Some COVID-19 patients experience persistent chronic fatigue six months after infection, finds study

A team of scientists from Germany has recently revealed that almost 50% of patients present with moderate to severe chronic fatigue syndrome six months after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. 

Background

Infection with SARS-CoV-2 is associated with a wide variety of symptoms, ranging from mild fever and cough to severe pulmonary and cardiovascular complications. Although almost 80% of coronavirus disease 2019 (COVID-19) patients remain asymptomatic or mildly symptomatic, a growing pool of evidence indicates that a significant fraction of COVID-19 patients present with persistent symptoms referred to as ‘long COVID’. Most commonly reported symptoms of long COVID are fatigue, cognitive impairment, and post-exertional malaise (worsening of symptoms after minor physical or mental exertion).

In the current study, the scientists have investigated mild to moderate COVID-19 patients who present with persistent fatigue and other related symptoms. They have also investigated whether these patients meet the diagnostic criteria for chronic fatigue syndrome/myalgic encephalomyelitis (ME/CFS), which is a neurological disease characterized by severe mental and physical fatigue, chronic pain, and sleep disorder.

Study design

A total of 42 COVID-19 patients presented with moderate to severe intensity chronic fatigue, exertion intolerance, cognitive dysfunction, and pain six months after SARS-CoV-2 infection were investigated in the study. All participants were diagnosed with mild to moderate COVID-19. A team of experienced clinical immunologists, rheumatologists, neurologists, and cardiologists was involved for an accurate diagnosis of ME/CFS in these patients based on the Canadian Consensus Criteria. The intensity and duration of post-exertional malaise (symptoms lasting for more than 14 hours) was considered to be the main diagnostic criterion for ME/CCFS.

Important observations

Of all enrolled patients, 32 had mild COVID-19 and 10 had moderate COVID-19 because of pneumonia. The numbers of male and female patients were 29 and 13, respectively, and the average age of the patients was 36 years (age range: 22 – 62 years).

Of 42 enrolled patients, 19 met the diagnostic criteria for ME/CFS and were found to have severe fatigue and functional impairment, severe stress intolerance, and hypersensitivity to noise, light, and temperature. The scientists categorized these patients as Chronic COVID-19 Syndrome/Chronic Fatigue Syndrome (CCS/CFS). The rest of the patients who were not diagnosed with ME/CFS mainly because of the relatively shorter duration of post-exertional malaise (2 – 10 hours) were referred to as CCS. The patients with ME/CFS showed significantly reduced hand grip strength than those without ME/CFS.

After 6 months of SARS-CoV-2 infection, all participants were found to have fatigue with different intensities. The most commonly observed symptoms were post-exertional malaise, cognitive impairment, and muscle pain. Although patients without ME/CFS exhibited less severe symptoms, most of them had severely impaired daily life activities. The majority of enrolled patients (n=28) were either unable to work or required a reduced work schedule because of post- Covid-19 symptoms.

In the study cohort, autonomic dysfunction was observed in most of the patients, with no significant difference in symptom intensity between patients with and without ME/CFS. The increase in systolic and diastolic blood pressure at standing position was significantly lower in patients with ME/CFS than those without it. Among patients with ME/CFS, four were diagnosed with postural tachycardia syndrome.         

Regarding biochemical parameters, only two patients in the entire study cohort showed mildly elevated C-reactive protein levels, indicating the absence of robust inflammatory response. Almost 50% of patients showed increased levels of interleukin 8 (IL-8), which is a clinical feature of severe COVID-19 patients. Moreover, a low level of mannose-binding lectin was observed in 22% of patients, indicating impaired immune functioning. An indication of autoimmune disorder was noticed in the study cohort as elevated levels of antinuclear antibody were found in 3 ME/CFS patients and 6 non-ME/CFS patients.

Study significance

The study reveals that even mildly affected COVID-19 patients can develop a severe chronic syndrome characterized by moderate to severe fatigue and exertion intolerance. Because most of the post-COVID symptoms considered in this study did not differ significantly between patients with and without ME/CFS, the scientists suggest that chronic COVID-19 syndrome is a more appropriate terminology than ME/CFS in defining long-term symptoms related to SARS-CoV-2 infection.

