Mass vaccination and available antiviral treatments have not prevented vaccinated individuals from experiencing lingering COVID-19 symptoms.
A recent study found that the majority of patients who suffered from long COVID during a time when vaccines and antiviral treatments were widely available were vaccinated.In the observational study published in the Journal of Clinical Medicine, researchers interviewed 390 people in Thailand who contracted COVID-19 during the “fifth wave of the COVID-19 pandemic” when the omicron variant was dominant. Patients were followed by phone from three months after their diagnosis for a year to monitor their physical condition, mental health, sleep disturbances, and quality of life.
Out of 390 people with COVID-19, 377 (97 percent) were vaccinated, 383 (98 percent) underwent antiviral treatment, and 330 (78 percent) developed long COVID syndrome. The most frequently reported symptoms were fatigue and cough. Other reported symptoms included depression, anxiety, and poor sleep quality. The study found that patients under age 60 with a cough as an initial symptom were more likely to develop the condition. In a subset of patients with long COVID, researchers found a notable correlation in females with headaches, dizziness, and brain fog.
“Despite the extensive distribution of vaccines and antiviral therapies, the prevalence of long COVID remains high,” the authors of the paper wrote.
Although definitions of long COVID differ, the Centers for Disease Control and Prevention (CDC) broadly defines long COVID as “signs, symptoms, and conditions that continue to develop after acute COVID-19 infection” that can last for “weeks, months, or years.” The term “long COVID” also includes post-acute sequelae of SARS-CoV-2 infection, long-haul COVID, and post-acute COVID-19.
According to the World Health Organization, while most people with COVID-19 recover and return to normal health, some patients, including those with mild illness, have symptoms that persist for weeks or months after recovering from acute illness.
Nearly 7 percent of U.S. adults surveyed by the CDC in 2022 said they’ve experienced long COVID. Although U.S. regulatory agencies claim vaccinating against COVID-19 can reduce the risk of developing long COVID, the current paper did not find a significant link between the presence of comorbidities or infection severity and the emergence of long COVID symptoms.
Studies Link Long COVID to Vaccination
A February report published by the CDC found that more than 8 percent of participants in seven U.S. states reported having experienced long COVID symptoms. In West Virginia, almost 11 percent of survey participants reported long COVID symptoms. However, the agency did not disclose whether survey respondents were vaccinated
Some research suggests long COVID may be caused by an immune overreaction to the SARS-CoV-2 spike protein that COVID-19 vaccines use to induce antibodies and that vaccination causes some people to generate a second round of antibodies that target the first.
In a February 2023 study published in the Journal of Medical Virology, researchers analyzed the levels of spike protein and viral RNA in patients hospitalized for COVID-19 with and without long COVID. They found that spike protein and viral RNA were more likely to be present in patients with long COVID.
In an August 2023 study published in the International Journal of Infectious Diseases, researchers found the risk of long COVID was lower in those who had previous SARS-CoV-2 infection, and the risk of getting long COVID did not differ by vaccination status. Researchers found that unvaccinated people infected with omicron had the lowest risk of long COVID.
In a 2023 study in the European Review for Medical and Pharmacological Sciences, researchers studied the serum of 81 individuals with long COVID. They found viral spike protein in one patient after the infection had cleared despite having a negative COVID-19 test, and vaccine spike protein in two patients two months after vaccination.
In a December 2022 study published in PLoS One, researchers found patients were more likely to experience long COVID if they had preexisting medical conditions, a higher number of symptoms during the acute phase of COVID-19 illness, if their infection was more severe or resulted in hospitalization, or if they had received two doses of a COVID-19 vaccine.
The peak of the COVID-19 pandemic may be behind us, but for many people, long COVID continues to cause symptoms weeks, months, or even years after the initial illness. Among the more than 200 symptoms reported for long COVID, brain fog — problems with thinking, understanding, focus and memory — is one of the most widespread and long-lasting.
What does the latest research tell us about brain fog in long COVID? Image credit: davit85/Getty Images.
The World Health Organization (WHO) declared COVID-19 a pandemicTrusted Source on March 11, 2020. Since then, the WHO has recorded almost 775 million confirmed cases worldwide. But there have, almost certainly, been many more that have not been confirmed, particularly with the decline in testing in most countries.
One study, published in Nature Reviews MicrobiologyTrusted Source in January 2023, suggests that around 10% of people experience long COVID following acute infection, with 50–70% of people who are hospitalized with COVID-19 experiencing lasting symptoms.
According to the United Kingdom’s Office of National Statistics Coronavirus (COVID-19) Infection Survey self-reported data, almost 3% of the U.K. population was experiencing long COVID in March 2023. Of these, 41% were still experiencing symptoms 2 years after initial infection with SARS-CoV-2.
In the United States, the CDC notes that 6.4%Trusted Source of adults have, at some time, reported long COVID symptoms.
These may be a continuation of those experienced in the acute infection, or may change, and can affect almost any part of the body, with one study — published ineClinicalMedicineTrusted Source in 2021 — finding that symptoms “affect multiple organ systems, with significant impacts on morbidity, mortality, and quality of life”.
The study from Nature Reviews Microbiology outlines lasting impacts on the heart, lungs, immune system, pancreas, gastrointestinal tract, kidneys, spleen, liver, blood vessels, reproductive system and neurological system.
Of course, a person with long COVID will not experience all of the 203 symptoms recorded by the wide-ranging international study from eClinicalMedicine. In this study, 91.8% of the cohort reported symptoms that lasted more than 35 weeks after initial infection, the most common and debilitating of which were fatigue, breathing issues and cognitive dysfunction, or brain fog.
This “classic” long COVID, characterized by brain fog, fatigue, dysautonomia, and postexertional malaiseTrusted Source, is more common in younger adults and in females. Older people and those with comorbidities are more likely to experience cardiovascular and metabolic effects.
Those who have had more severe COVID-19, with hypoxia, a need for ventilation, and psychological trauma, are at higher risk of lasting psychological effects or cognitive dysfunction.
But anyone who has had COVID-19 has a greater riskTrusted Source of neurological or psychiatric symptoms following their initial illness than someone who has not had a SARS-CoV-2 infection.
Some symptoms, such as mood and anxiety disorders, increase for a short time after infection, but then reduce back to baseline levels. However, others continue for much longer. And one of these is brain fog, which a recent study published in Scientific ReportsTrusted Source found in 89% of people with long COVID.
