbeknown to the participants, the researchers measured how much of each curry the participants ate. They found that those whose OFCs were most sensitive to fatty texture were more likely to eat more of the high-fat curry compared with those who weren’t as sensitive to fatty texture.

These findings could help to shape formulations of low-calorie foods and understand the neural mechanisms of overeating, Grabenhorst says.

doi: https://doi.org/10.1038/d41586-023-03243-8

References

Khorisantono, P. A., et al. J. Neurosci. https://doi.org/10.1523/JNEUROSCI.1473-23.2023 (2023).

Edited to update title and info accordingly.

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

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.

It’s now explicitly against Disney Plus’s policies for Canadian subscribers to share passwords outside of their household.

Tainted CPAP machines and ventilators went to children, the elderly and at least 700,000 veterans despite internal warnings. Company insiders said the devices posed an “unacceptable” risk.

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

I'm speaking of online data harvested through apps, websites, hardware (such as phones/streaming devices).

I mean if multiple versions of the same harvested data are being sold, wouldn't the value decrease because of the competition? When it comes to aggregate data, how much financial value can there really be in knowing that a million office workers just clicked on the same cat meme?

How does the quantity of time and expense toward "personalization" not simply overshadow the return, given that no one can click on even a small percentage of those numerous ads, let alone buy the shit being advertised?

It just seems like there would come a time when the value of user data is sucked dry, or at least significantly decreased.

"Four free tests will be available for each household to request through the government's COVIDTests.gov portal beginning on Monday, Sept. 25."