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Infusion of Young Blood Reverses Age-Related Impairments in Mice

A newly published study from Stanford University found that an infusion of young blood can counteract and reverse pre-existing effects of brain aging at the molecular, structural, functional and cognitive level in mice.

Something — or some things — in the blood of young mice has the ability to restore mental capabilities in old mice, a new study by Stanford University School of Medicine investigators has found.

If the same goes for humans, it could spell a new paradigm for recharging our aging brains, and it might mean new therapeutic approaches for treating dementias such as Alzheimer’s disease.

In the study, published online May 4 in Nature Medicine, the researchers used sophisticated techniques to pin down numerous important molecular, neuroanatomical and neurophysiological changes in the brains of old mice that shared the blood of young mice.

But they also conducted a critical experiment that was far from sophisticated, said Tony Wyss-Coray, PhD, the senior author of the study and a professor of neurology and neurological sciences. The scientists simply compared older mice’s performance on standard laboratory tests of spatial memory after these mice had received infusions of plasma (the cell-free part of blood) from young versus old mice, or no plasma at all.

“This could have been done 20 years ago,” said Wyss-Coray, who is also senior research career scientist at the Veterans Affairs Palo Alto Health Care System. “You don’t need to know anything about how the brain works. You just give an old mouse young blood and see if the animal is smarter than before. It’s just that nobody did it.”

Wyss-Coray has co-founded a biotechnology company, Alkahest, to explore the therapeutic implications of the new study’s findings. He serves as the director of Alkahest’s scientific advisory board.

The study’s lead author, Saul Villeda, PhD, now has an active lab of his own as a faculty fellow in anatomy at the University of California-San Francisco. Villeda was a graduate student at Stanford and, briefly, a postdoctoral scholar under Wyss-Coray’s direction when the bulk of the work was performed.

Reversing impairments

“We’ve shown that at least some age-related impairments in brain function are reversible. They’re not final,” Villeda said.

Previous experiments by Wyss-Coray, Villeda and their colleagues, described in a paper published in 2011 in Nature, had revealed that key regions in the brains of old mice exposed to blood from young mice produced more new nerve cells than did the brains of old mice similarly exposed to blood from old mice. Conversely, exposing young mice to blood from old mice had the opposite effect with respect to new nerve-cell production, and also reduced the young mice’s ability to navigate their environments.

But that earlier work didn’t directly assess the impact of young mouse blood on older mice’s behavior. This time, the researchers checked both for changes within nerve circuits and individual nerve cells and for demonstrable improvements in learning and memory. First, they examined pairs of mice whose circulatory systems had been surgically conjoined. Members of such pairs, known as parabiotic mice, share a pooled blood supply.

Wyss-Coray’s group paid special attention, in these parabiotic mice, to a brain structure called the hippocampus. In both mice and humans, this structure is critical for forming certain types of memories, notably the recollection and recognition of spatial patterns. “That’s what you need to use when, for example, you try to find your car in a parking lot or navigate around a city without using your GPS system,” Wyss-Coray said.

Experience alters hippocampal activity and anatomy. Studies have found, for instance, that a veteran London cabdriver’s hippocampus is larger than it was when the driver was first hired, and larger than the average person’s. The hippocampus is also extremely vulnerable to the normal aging process, showing early erosion in function as people grow older. In dementia such as Alzheimer’s disease, this hippocampal deterioration is accelerated, leading to an inability to form new memories.

“We know that detrimental anatomical and functional changes occur in the hippocampus as mice and people get older,” said Villeda. “This is just from natural aging. We’re all heading in that direction.”

When the investigators compared hippocampi from old mice whose circulatory systems had been conjoined with those of young mice to hippocampi from old mice that had been paired with other old mice, they found consistent differences in a number of biochemical, anatomical and electrophysiological measures known to be important to nerve-cell circuits’ encoding of new experiences for retention in the cerebral cortex.