In this study, 89% of participants also reported fatigue, and 77% difficulty concentrating. When researchers assessed them using the Montreal Cognitive Assessment, they found that 46% had mild cognitive dysfunction.
Often the result of, among other things, inflammation, concussion, hormonal changes, or medication, brain fog is one of the most common symptoms reported by people with long COVID.
A person with brain fog may have problems with memory, focus, thinking and understanding, as well as often experiencing stress and fatigue.
Prof. Stephen Griffin, virologist at the University of Leeds School of Medicine, and co-chair of Independent SAGE told Medical News Today:
“Symptoms can vary, but some of the major issues include a lack of recall for things like names, places, events, etc., as well as a general inability to process complex tasks, hold concentration over time and multi-task.”
“In some instances, general alertness can be affected as well which, when combined with the intense fatigue experienced by many, can be extremely debilitating in terms of interacting socially or functioning at school or work,” he added.
The study from eClinicalMedicine, which looked into the lasting effects of COVID-19, recorded brain fog, cognitive dysfunction and memory impairment in 85.1% of respondents. And almost 90% of those who worked reported that brain fog impaired their ability to work to some extent.
This study found that two SARS-CoV-2 variants, the original wild type and Omicron, were best able to induce cell stress and damage components of the BBB.
However, Dr. Giovanni Schifitto, professor of neurology at the University of Rochester Medical Center, NY, believes that the cause of long covid is likely to be multifactorial.
“The physical presence of SARS-CoV-2 in the brain, especially in the chronic phase, is unlikely to be the culprit. However, systemic virus persistence can create a more chronic systemic inflammatory status and that can contribute to multi-organ dysfunction,” he told us.
There is more support for the suggestion that brain fog in long COVID may result from immune dysfunction and inflammation.
One recent study, which appeared in Nature CommunicationsTrusted Source, showed that people with COVID had raised levels of four brain injury biomarkers, and that two of these persisted long after the initial infection, particularly in those who experienced neurological complications during the acute infection.
The authors of this research suggest these abnormal immune responses may be causing ongoing inflammation. And inflammation can lead to brain fog.
They believe that if they can find out why these immune responses are triggered, treatments could be developed to target them.
Whether the effects are due to viral invasion or immune dysfunction, research has found that SARS-CoV-2 infection can lead to changes in the brain.
A study — published in NatureTrusted Source in March 2022 — using data from the UK Biobank compared brain scans conducted on people before and after they had COVID-19.
Those who had had SARS-CoV-2 infection had a reduction in grey matter thickness, markers of tissue damage in olfactory regions, and changes in brain volume, as well as slightly lower cognitive abilities than those who had not.
Prof. Griffin explained:
“As with many issues around long COVID, brain fog is likely a combination of persistent infection by SARS-CoV-2 [as reported in a new studyTrusted Source published in 2023] and host immune/metabolic changes that occur either concomitantly or as a follow-on. Worryingly, changes to the brain, including reductions in grey matter, have been noted even in patients that aren’t necessarily associated with neurological symptoms.”
Research reported in Nature NeuroscienceTrusted Source, which used dynamic contrast-enhanced magnetic resonance imagingTrusted Source (DCE-MRI) on people with long COVID with or without reported brain fog, has backed up these findings. The researchers found not only significantly increased BBB permeability in the group with brain fog, but also reduced global brain volume and white matter volume.
The researchers suggest that “long COVID-derived brain fog is associated with BBB disruption and sustained systemic inflammation,” adding that their “data suggest that BBB disruption occurs during acute infection and long COVID, where it is strongly associated with cognitive impairment.”
following a healthy diet, rich in fresh fruits and vegetables and limiting processed food
doing regular exercise
having good sleep hygiene
managing stress.
Dr. Schifitto advised that:
“General principals are avoid deconditioning, thus keep routine physical activity although [this] will need to be titrated to tolerance. Be aware of mental fatigue so spread intellectual work throughout the day. Because often there are also depressive symptoms present, maintain social connections.”
And Prof. Griffin warned that anyone with long COVID brain fog should “ensure that you pace yourself when experiencing this or other long COVID symptoms. Over-exertion can sometimes exacerbate things.”
He suggested that using tech, and setting reminders and alarms can help people cope with the brain fog and fatigue of long COVID.
As has become increasingly clear, COVID, like many other viral diseases, can have effects long beyond the initial infection, and research is only now starting to discover why.
Avoiding infection is, of course, the best way to avoid long-term effects, but there is increasing evidence that vaccination and antiviral treatment in the early stages of infection reduces the risk of long COVID.
But Prof. Griffin is frustrated about the lack of action taken to prevent infection and counter the long-term effects of COVID-19.
“Like a lot of aspects of SARS-CoV-2 infection, because it [brain fog] doesn’t necessarily manifest during acute disease it tends to be overlooked. This, to me, is another reason why the reluctance of western governments to suppress prevalence of this virus is […] mind-bogglingly negligent,” he told us.
“There are already record numbers of people out of work due to chronic illness, also many that struggle on, plus cognitive impairment on this scale makes for a less productive population as a whole,“ said Prof Griffin.
“Adding brain fog to the already staggering list of longer term problems caused by COVID must surely make us question what we’re allowing to happen to those being exposed to multiple infections with this virus, including our children,” he emphasized.
Researchers have made a groundbreaking discovery about Long COVID’s neurological effects, including brain fog and cognitive decline. By identifying blood vessel disruption in the brain, they offer new insights for diagnosing and treating the condition, potentially transforming the approach to post-viral neurological syndromes.
Scientists uncover crucial links between Long COVID and brain blood vessel integrity, offering hope for new treatments and diagnostic methods.
A team of scientists from Trinity College Dublin and investigators from FutureNeuro announced a major discovery that has profound importance for our understanding of brain fog and cognitive decline seen in some patients with Long COVID.
In the months after the emergence of the novel coronavirus SARS-CoV2 in late 2019 a patient-reported syndrome termed Long-COVID began to come to the fore as an enduring manifestation of acute infection.
Understanding Long COVID
Long COVID has up to 200 reported symptoms to date, but in general, patients report lingering symptoms such as fatigue, shortness of breath, problems with memory and thinking, and joint/muscle pain. While the vast majority of people suffering from COVID-19 make a full recovery, any of these symptoms that linger for more than 12 weeks post-infection can be considered Long COVID.
Long COVID has now become a major public health issue since the outbreak of the pandemic in 2020. While international incidence rates vary, it is estimated to affect up to 10% of patients infected with the SARS-CoV2 virus. Of these patients suffering from Long-COVID, just under 50% of them report some form of lingering neurological effect such as cognitive decline, fatigue, and brain fog.
