Category: COVID

Categories : COVIDTags :

Certain Nasal Bacteria May Boost the Risk for COVID-19 Infection

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Methicillin resistant Staphylococcus aureus (MRSA) – Credit: CDC

A new study from researchers at the George Washington University has found that certain bacteria living in the nose may influence how likely someone is to get a COVID-19 infection. Published in EBioMedicine, the research reveals that certain types of nasal bacteria can affect the levels of key proteins the virus needs to enter human cells, offering new insight into why some people are more vulnerable to COVID-19 than others.

“We’ve known that the virus SARS-CoV-2 enters the body through the respiratory tract, with the nose being a key entry point. What’s new – and surprising – is that bacteria in our noses can influence the levels of proteins that the virus uses to infect cells,” said Cindy Liu, associate professor of environmental and occupational health at the GW Milken Institute School of Public Health.

Higher Gene Expression of Viral Entry Proteins Increases COVID-19 Infection Risk

In the study, Liu and her team analysed nasal swab samples from over 450 people, including some who later tested positive for COVID-19. They found that those who became infected had higher levels of gene expression for two key proteins: ACE2 and TMPRSS2. ACE2 allows the virus to enter nasal cells, while TMPRSS2 helps activate the virus by cleaving its spike protein.

Those with high expression for these proteins were more than three times as likely to test positive for COVID-19, while those with moderate levels had double the risk. The study also found that people who became infected had more unstable levels of gene expression, with the sharpest increases just days before testing positive, suggesting rising expression levels may signal increased vulnerability to the virus.

Notably, while women generally had higher gene expression levels of these proteins – consistent with previous studies showing higher COVID-19 infection rates in women – men with higher levels were more likely to get infected, indicating elevated protein levels may present a greater risk for men.

Nasal Bacteria May Play a Role in COVID-19 Risk

To understand what could impact the expression levels of these viral entry proteins, the researchers turned to the nasal microbiome – the diverse community of bacteria that naturally reside in the nose. They found that certain nasal bacteria may affect the expression levels of ACE2 and TMPRSS2, influencing the respiratory tract’s susceptibility to COVID-19.

The study identified three common nasal bacteria – Staphylococcus aureus, Haemophilus influenzae, and Moraxella catarrhalis/nonliquefaciens – that were linked to higher expression levels of ACE2 and TMPRSS2 and increased COVID-19 risk. On the other hand, Dolosigranulum pigrum, another common type of nasal bacteria, was connected to lower levels of these key proteins and may offer some protection against the virus.

“Some bacteria in your nose may be setting the stage – or even holding the door open – for viruses like SARS-CoV-2 to get in,” said Daniel. Park, a senior research scientist at GW and the first author of the study.

While some of the high-risk bacteria were less common, 20% of participants carried enough S. aureus to nearly double their risk for having elevated ACE2 and TMPRSS2 expression, making it a major nasal microbiome risk factor for increasing individuals’ risk for COVID-19 infection.

Why This Matters

The findings offer new potential ways to predict and prevent COVID-19 infection. The study suggests that monitoring ACE2 and TMPRSS2 gene expression could help identify individuals at higher risk for infection. The research also highlights the potential of targeting the nasal microbiome to help prevent viral infections.

“We’re only beginning to understand the complex relationship between the nasal microbiome and our health,” said Liu. “This study suggests that the bacteria in our nose – and how they interact with the cells and immune system in our nasal cavity – could play an important role in determining our risk for respiratory infections like COVID-19.”

The team plans to explore whether modifying the nasal microbiome, such as through nasal sprays or live biotherapeutics, could reduce the risk of infection – potentially paving the way for new ways to prevent respiratory viral infections in future pandemics.

Source: George Washington University

Categories : COVIDTags :

New Antibodies Potentially Effective Against All SARS-CoV-2 Variants

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Image by Fusion Medical on Unsplash

SARS-COV-2 has been very good at mutating to keep infecting people – so good that most antibody treatments developed during the pandemic are no longer effective. Now a team led by Stanford University researchers may have found a way to pin down the constantly evolving virus and develop longer-lasting treatments.

The researchers discovered a method to use two antibodies, one to serve as a type of anchor by attaching to an area of the virus that does not change very much and another to inhibit the virus’s ability to infect cells. This pairing of antibodies was shown to be effective against the initial SARS-CoV-2 virus that caused the pandemic and all its variants through omicron in laboratory testing. The findings are detailed in the journal Science Translational Medicine.

“In the face of an ever-changing virus, we engineered a new generation of therapeutics that have the ability to be resistant to viral evolution, which could be useful many years down the road for the treatment of people infected with SARS-CoV-2,” said Christopher O. Barnes, the study’s senior author, an assistant professor of biology.