Recharging old brains

The hippocampi of older mice that had been conjoined to younger mice more closely resembled those of younger mice than did the hippocampi of older mice similarly paired with old mice. The old mice paired with young mice made greater amounts of certain substances that hippocampal cells are known to produce when learning is taking place, for example. Hippocampal nerve cells from older members of old-young parabiotic pairs also showed an enhanced ability to strengthen the connections between one nerve cell and another — essential to learning and memory.

“It was as if these old brains were recharged by young blood,” Wyss-Coray said.

Villeda, Wyss-Coray and their associates next subjected regular older mice to a test in which the mice were trained to quickly locate a submerged platform in a water-filled container. The mice had to speedily orient themselves using memory cues provided by their surroundings. The investigators injected old mice intravenously with plasma from young or old mice and ran them through the test. Typically, untreated older mice did poorly compared to young mice, as they did when injected with plasma from old mice. But if they were infused with young mice’s plasma they did much better.

This was likewise the case on another test in which mice were trained to freeze in fear when plunked into a particular environment. The better they recognized that environment, the longer they would freeze. Older mice typically freeze for a shorter period of time than younger ones do. Again, “freezing” times for older mice given young plasma, but not old plasma, increased significantly.

Finding the factors

In both tests, the improvement vanished if the plasma provided to the old mice had first been subjected to high temperatures. Heat treatment can denature proteins, so this hints that a blood-borne protein, or group of them, may be responsible for the cognitive improvements seen in old mice given young mouse plasma.

“There are factors present in blood from young mice that can recharge an old mouse’s brain so that it functions more like a younger one,” Wyss-Coray said. “We’re working intensively to find out what those factors might be and from exactly which tissues they originate.”

“We don’t know yet if this will work in humans,” he said, adding that he hopes to find out sooner rather than later. A near-term goal of his company is to test this proposition through a clinical trial.

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Scientists Succeed In Growing A Beating Human Heart From Stem Cells

Scientists from Massachusetts General Hospital and Harvard Medical school have successfully grown a human heart from adult skin cells, according to a study published recently.

The breakthrough could be huge news for the 4,000 Americans currently awaiting heart transplants, and the more than 25 million people who suffer heart failure each year. In the United States, approximately 2,500 of the 4,000 people in line for heart transplants actually receive them, indicating a shortage that research like this might be able to address.

According to the journal, the scientists took 73 donor hearts deemed unfit for transplantation, stripped away cells on those hearts and replaced them with skin cells that — using messenger RNA — had been turned into pluripotent stem cells, the kinds of cells that can be specialized to any part of the human body. After causing the stem cells to develop into two types of cardiac cells, the researchers then mimicked the environment a human heart would typically grow within and infused the cardiac cells with a nutrient solution that facilitated growth.

After two weeks, they shocked the hearts with electricity, and lo and behold, the hearts began beating. The tissue inside appeared to be well-structured and functional. Scientists compared the growth of the heart as "building a house with the frame already constructed." 

Ultimately, the researchers aim to grow an entire human heart that is capable of being transplanted. 

"To show that functional myocardial tissue of human scale can be built on this platform, we then partially recellularized human whole-heart scaffolds with human induced pluripotent stem cell–derived cardiomyocytes," the team of scientists wrote in their journal. "Under biomimetic culture, the seeded constructs developed force-generating human myocardial tissue and showed electrical conductivity, left ventricular pressure development, and metabolic function."

The technological development was celebrated on social media. As one user wrote: "Living in the future is awesome."

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Experts Explain How Vit D Deficiency Can Cause Heart Failure

A daily dose of sunshine, which stimulates production of Vitamin D in the body, is vital not just for the well-being of your bones but may also be good for your heart.

The problem of vitamin D deficiency affecting bone health is well known for decades. For some years, scientists have also seen vitamin D deficiency as a factor that determines health of your heart. Now Indian researchers have deciphered how exactly vitamin D deficiency can cause heart failure.