Now, the findings reported by the Trinity team in the top international journal Nature Neuroscience showed that there was disruption to the integrity of the blood vessels in the brains of patients suffering from Long COVID and brain fog. This blood vessel “leakiness” was able to objectively distinguish those patients with brain fog and cognitive decline compared to patients suffering from Long-COVID but not with brain fog.
The team led by scientists at the Smurfit Institute of Genetics in Trinity’s School of Genetics and Microbiology and neurologists in the School of Medicine have also uncovered a novel form of MRI scan that shows how Long-COVID can affect the human brain’s delicate network of blood vessels.
“For the first time, we have been able to show that leaky blood vessels in the human brain, in tandem with a hyperactive immune system may be the key drivers of brain fog associated with Long COVID. This is critically important, as understanding the underlying cause of these conditions will allow us to develop targeted therapies for patients in the future,” said Prof. Matthew Campbell, Professor in Genetics and Head of Genetics at Trinity, and Principal Investigator at FutureNeuro.
This project was initiated by a rapid response grant funded by Science Foundation Ireland (SFI) at the height of the pandemic in 2020 and involved recruiting patients suffering from the effects of Long-COVID as well as patients who were hospitalized in St James’ Hospital.
“Undertaking this complicated clinical research study at a time of national crisis and when our hospital system was under severe pressure is a testament to the skill and resource of our medical trainees and staff. The findings will now likely change the landscape of how we understand and treat post-viral neurological conditions. It also confirms that the neurological symptoms of Long Covid are measurable with real and demonstrable metabolic and vascular changes in the brain,” said Prof. Colin Doherty, Professor of Neurology and Head of the School of Medicine at Trinity, and Principal Investigator at FutureNeuro.
Moving Beyond COVID-19
In recent years, it has become apparent that many neurological conditions such as Multiple sclerosis (MS) likely have a viral infection as the initiating event that triggers the pathology. However, proving that direct link has always been challenging.
Prof. Campbell added: “Here, the team at Trinity was able to prove that every patient that developed Long-COVID had been diagnosed with SARS-CoV2 infection, because Ireland required every documented case to be diagnosed using the more accurate PCR-based methods. The concept that many other viral infections that lead to post-viral syndromes might drive blood vessel leakage in the brain is potentially game-changing and is under active investigation by the team.”
Dr. Chris Greene, Postdoctoral research fellow and first author of the study, added: “Our findings have now set the stage for further studies examining the molecular events that lead to post-viral fatigue and brain fog. Without doubt, similar mechanisms are at play across many disparate types of viral infection and we are now tantalizingly close to understanding how and why they cause neurological dysfunction in patients.”
During the early stages of the Covid-19 pandemic, reports emerged that persons who had been infected with SARS-CoV-2 were having lingering health problems. Such long-term issues were collectively referred to as “long Covid” and were reported to affect nearly every organ system.1 The cardinal features of long Covid include fatigue, dysautonomia (or postural orthostatic tachycardia syndrome), postexertional malaise, and cognitive difficulties that are colloquially referred to as “brain fog.”
Several large studies then emerged documenting the presence of neurologic sequelae — including cognition and memory problems — in the postacute phase of SARS-CoV-2 infection.2,3 A recent analysis of the U.S. Current Population Survey showed that after the start of the Covid-19 pandemic, an additional one million U.S. residents of working age reported having “‘serious difficulty’ remembering, concentrating, or making decisions” than at any time in the preceding 15 years.4 Whether these changes are attributable solely to long Covid is unclear, but that report represents a change in the cognitive health of U.S. residents from prepandemic levels.
In a study published in this issue of the Journal, Hampshire et al.5 bring greater clarity to how SARS-CoV-2 infection may affect cognition. They studied 800,000 adults from a larger community sample of more than 3 million persons in the Real-Time Assessment of Community Transmission (REACT) study of SARS-CoV-2 transmission in England. Using an online assessment tool for cognitive function with eight domains, the investigators estimated global cognitive scores among participants who had been previously infected with SARS-CoV-2 and had had symptoms that persisted at least 12 weeks, whether resolved or not, and among uninfected participants.
Modest cognitive decline occurred with the original virus and with each viral variant, including B.1.1.529 (omicron). As compared with uninfected participants (control), cognitive deficit — commensurate with a 3-point loss in IQ — was evident even in participants who had had mild Covid-19 with resolved symptoms. Participants with unresolved persistent symptoms had the equivalent of a 6-point loss in IQ, and those who had been admitted to the intensive care unit had the equivalent of a 9-point loss in IQ. Of importance, these deficits were associated with many of the other symptoms that have been reported by persons with long Covid. The greatest deficits in cognitive function were associated with the original strain of the virus (before December 1, 2020) and the early B.1.1.7 (alpha) variant (from December 1, 2020, to April 30, 2021). Longer hospital stays and durations of acute illness were predictors of persistent global deficits. Memory, reasoning, and executive function (i.e., planning) tasks were the most sensitive indicators of impaired function, and scores on these tasks tended to correlate with brain fog. Vaccinations provided a small cognitive advantage. Reinfection contributed an additional loss in IQ of nearly 2 points, as compared with no reinfection.Figure 1.Putative Mechanisms of Cognitive Dysfunction in Long Covid.
The mechanisms of cognitive dysfunction after SARS-CoV-2 infection still need to be elucidated (Figure 1). Studies involving humans and mouse organoids showed that SARS-CoV-2 infection induces fusion of neurons, which compromises neuronal activity. Studies involving humans have shown prolonged neuroinflammatory responses, structural abnormalities, and accelerated aging in the brains of persons with mild-to-moderate SARS-CoV-2 infection.6-8 Virus was present in brain-tissue samples obtained during autopsy from persons who had had severe Covid-19.8 Gut dysbiosis, dysfunctional hypothalamic–pituitary response, and low-serotonin–induced dysfunction in vagal signaling may also play a role in impaired cognition after SARS-CoV-2 infection.9,10
The results of the study by Hampshire and colleagues are of concern, and the broader implications require evaluation. For example, what are the functional implications of a 3-point loss in IQ? Whether one group of persons is affected more severely than others is not clear. Whether these cognitive deficits persist or resolve along with predictors and trajectory of recovery should be investigated. Will Covid-19–associated cognitive deficits confer a predisposition to a higher risk of Alzheimer’s disease or other forms of dementia later in life? The effects on educational attainment, work performance, accidental injury, and other activities that require intact cognitive abilities should also be evaluated. SARS-CoV-2 infection happened in the context of a global pandemic that disrupted many facets of our lives; disentangling the effects of the infection from those of the pandemic (e.g., social isolation, grief, and trauma) should also be undertaken.
