Just a few days ago, I came across a comment here in a diary about COVID. The Kossack pushed the sentiment that COVID is due to become endemic, will join other seasonal coronaviruses that cause the common cold, and that we should all just hunker down. I consider this type of comment to be, “Well, it’s all over; stop trying to save yourselves. Get used to it. There’s nothing you can do.” To me, this is a call to drop defenses.

We have a lot on our plates right now (Ukraine still at war, Roe slated to die, white supremacy and mass shootings coming to a head, January 6 committee front and center), but COVID is still one of them. It’s just that, as a nation, we’re simply not talking about it.

Here is a smattering of COVID news from the past few weeks. (Emphases below are mine.) We can’t afford to pretend the danger has passed. We’re still in the thick of it.

‘We’re playing with fire’: US Covid cases may be 30 times higher than reported

(The Guardian, June 2, 2022)

Covid cases could be undercounted by a factor of 30, an early survey of the surge in New York City indicates. “It would appear official case counts are under-estimating the true burden of infection by about 30-fold, which is a huge surprise,” said Denis Nash, an author of the study and a distinguished professor of epidemiology at the City University of New York School of Public Health.

About one in five – 22% – of adult New Yorkers likely had Covid between 23 April and 8 May, according to the preprint study, which has not been peer-reviewed or published. That would mean 1.5 million adults in the city had Covid in a single two-week period – far higher than official counts during that time. …

There is also a “huge disincentive” for many people to get tested for Covid, said Lara Jirmanus, a family physician and clinical instructor at Harvard Medical School. Americans have been told the virus is mild and won’t affect their lives, she said, but if they test positive, they need to stay home from work and school.

It’s almost as though we’ve created a national ‘don’t ask, don’t tell’ Covid policy – and that is a perfect way to promise that Covid will spread rapidly,” she said – especially concerning given as much as 60% of Covid transmission happens from people who never have any symptoms.

… “To just decide that it’s perfectly fine for everyone to be infected three to four times a year in the future with a new virus whose effects we don’t fully understand is a huge, huge gamble,” she continued. “We just don’t know what Covid could lead to in the future… We’re playing with fire.”

Association between long-term exposure to ambient air pollution and COVID-19 severity

(Canadian Medical Association Journal, May 24, 2022)

We observed that people with SARS-CoV-2 infection who lived in areas of Ontario with higher levels of common air pollutants (PM2.5, NO2 and O3) were at elevated risk of being admitted to the ICU after we adjusted for individual and contextual confounding factors, even when the air pollution level was relatively low. In addition, we found that chronic exposure to PM2.5 and O3 was associated with elevated risk of COVID-19–related hospital admission, and exposure to O3 was also associated with elevated risk of death due to COVID-19. These results suggest that chronic exposure to air pollution before SARS-CoV-2 infection may contribute to COVID-19 severity, particularly chronic exposure to O3.

(PM2.5 refers to particulate matter larger than 2.5 nanometers; NO2 is nitrogen dioxide, O3 is ozone.)

Covid infection may induce severe bone loss, suggests animal study

(The Tribune India, May 27, 2022)

To study the effects of SARS-CoV-2 infection on bone metabolism, the researchers from the University of Hong Kong infected Syrian hamsters with SARS-CoV-2.

They then collected their bone tissues after the infection and analysed them using three-dimensional micro-computerised tomography scans.

The study found that SARS-CoV-2 infection induced severe bone loss from 20 per cent to 50 per cent progressively in particular to the trabecular bone in the long bones and lumbar vertebrae.

The cytokine dysregulation or inability to control inflammation, induced by SARS-CoV-2, triggered an amplified pro-inflammatory cascade in the skeletal tissues to augment their breakdown.

The researchers said their team is the first in the world to report the effects of SARS-CoV-2 on bone metabolism using a well-established Syrian hamster model that closely mimics covid-19 in humans.

(Original study published in Nature Communications, May 9, 2022.)

Risk of blood clots in lungs doubles for Covid survivors, study says

(The National, May 27, 2022)

One in five people who catch Covid-19 are likely to go on to develop another health condition, research says.

The study from the US Centres for Disease Control and Prevention found survivors were twice as likely to develop a pulmonary embolism or respiratory illness compared to people who were never infected.

A pulmonary embolism is a clot that develops in a blood vessel that travels to an artery that goes from the heart to the lungs, which can block the normal flow of blood.

Researchers studied the electronic health records of almost two million people, around 353,000 of whom had the virus, from March 2020 to November last year.

One in five of those who had the virus in the 18–64 age group and one in four survivors aged 65 years or older experienced at least one ‘incident,’ such as a blood clot or pulmonary embolism, that might be attributable to a previous infection.

(Original findings at CDC.)

In Long COVID, Blood Markers Are Linked to Neuropsychiatric Symptoms

(Neuroscience News, May 28, 2022)

The researchers first isolated protein-filled sacs, called exosomes, released into the blood by all kinds of cells, then selected for only those exosomes derived from neurons and supporting cells known as astrocytes. Goetzl sees this approach as a proxy measure reflecting the disruption that occurs to cells in the brain in the aftermath of SARS-CoV-2 infection.

The analysis detected much higher average levels of two SARS-CoV-2 viral proteins they measured—the nucleocapsid protein and the spike protein—in blood plasma samples collected between six and 12 weeks after diagnosis from patients infected with COVID who had neuropsychiatric symptoms in comparison to samples from those who had long COVID, but who did not have neuropsychiatric symptoms.