The new study has shown that vitamin D deficiency alone can lead to heart failure, possibly through insulin resistance. It has found that cardiac insulin leads to functional deterioration of heart in animals with low vitamin D levels.

The utilization of glucose and fatty acids – key fuels for energy generation in heart – is adversely affected due to insulin resistance in heart cells. Insulin plays a critical role in regulation of cellular metabolism in many tissues in the body.

To study if vitamin D deficiency could cause cardiac damage similar to other risk factors like consumption of high fats and high calorie food, researchers designed an experiment with rats. They manipulated diets of animals and divided them into three groups – one with adequate vitamin D, second set had vitamin D deficiency, while the third group was fed with high fat and high fructose diet.

At the end of 20 weeks, it was found that the hearts of vitamin D deficient animals were failing. They showed molecular and functional changes similar to the hearts of rats in high fat high fructose diet group. “The cardiac dysfunction caused by vitamin D deficiency alone was very similar to that by the other risk factor – high calorie diet – sometimes even to a greater extent in some parameters. For example, cardiac inflammation was higher in vitamin D deficiency diet than high calorie diet,” researchers have observed in the study.

Researchers found greater expression of genes involved in enlargement of cardiac muscles. These findings were confirmed when scientists measured heart wall thicknesses, chamber internal diameters and contracting capacity of heart. Left ventricular posterior wall thickness was found to be increased in rats with vitamin D deficiency. This happens when cardiac workload increases and turns pathological if no remedial measures are taken, finally progressing to heart failure. In such condition, the pumping action of the heart can no longer meet the metabolic demands of the body.

“We have shown the link between vitamin D deficiency and cardiac dysfunction and how it may lead to heart failure. Vitamin D and its signalling modulate myocardial insulin sensitivity, the insufficiency of which induces impaired glucose utilization, remodeling response, and heart failure,” explained a senior scientist.

The group, in its study in 2016 involving a South Indian population, had shown that low vitamin D levels were associated with diabetes as well as diabetes plus coronary artery disease. However, it had not provided any cause-effect relationship. “Our study now tackles exactly that issue with animal experiments and provides conclusive evidence,” Dr. added.

The new findings have both public health and therapeutic implications. The insights gained on how vitamin D signalling affects myocardial insulin sensitivity may help scientists design new drugs for management of heart failure by targeting activation of vitamin D receptor.

With vitamin D deficiency emerging as a risk factor for heart disease, public health policies will have to take note of it since metabolic disorders are already a major health challenge in India. “We have evidence to show that widespread vitamin D deficiency in Indians definitely contributes to insulin resistance and diabetes. Our previous research and ongoing work in Indian population have indicated that supplementation with vitamin D may help in ameliorating insulin resistance and decreasing blood glucose levels,” commented a Dr.

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New Method to Help Predict Mortality in Elderly

Researchers have developed a method to assess the 'age' of patients' immune systems, thus predicting mortality in older adults. According to researchers, the immune age is a kind of biological clock that will help identify an early weakening of the immune system.
The new model will help devise preventive measures to reduce disease and mortality, Xinhua news agency reported. In the study, Technion scientists, along with a team from the Stanford University in California, were able to quantify the changes in the immune system that happen over the years.

 In nine years, they characterised the immune systems of 135 healthy people of different ages once a year and built a model that quantifies these changes in a specific person. The data enabled the researchers to quantify the immune age in an index called 'IMM-AGE score', which provides information that the chronological age cannot tell.

Using the new method, the team quantified the immunisation age of more than 2,000 elders. The researchers believe that with the new method, they will also be able to characterise genes that affect immunisation age, and even identify lifestyle, habits and medications that affect the 'age'.

With an increase in inflammatory processes, the human body undergoes slow and constant functional weakening of the immune system. Ageing of the immune system has devastating consequences, including an inability to cope with infections and an increased risk of chronic diseases such as cancer.

The quantification of the immune system's ageing is a complex challenge that requires multidimensional monitoring over time.

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