There are limitations to the study conducted by Hampshire and colleagues. The study was based on an engagement survey; hence, there may be a degree of response and ascertainment bias, such that either more persons with long Covid may have opted to enroll and that persons who were sick and had disability would not participate in the surveys. Also, there was a lack of racial diversity, which will lead to uncertainty with regard to the effects of long Covid on cognition in underrepresented populations.
The SARS-CoV-2 pandemic produced in its wake millions of persons affected with long Covid, some of whom have had or are currently having cognitive challenges. A deeper understanding of the biology of cognitive dysfunction after SARS-CoV-2 infection and how best to prevent and treat it are critical for addressing the needs of affected persons and preserving the cognitive health of populations.
The peak of the COVID-19 pandemic may be behind us, but for many people, long COVID continues to cause symptoms weeks, months, or even years after the initial illness. Among the more than 200 symptoms reported for long COVID, brain fog — problems with thinking, understanding, focus and memory — is one of the most widespread and long-lasting.What does the latest research tell us about brain fog in long COVID? Image credit: davit85/Getty Images.
The World Health Organization (WHO) declared COVID-19 a pandemicTrusted Source on March 11, 2020. Since then, the WHO has recorded almost 775 million confirmed cases worldwide. But there have, almost certainly, been many more that have not been confirmed, particularly with the decline in testing in most countries.
One study, published in Nature Reviews MicrobiologyTrusted Source in January 2023, suggests that around 10% of people experience long COVID following acute infection, with 50–70% of people who are hospitalized with COVID-19 experiencing lasting symptoms.
According to the United Kingdom’s Office of National Statistics Coronavirus (COVID-19) Infection Survey self-reported data, almost 3% of the U.K. population was experiencing long COVID in March 2023. Of these, 41% were still experiencing symptoms 2 years after initial infection with SARS-CoV-2.
In the United States, the CDC notes that 6.4%Trusted Source of adults have, at some time, reported long COVID symptoms.
These may be a continuation of those experienced in the acute infection, or may change, and can affect almost any part of the body, with one study — published ineClinicalMedicineTrusted Source in 2021 — finding that symptoms “affect multiple organ systems, with significant impacts on morbidity, mortality, and quality of life”.
The study from Nature Reviews Microbiology outlines lasting impacts on the heart, lungs, immune system, pancreas, gastrointestinal tract, kidneys, spleen, liver, blood vessels, reproductive system and neurological system.
Of course, a person with long COVID will not experience all of the 203 symptoms recorded by the wide-ranging international study from eClinicalMedicine. In this study, 91.8% of the cohort reported symptoms that lasted more than 35 weeks after initial infection, the most common and debilitating of which were fatigue, breathing issues and cognitive dysfunction, or brain fog.
This “classic” long COVID, characterized by brain fog, fatigue, dysautonomia, and postexertional malaiseTrusted Source, is more common in younger adults and in females. Older people and those with comorbidities are more likely to experience cardiovascular and metabolic effects.
Those who have had more severe COVID-19, with hypoxia, a need for ventilation, and psychological trauma, are at higher risk of lasting psychological effects or cognitive dysfunction.
But anyone who has had COVID-19 has a greater riskTrusted Source of neurological or psychiatric symptoms following their initial illness than someone who has not had a SARS-CoV-2 infection.
Some symptoms, such as mood and anxiety disorders, increase for a short time after infection, but then reduce back to baseline levels. However, others continue for much longer. And one of these is brain fog, which a recent study published in Scientific ReportsTrusted Source found in 89% of people with long COVID.
In this study, 89% of participants also reported fatigue, and 77% difficulty concentrating. When researchers assessed them using the Montreal Cognitive Assessment, they found that 46% had mild cognitive dysfunction.
Often the result of, among other things, inflammation, concussion, hormonal changes, or medication, brain fog is one of the most common symptoms reported by people with long COVID.
A person with brain fog may have problems with memory, focus, thinking and understanding, as well as often experiencing stress and fatigue.
Prof. Stephen Griffin, virologist at the University of Leeds School of Medicine, and co-chair of Independent SAGE told Medical News Today:
“Symptoms can vary, but some of the major issues include a lack of recall for things like names, places, events, etc., as well as a general inability to process complex tasks, hold concentration over time and multi-task.”
“In some instances, general alertness can be affected as well which, when combined with the intense fatigue experienced by many, can be extremely debilitating in terms of interacting socially or functioning at school or work,” he added.
The study from eClinicalMedicine, which looked into the lasting effects of COVID-19, recorded brain fog, cognitive dysfunction and memory impairment in 85.1% of respondents. And almost 90% of those who worked reported that brain fog impaired their ability to work to some extent.
This study found that two SARS-CoV-2 variants, the original wild type and Omicron, were best able to induce cell stress and damage components of the BBB.
However, Dr. Giovanni Schifitto, professor of neurology at the University of Rochester Medical Center, NY, believes that the cause of long covid is likely to be multifactorial.
“The physical presence of SARS-CoV-2 in the brain, especially in the chronic phase, is unlikely to be the culprit. However, systemic virus persistence can create a more chronic systemic inflammatory status and that can contribute to multi-organ dysfunction,” he told us.
There is more support for the suggestion that brain fog in long COVID may result from immune dysfunction and inflammation.
One recent study, which appeared in Nature CommunicationsTrusted Source, showed that people with COVID had raised levels of four brain injury biomarkers, and that two of these persisted long after the initial infection, particularly in those who experienced neurological complications during the acute infection.
The authors of this research suggest these abnormal immune responses may be causing ongoing inflammation. And inflammation can lead to brain fog.
They believe that if they can find out why these immune responses are triggered, treatments could be developed to target them.
Whether the effects are due to viral invasion or immune dysfunction, research has found that SARS-CoV-2 infection can lead to changes in the brain.
A study — published in NatureTrusted Source in March 2022 — using data from the UK Biobank compared brain scans conducted on people before and after they had COVID-19.
Those who had had SARS-CoV-2 infection had a reduction in grey matter thickness, markers of tissue damage in olfactory regions, and changes in brain volume, as well as slightly lower cognitive abilities than those who had not.