Levels of these proteins from neuronal exosomes in long COVID patients without neuropsychiatric illness were still higher than levels from patients without long COVID.

(Original study published by Annals of Neurology, March 13, 2022.)

Babies Exposed to COVID in the Womb Show Neurodevelopmental Changes

(Neuroscience News, June 6, 2022)

Researchers found that babies born to mothers who had been infected show greater difficulties in relaxing and adapting their bodies when they are being held, when compared to infants from non-infected mothers, especially when infection took place in late pregnancy.

Moreover, infants born from infected mothers tend to show greater difficulty in controlling head and shoulder movement. These alterations suggest a possible COVID-19 effect on motor function (movement control). …

The researchers are presenting the data on pregnancy and post-natal assessment at 6 weeks after birth, but the project will continue to see if there are longer-term effects. The group will monitor infant language and motor development between 18 and 42 months old.

(This research was presented at the 30th European Congress of Psychiatry.)

“Long COVID” May Be Caused by High Levels of Virus-Specific T Cells

(Contagion Live, June 9, 2022)

A recent study, published in PLOS Pathogens, compared the frequencies of COVID-19-specific T cells and inflammatory markers with lung function in patients who had either pulmonary PASC or resolved COVID-19.

“The persistence of high numbers of virus-specific T cells in individuals with long COVID suggests that there may be hidden viral reservoirs that are maintaining and leading to long-term symptoms,” said Brent Palmer, PhD, the study’s senior author and an associate professor of allergy and clinical immunology at the University of Colorado School of Medicine. …

Palmer and fellow investigators found that patients who suffered from long COVID had virus-specific T cell levels that were more than 100 times higher than in patients who made a full recovery. The patients with PASC had frequencies of IFN-γ- and TNF-α-producing SARS-CoV-2-specific CD4+ and CD8+ T cells in peripheral blood that were 6-105 times higher.

Covid can cause ongoing damage to heart, lungs and kidneys, study finds

(The Guardian, May 23, 2022)

The authors write that, compared with controls, those who had been hospitalised with Covid showed several abnormalities, including in results from imaging of the heart, lungs and kidneys.

The team found about 13%, or one in eight, of those hospitalised for Covid were deemed by experts to be very likely to have myocarditis, or heart inflammation, compared with just one control participant. …

The likelihood of myocarditis was higher among healthcare workers and those with acute kidney injury, as well as those with more severe disease requiring invasive ventilation.

(Original study published at Nature Medicine, May 23, 2022.)

Over 75 Percent of Long Covid Patients Were Not Hospitalized for Initial Illness, Study Finds

(New York Times, May 18, 2022)

The study, conducted by FAIR Health, a nonprofit organization that focuses on health care costs and insurance issues, found that 76 percent of the long Covid patients did not require hospitalization for their initial coronavirus infection. …

More than three-quarters of the patients in the study were infected in 2021, most of those in the last half of the year. On average, patients were still experiencing long Covid symptoms that qualified for the diagnosis four and a half months after their infection. …

Because the study captured only a privately insured population, Dr. Ssentongo said, it almost certainly understates the scope and burden of long Covid, especially since low-income communities have been disproportionately affected by the virus and often have less access to health care. “I think it may even be worse if we added in the Medicaid population and all these other people that would have been missed” in the study’s data, he said.

(Original white paper by FAIR Health, May 18, 2022.)

COVID-19 increases risk of psychiatric diagnoses in the months after infection, Oregon State University study finds

(Oregon State University Newsroom, June 7, 2022)

A recent Oregon State University study found that COVID-19 patients had a roughly 25% increased risk of developing a psychiatric disorder in the four months following their infection, compared with people who had other types of respiratory tract infections. …

Researchers found that COVID patients had a 3.8% rate of developing a psychiatric disorder compared with 3.0% for other respiratory tract infections. The 0.8% difference amounts to about a 25% increased relative risk.

They looked specifically at anxiety disorders and mood disorders and found a minor but significant increase in risk for anxiety disorders and no change in risk for mood disorders.

(Original study published in World Psychiatry, May 7, 2022.)

Long COVID associated with extensive in-vivo neuroinflammation on [18F]DPA-714 PET

(medRxiv, June 4, 2022)

In this study, we report widespread and large increases in [18F]DPA-714 binding throughout the brain in the first two patients included in our in-vivo study of neuroinflammation. Although far from definitive, these findings are striking in extent and magnitude. As such, they implicate profound neuroinflammation in the pathophysiology of long COVID.

The extent of neuroinflammation in these patients with long COVID is remarkable. Whereas earlier post-mortem studies of acute COVID-19 patients have shown elevated neuroinflammation primarily in olfactory bulbs, medulla, brainstem and cerebellum, the current study suggests that the process of neuroinflammation may be more widespread in long COVID. Furthermore, as can be visually appreciated, we found high binding in the thalamus for both patients. This has also been reported in MS, using similar (TSPO) PET ligands. The thalamus is considered an important regulator, in relation to fatigue and cognitive functioning and may offer a clue towards the etiology of these symptoms in long COVID.

([18F]DPA-714 is a tracer molecule used for imaging in positron emission tomography. The image heading the diary relates to this study. The image is not a heat map but rather shows the extensiveness and globality of the inflammation.)

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