Prof. Griffin explained:
“As with many issues around long COVID, brain fog is likely a combination of persistent infection by SARS-CoV-2 [as reported ina new studyTrusted Sourcepublished in 2023] and host immune/metabolic changes that occur either concomitantly or as a follow-on. Worryingly, changes to the brain, including reductions in grey matter, have been noted even in patients that aren’t necessarily associated with neurological symptoms.”
Research reported in Nature NeuroscienceTrusted Source, which used dynamic contrast-enhanced magnetic resonance imagingTrusted Source (DCE-MRI) on people with long COVID with or without reported brain fog, has backed up these findings. The researchers found not only significantly increased BBB permeability in the group with brain fog, but also reduced global brain volume and white matter volume.
The researchers suggest that “long COVID-derived brain fog is associated with BBB disruption and sustained systemic inflammation,” adding that their “data suggest that BBB disruption occurs during acute infection and long COVID, where it is strongly associated with cognitive impairment.”
following a healthy diet, rich in fresh fruits and vegetables and limiting processed food
doing regular exercise
having good sleep hygiene
managing stress.
Dr. Schifitto advised that:
“General principals are avoid deconditioning, thus keep routine physical activity although [this] will need to be titrated to tolerance. Be aware of mental fatigue so spread intellectual work throughout the day. Because often there are also depressive symptoms present, maintain social connections.”
And Prof. Griffin warned that anyone with long COVID brain fog should “ensure that you pace yourself when experiencing this or other long COVID symptoms. Over-exertion can sometimes exacerbate things.”
He suggested that using tech, and setting reminders and alarms can help people cope with the brain fog and fatigue of long COVID.
As has become increasingly clear, COVID, like many other viral diseases, can have effects long beyond the initial infection, and research is only now starting to discover why.
Avoiding infection is, of course, the best way to avoid long-term effects, but there is increasing evidence that vaccination and antiviral treatment in the early stages of infection reduces the risk of long COVID.
But Prof. Griffin is frustrated about the lack of action taken to prevent infection and counter the long-term effects of COVID-19.
“Like a lot of aspects of SARS-CoV-2 infection, because it [brain fog] doesn’t necessarily manifest during acute disease it tends to be overlooked. This, to me, is another reason why the reluctance of western governments to suppress prevalence of this virus is […] mind-bogglingly negligent,” he told us.
“There are already record numbers of people out of work due to chronic illness, also many that struggle on, plus cognitive impairment on this scale makes for a less productive population as a whole,“ said Prof Griffin.
“Adding brain fog to the already staggering list of longer term problems caused by COVID must surely make us question what we’re allowing to happen to those being exposed to multiple infections with this virus, including our children,” he emphasized.
From work to school to socializing, COVID-19 has impacted just about every part of our lives—and now Boston University research has shown that also includes what happens in the bedroom. A study of more than 2,000 cisgender women found the coronavirus disease can impair sexual function, with long COVID having an especially detrimental effect.
“If you’re sick with COVID, you’re probably less interested in sex and maybe your body is less prepared to have sex,” says Amelia M. Stanton, a BU College of Arts & Sciences assistant professor of psychological and brain sciences. “But what might be surprising to some folks is that long COVID symptoms really may have a physiological and psychological impact on sexual well-being for women.”
Although previous research has investigated the effect of the pandemic on peoples’ sex lives—particularly in men—Stanton says this is the first study to highlight long COVID’s fallout on sexual health in women. An expert on sexual and mental health, she helped lead the study with researchers from Middlebury College, McLean Hospital, and the University of Vermont. The findings were recently published in the Journal of Sexual Medicine.
Long COVID and sexual dysfunction
To figure out COVID’s impact on intimacy, Stanton and her colleagues conducted an online survey. Roughly half of the women taking part had reported never having had COVID, the rest said they’d tested positive. Participants were quizzed using the Female Sexual Function Index (FSFI), an established tool that measures factors like arousal and satisfaction with questions such as, “Over the past 4 weeks, how often did you feel sexual desire?” Only women who’d had sex in the previous month were included in the results.
Among those who’d had COVID, levels of desire, arousal, lubrication, and satisfaction were all lower than in those who hadn’t; orgasm and pain scores weren’t significantly different between the two groups. But while women in the COVID group were still classed within the index’s functional range, participants with long COVID had “an average FSFI full scale score in the dysfunctional range,” according to the researchers. They found women with long COVID—a broad condition with cognitive and physical symptoms that linger for weeks, sometimes months, after an initial infection—had markedly worse arousal, lubrication, orgasm, and pain scores.
“I hope it’s validating. If women type in ‘sex long COVID,’ something will come up now,” says Stanton, who is also a clinical health psychologist at The Fenway Institute, a Boston clinic focused on the health of sexual and gender minorities. “Sex, sexuality, and sexual function are still relatively taboo subjects. But this offers something patients can bring to their providers and say, ‘This is going on for me,’ and maybe create an open dialogue around sex.”
In their paper, Stanton and her colleagues say the results suggest “that COVID-19 infection may be associated with impairment of both cognitive and physiological aspects of sexual function.” Just as the body and mind might take some time to get back to firing on all cylinders when it comes to work, study, and exercise, the same may apply to sex. They also speculate that wider societal changes caused by the pandemic may be a factor, with fewer social events and kids hanging around at home more reducing opportunities for shared or solo sexual activities.
Talking about sex
While a COVID infection might impact women’s sexual health, previous BU research has found vaccination does not cause infertility, reduce pregnancy chances, or have a significant impact on menstruation.
“COVID-19 vaccination in either partner is unrelated to fertility among couples trying to conceive through intercourse,” Amelia Wesselink, an SPH research assistant professor of epidemiology, told The Brink in 2022 when discussing her study on vaccines and fertility. That same research did, however, find that men who’d tested positive for COVID within the past 60 days had reduced fertility.
Stanton is the principal investigator of BU’s Sexual, Reproductive, and Mental Health Disparities Program—an effort to explore sexual and mental health in minoritized and marginalized populations—and says possible future routes for the latest project would be to expand the study’s sexual and gender minority diversity, talk to women for their qualitative experiences, and design tools to help providers better support their patients.
“I’m an interventionist, so I always think about intervention design as a next step,” says Stanton. In other research, she’s working to develop new approaches clinicians can use to talk about sex with their patients, as well as studying how to improve sexual well-being and mental health in low-resource communities.
“I always encourage providers to initiate conversations about sex,” says Stanton. “If they have someone who’s coming in for long COVID, maybe ask, ‘How are you doing sexually?’ Asking that one question could open the door for people to say, ‘You know, I’ve been ashamed to say that this is going on, and I really need help.’ Any way we can iterate to folks that there is hope and there are strategies—your symptoms are meaningful and relevant, and they’re important to talk about.”
Brain fog is one of the most commo.n, persistent complaints in patients with long COVID. It affects as many as 46% of patients who also deal with other cognitive concerns like memory loss and difficulty concentrating.
Now, researchers believe they know why. A new study has found that these symptoms may be the result of a viral-borne brain injury that may cause cognitive and mental health issues that persist for years.
Researchers found that 351 patients hospitalized with severe COVID-19 had evidence of a long-term brain injury a year after contracting the SARS-CoV-2 virus. The findings were based on a series of cognitive tests, self-reported symptoms, brain scans, and biomarkers.
Brain Deficits Equal to 20 Years of Brain Aging
As part of the preprint study, participants took a cognition test with their scores age-matched to those who had not suffered a serious bout of COVID-19. Then a blood sample was taken to look for specific biomarkers, showing that elevated levels of certain biomarkers were consistent with a brain injury. Using brain scans, researchers also found that certain regions of the brain associated with attention were reduced in volume.
Patients who participated in the study were “less accurate and slower” in their cognition, and suffered from at least one mental health condition, such as depression, anxiety, or posttraumatic stress disorder, according to researchers.
The brain deficits found in COVID-19 patients were equivalent to 20 years of brain aging and provided proof of what doctors have feared: that this virus can damage the brain and result in ongoing mental health issues.
“We found global deficits across cognition,” said lead study author Benedict Michael, PhD, director of the Infection Neuroscience Lab at the University of Liverpool in Liverpool, England. “The cognitive and memory problems that patients complained of were associated with neuroanatomical changes to the brain.”
Proof That Symptoms Aren’t ‘Figment’ of Patients’ Imaginations
Cognitive deficits were common among all patients, but the researchers said they don’t yet know whether the brain damage causes permanent cognitive decline. But the research provides patients who have been overlooked by some clinicians with proof that their conditions aren’t a figment of their imaginations, said Karla L. Thompson, PhD, lead neuropsychologist at the University of North Carolina School of Medicine’s COVID Recovery Clinic.
“Even though we’re several years into this pandemic, there are still a lot of providers who don’t believe that their patients are experiencing these residual symptoms,” said Thompson, “That’s why the use of biomarkers is important, because it provides an objective indication that the brain has been compromised in some way.”
Some patients with long COVID have said that getting their doctors to believe they have a physical ailment has been a persistent problem throughout the pandemic and especially as it relates to the sometimes-vague collection of symptoms associated with brain fog. One study found that as many as 79% of study respondents reported negative interactions with their healthcare providers when they sought treatment for their long-COVID symptoms.
How Do COVID-Related Brain Injuries Happen?
Researchers are unsure what’s causing these brain injuries, though they have identified some clues. Previous research has suggested that such injuries might be the result of a lack of oxygen to the brain, especially in patients who were hospitalized, like those in this study, and were put on ventilators.
Brain scans have previously shown atrophy to the brain’s gray matter in COVID-19 patients, likely caused by inflammation from a heightened immune response rather than the virus itself. This inflammatory response seems to affect the central nervous system. As part of the new study, researchers found some neuroprotective effects of using steroids during hospitalization to reduce brain inflammation.
The results suggest that clinicians should overcome their skepticism and consider the possibility that their patients have suffered a brain injury and should be treated appropriately, said James C. Jackson, PsyD, a neuropsychiatrist at Vanderbilt University School of Medicine. “The old saying is that if it walks like a duck and talks like a duck, it’s a duck,” said Jackson.
He contends that treatments used for patients who have brain injuries have also been shown to be effective in treating long COVID–related brain fog symptoms. These may include speech, cognitive, and occupational therapy as well as meeting with a neuropsychiatrist for the treatment of related mental health concerns.
A New Path Forward
Treating long-COVID brain fog like a brain injury can help patients get back to some semblance of normalcy, researchers said. “What we’re seeing in terms of brain injury biomarkers and differences in brain scans correlates to real-life problems that these patients are dealing with on a daily basis,” said Jackson. These include problems at work and in life with multitasking, remembering details, meeting deadlines, synthesizing large amounts of information, and maintaining focus on the task at hand, he said.
There’s also a fear that even with treatment, the aging of the brain caused by the virus might have long-term repercussions and that this enduring injury may cause the early onset of dementia and Alzheimer’s disease in those who were already vulnerable to it. One study, from the National Institute of Neurological Disorders and Stroke (NINDS), found that in those infected with COVID-19 who already had dementia, the virus “rapidly accelerated structural and functional brain deterioration.”
“We already know the role that neuroinflammation plays in the brains of patients with Alzheimer’s disease,” said Thompson. “If long COVID is involved in prolonged inflammation of the brain, it goes a long way in explaining the mechanism underlying [the study’s reported] brain aging.”
Still More to Learn
In some ways, this study raises nearly as many questions as it does answers. While it provides concrete evidence around the damage the virus is doing to the brains of patients who contracted severe COVID-19, researchers don’t know about the impact on those who had less serious cases of the virus.
For Ziyad Al-Aly, MD, chief of research and development at the Veterans Affairs St. Louis Health Care System, the concern is that some long-COVID patients may be suffering from cognitive deficits that are more subtle but still impacting their daily lives, and that they’re not getting the help they need.
What’s more, said Al-Aly, it’s unclear whether the impacts of the brain damage are permanent or how to stop them from worsening. Researchers and clinicians need a better understanding of the mechanism that allows this virus to enter the brain and do structural damage. If it’s inflammation, will anti-inflammatory or antiviral medications work at preventing it? Will steroids help to offset the damage? “It’s critical we find some answers,” he said.
“SARS-CoV-2 isn’t going anywhere. It will continue to infect the population, so if this is indeed a virus that damages the brain in the long term or permanently, we need to figure out what can be done to stop it,” said Al-Aly.
From work to school to socializing, COVID-19 has impacted just about every part of our lives—and now Boston University research has shown that also includes what happens in the bedroom. A study of more than 2,000 cisgender women found the coronavirus disease can impair sexual function, with long COVID having an especially detrimental effect.
“If you’re sick with COVID, you’re probably less interested in sex and maybe your body is less prepared to have sex,” says Amelia M. Stanton, a BU College of Arts & Sciences assistant professor of psychological and brain sciences. “But what might be surprising to some folks is that long COVID symptoms really may have a physiological and psychological impact on sexual well-being for women.”
Although previous research has investigated the effect of the pandemic on peoples’ sex lives—particularly in men—Stanton says this is the first study to highlight long COVID’s fallout on sexual health in women. An expert on sexual and mental health, she helped lead the study with researchers from Middlebury College, McLean Hospital, and the University of Vermont. The findings were recently published in the Journal of Sexual Medicine.
Long COVID and sexual dysfunction
To figure out COVID’s impact on intimacy, Stanton and her colleagues conducted an online survey. Roughly half of the women taking part had reported never having had COVID, the rest said they’d tested positive. Participants were quizzed using the Female Sexual Function Index (FSFI), an established tool that measures factors like arousal and satisfaction with questions such as, “Over the past 4 weeks, how often did you feel sexual desire?” Only women who’d had sex in the previous month were included in the results.
Among those who’d had COVID, levels of desire, arousal, lubrication, and satisfaction were all lower than in those who hadn’t; orgasm and pain scores weren’t significantly different between the two groups. But while women in the COVID group were still classed within the index’s functional range, participants with long COVID had “an average FSFI full scale score in the dysfunctional range,” according to the researchers. They found women with long COVID—a broad condition with cognitive and physical symptoms that linger for weeks, sometimes months, after an initial infection—had markedly worse arousal, lubrication, orgasm, and pain scores.
“I hope it’s validating. If women type in ‘sex long COVID,’ something will come up now,” says Stanton, who is also a clinical health psychologist at The Fenway Institute, a Boston clinic focused on the health of sexual and gender minorities. “Sex, sexuality, and sexual function are still relatively taboo subjects. But this offers something patients can bring to their providers and say, ‘This is going on for me,’ and maybe create an open dialogue around sex.”
In their paper, Stanton and her colleagues say the results suggest “that COVID-19 infection may be associated with impairment of both cognitive and physiological aspects of sexual function.” Just as the body and mind might take some time to get back to firing on all cylinders when it comes to work, study, and exercise, the same may apply to sex. They also speculate that wider societal changes caused by the pandemic may be a factor, with fewer social events and kids hanging around at home more reducing opportunities for shared or solo sexual activities.
Talking about sex
While a COVID infection might impact women’s sexual health, previous BU research has found vaccination does not cause infertility, reduce pregnancy chances, or have a significant impact on menstruation.
“COVID-19 vaccination in either partner is unrelated to fertility among couples trying to conceive through intercourse,” Amelia Wesselink, an SPH research assistant professor of epidemiology, told The Brink in 2022 when discussing her study on vaccines and fertility. That same research did, however, find that men who’d tested positive for COVID within the past 60 days had reduced fertility.
Stanton is the principal investigator of BU’s Sexual, Reproductive, and Mental Health Disparities Program—an effort to explore sexual and mental health in minoritized and marginalized populations—and says possible future routes for the latest project would be to expand the study’s sexual and gender minority diversity, talk to women for their qualitative experiences, and design tools to help providers better support their patients.
“I’m an interventionist, so I always think about intervention design as a next step,” says Stanton. In other research, she’s working to develop new approaches clinicians can use to talk about sex with their patients, as well as studying how to improve sexual well-being and mental health in low-resource communities.
“I always encourage providers to initiate conversations about sex,” says Stanton. “If they have someone who’s coming in for long COVID, maybe ask, ‘How are you doing sexually?’ Asking that one question could open the door for people to say, ‘You know, I’ve been ashamed to say that this is going on, and I really need help.’ Any way we can iterate to folks that there is hope and there are strategies—your symptoms are meaningful and relevant, and they’re important to talk about.”
A study offers new clues on why long COVID persists in some individuals. krisanapong detraphiphat
Despite the debilitating nature of long COVID, there is an absence of diagnostic tests and therapeutic tools for long COVID.
A new study analyzed blood samples from long COVID patients and healthy individuals. The findings suggest a dysregulation of the complement pathway, a part of the immune system, and the blood clotting pathways in individuals with long COVID at six months.
Changes in certain molecules in these immune and blood clotting pathways were predictive of the persistence of long COVID symptoms at 6 and 12 months, indicating the utility of these measures in developing diagnostic tools for long COVID.
The dysregulation of these immune and blood clotting pathways suggests that therapies targeting these pathways could help treat long COVID.
Approximately 10%-20%Trusted Source of individuals with a SARS-CoV-2 infection experience lingering symptoms beyond three months after symptom onset. These symptoms referred to as long COVID, can be debilitating, but there is a lack of diagnostic or therapeutic tools.
A new study published in Sciencefound that patients experiencing long COVID symptoms six months after the SARS-CoV-2 infection show dysregulation of the blood clotting or coagulation system and the complement pathway, which is a part of the immune system.
These changes in the coagulation and immune systems in long COVID patients were shown to predict the persistence of symptoms at six months. They may have the potential for the development of diagnostic tools. Moreover, therapeutics to counter the changes in the blood clotting and immune system could help alleviate long COVID symptoms.
Dr. Wolfram Ruf, Scientific Director at the Center for Thrombosis and Hemostasis (CTH), Johannes Gutenberg University, wrote in an accompanying editorial:
“Although therapeutic interventions with coagulation and complement inhibitors in acute COVID-19 produced mixed results, the pathological features specific for Long Covid suggest potential interventions for clinical testing.”
Long COVID refers to one or more symptoms that persist or develop after the acute phase of a SARS-CoV-2 infection. Common symptoms of long COVID include muscle weakness, fatigue, and brain fog.
Tissue damage, persistent inflammation, production of autoantibodies, and reactivation of latent virus reservoirs are some factors that have been hypothesizedTrusted Source to cause long COVID. However, the lack of knowledge about the precise mechanisms underlying long COVID has hampered the development of diagnostic tools and targeted therapies.
Several studies have shown that individuals with long COVID show immune system dysregulationTrusted Source. The present study further examined changes in the immune system associated with long COVID at six months.
The study included 39 healthy participants and 113 individuals with confirmed SARS-CoV-2 infection. During the 12-month follow-up period after the onset of a SARS-CoV-2 infection, 40 out of the 113 participants with an acute SARS-CoV-2 infection had at least one persistent symptom at the 6-month follow-up visit.
Serum samples were collected from the participants during the acute phase of the infection and six months after the infection. These serum samples were used to quantify changes in more than 6,500 proteins.
The participants with long COVID symptoms at six months showed changes in serum proteins belonging to the complement system compared with healthy individuals or those without long COVID at six months. The complement system is a part of the innate immune system, which serves as the first line of defense against germs.
The complement system activation helps elicit an immune response against pathogens or damaged tissue. During the activation of the complement pathway, the plasma proteins belonging to the complement system interact with each other to form a terminal complement complex. The terminal complement complex binds to the surface of or inserts into the membrane of pathogens and damaged cells to induce cell death or promote their removal by engulfment Trusted Sourceby phagocytes.
Among patients with long COVID at six months, the researchers found increased activation of the complement pathway during acute SARS-CoV-2 infection and at six months after diagnosis. Increased activation of the complement pathway and terminal complement complex formation in 6-month long COVID patients could lead to tissue damage.
The proteins in the complement system can be activated by three distinct pathways, each involving different types of molecules. The three complement activation pathways include the classical pathway, the alternative pathway, and the lectin pathway.
Individuals with long COVID at six months showed increased expression of molecules involved in forming the terminal complement complex via the activation of the classical and alternative pathways than those without long COVID or healthy patients.
In addition to the three complement activation pathways, thrombin, a protein that promotes blood coagulation, can also cause the activation of the complement pathway and lead to the formation of the terminal complement complex.
Patients with long COVID symptoms at the 6-month follow-up showed lower levels of antithrombin III, an enzyme that inhibits thrombin, during the acute phase and at six months after the onset of a SARS-CoV-2 infection than healthy individuals. The lower antithrombin III levels were accompanied by increased expression of markers of thrombosis, a state characterized by the formation of clots in the absence of bleeding.
Patients with long COVID at six months simultaneously showed increased markers for inflammation and those for thrombosis. The cooccurrence of inflammation and thrombosis is referred to as thromboinflammation.
Signs of thromboinflammation observed in individuals with long COVID at six months included destruction of red blood cells and dysfunction of endothelial cells that line blood vessels. Moreover, these patients also showed increased markers of tissue damage in the blood.
These changes associated with thromboinflammation reflect the dysregulation of the complement system in patients with 6-month long COVID. The dysregulation of the coagulation system in long COVID patients also underscores the need for cardiovascular health assessment.
The researchers found that changes in specific complement protein levels, coagulation system biomarkers, and age and body mass index predicted long COVID at 6 and 12 months.
MNT spoke with Dr. Hrishikesh Kulkarni, Assistant Professor of Medicine at Washington University School of Medicine, who was not involved in the study. Dr. Kulkarni said:
“By utilizing an unbiased screen and confirming it using distinct components of the membrane attack complex by which the complement system damages cells, the authors demonstrate that persistently increased complement activation is a key feature of Long COVID. Moreover, their models that incorporate the measurement of 2 protein ratios improve an already good clinical model comprising of age and body-mass index, most notably for 12-month Long COVID.”
The classical complement pathway is activated upon antibodies binding to viral proteins or autoantibodies in the body’s tissue. In the present study, the serum from patients with 6-month long COVID showed increased antibodies against cytomegalovirus, a type of herpesvirus.
This is consistent with evidence suggesting that long COVID symptoms may arise, in part, due to an inflammatory response to the reactivation of a prior herpesvirus infection. The persistence of SARS-CoV-2 in some tissues may also produce an immune response.
These results suggest that binding of the antibodies to proteins from a herpesvirus could contribute to the activation of the complement system. Besides explaining the increased complement activation, these results suggest that antivirals targeting the herpesvirus and SARS-CoV-2 could have the potential to ameliorate long COVID symptoms.
Researchers found several immune and hormonal differences between people with Long COVID and those without.
The findings shed light on possible causes of Long COVID and could eventually lead to more sensitive testing and personalized treatments.
Researchers are making progress in understanding the underlying causes of Long COVID. ShowRecMedia / Shutterstock
Some people may experience chronic symptoms for months or years after an acute viral infection. Long COVID, a syndrome that develops in some people after an acute SARS-CoV-2 infection, is a prominent recent example. More than 200 Long COVID symptoms have been documented. Typical ones include extreme fatigue, cognitive impairment, post-exertional malaise, and respiratory problems. Research suggests that about one in eight people who survive an acute SARS-CoV-2 infection go on to have persistent symptoms. The processes that give rise to Long COVID remain unclear.
To shed light on the biology underlying Long COVID, a research team with NIH funding, partly through the RECOVER(link is external) Initiative, conducted a study of more than 250 people. The participants included people who had been infected with SARS-CoV-2 and uninfected people. Among those who had been infected, some had Long COVID and some did not. The researchers measured levels of various immune cells and markers in the participants’ blood. They also measured antibody responses to SARS-CoV-2 and a range of other viruses. The results appeared in Nature on September 25, 2023.
The team found significant differences in the immune cells of participants with and without Long COVID. Those with Long COVID had higher levels of cells called non-conventional monocytes and activated B lymphocytes. They had lower levels of type 1 conventional dendritic cells and central memory T cells. These differences did not depend on age, sex, or body mass index. Participants with Long COVID also had different levels of immune signaling molecules.
Participants with Long COVID had much stronger antibody responses against the SARS-CoV-2 spike protein than those without Long COVID. They also had much stronger responses to an unrelated virus, Epstein-Barr virus (EBV). EBV is a common herpesvirus that causes mononucleosis. After infection, it remains latent in the body and can sometimes reactivate. The higher levels of antibodies to EBV suggest recent reactivation of this virus.
When the researchers used machine learning to identify which features could best predict Long COVID status, they found that the strongest predictor was the stress hormone cortisol. People with Long COVID had much lower cortisol levels than those without. Other strong predictors of Long COVID included elevated levels of a protein called galectin-1, elevated antibodies against EBV, and reduced levels of certain immune cells.
These findings identify potential biomarkers that could help with diagnosing Long COVID. They also suggest possible mechanisms that contribute to Long COVID. These include a lingering presence of SARS-CoV-2 components in the body, reactivation of latent EBV, and chronic inflammation.
“These findings are important,” says Dr. David Putrino of the Icahn School of Medicine at Mount Sinai, one of the senior authors. “They can inform more sensitive testing for Long COVID patients and personalized treatments for Long COVID that have, until now, not had a proven scientific rationale. This is a decisive step forward in the development of valid and reliable blood testing protocols for Long COVID.”
Dr. Akiko Iwasaki of the Yale University School of Medicine, another senior author, says, “These findings tell us something about the underlying disease pathogenesis of Long COVID and suggest potential paths for therapy.”
Putative Mechanisms of Cognitive Dysfunction in Long Covid.
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