An overlooked option

The team led by Barnes and first author Adonis Rubio, a doctoral candidate in the Stanford School of Medicine, conducted this investigation using donated antibodies from patients who had recovered from COVID-19. Analysing how these antibodies interacted with the virus, they found one that attaches to a region of the virus that does not mutate often.

This area, within the Spike N-terminal domain, or NTD, had been overlooked because it was not directly useful for treatment. However, when a specific antibody attaches to this area, it remains stuck to the virus. This is useful when designing new therapies that enable another type of antibody to get a foothold and attach to the receptor-binding domain, or RBD, of the virus, essentially blocking the virus from binding to receptors in human cells.

An illustration of the bispecific antibodies the Stanford-led research team developed to neutralise the virus that causes COVID-19. Named “CoV2-biRN,” these two antibodies work together by attaching to different areas of the virus.
The bispecific antibodies target two areas of the virus: One attaches to the “NTD,” or Spike N-terminal domain, an area on the virus that does not change very much. This allows the second antibody to attach to the “RBD,” or receptor-binding domain, essentially preventing the virus from infecting human cells. | Christopher O. Barnes and Adonis Rubio using Biorender stock images

The researchers designed a series of these dual or “bispecific” antibodies, called CoV2-biRN, and in laboratory tests they showed high neutralisation of all the variants of SARS-CoV-2 known to cause illness in humans. The antibodies also significantly reduced the viral load in the lungs of mice exposed to one version of the omicron variant.

More research, including clinical trials, would have to be done before this discovery could be used as a treatment in human patients, but the approach is promising – and not just for the virus that causes COVID-19.

Next, the researchers will work to design bispecific antibodies that would be effective against all coronaviruses, the virus family including the ones that cause the common cold, MERS, and COVID-19. This approach could potentially also be effective against influenza and HIV, the authors said.

“Viruses constantly evolve to maintain the ability to infect the population,” Barnes said. “To counter this, the antibodies we develop must continuously evolve as well to remain effective.”

Source: Stanford University

Categories : COVIDTags :

Study Tracks Physical and Cognitive Impairments Associated with Long COVID

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Researchers following nearly 1000 people with post-COVID-19 syndrome found few changes to their symptoms in the second year of illness

Photo by Usman Yousaf on Unsplash

Two-thirds of people with post-COVID-19 syndrome have persistent, objective symptoms – including reduced physical exercise capacity and reduced cognitive test performances – for a year or more, with no major changes in symptom clusters during the second year of their illness, according to a new study published January 23rd in the open-access journal PLOS Medicine by Winfried Kern of Freiburg University, Germany, and colleagues.

Self-reported health problems following SARS-CoV-2 infection have commonly been described and may persist for months. However, the long-term prognosis of post-COVID-19 syndrome (PCS) is unknown.

In the new study, researchers studied 982 people aged 18 to 65 who had previously been identified as having PCS, as well as 576 controls. All participants visited one of several university health centers in southwestern Germany for comprehensive assessments, including neurocognitive, cardiopulmonary exercise, and laboratory testing.

The predominant symptom clusters among people with PCS were fatigue/exhaustion, neurocognitive disturbances, chest symptoms/breathlessness, and anxiety/depression/sleep problems. Nearly 68% of people who originally reported PCS still struggled with symptoms in the second year. Exercise intolerance with post-exertional malaise was reported by 35.6% of people with persistent PCS, and these people had worse outcomes and more severe symptoms. People with lower educational attainment, obesity, or more severe illness during the initial COVID-19 infection were also at higher risk of prolonged symptoms.

When they looked at objective measures of health and cognition, the team found that people with persistent PCS had significant reductions in handgrip strength, maximal oxygen consumption, and ventilatory efficiency. Patients with persistent PCS and post-exertional malaise scored lower than control patients on cognitive tests measuring memory, attention, and processing speed; however, the researchers point out that they had no data on cognition before acute COVID-19 infection. The team was not able to identify differences in cardiac function or laboratory values, including tests of viral persistence.

“The results call for the inclusion of cognitive and exercise testing in the clinical evaluation and monitoring of patients with suspected PCS,” the authors say. “Observational studies with longer follow-up are urgently needed to evaluate factors for improvement and non-recovery from PCS.”

The authors add, “Grave symptoms with mental and physical exercise dysfunction, but no laboratory markers in Long Covid/post-Covid syndrome.”

Provided by PLOS

Categories : Cancer COVIDTags :

COVID Caused Cancer Tumours to Shrink in Mice – New Study

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SARS-CoV-2 infecting a human cell. Credit: NIH

Justin Stebbing, Anglia Ruskin University

A fascinating new study, published in the Journal of Clinical Investigation, has revealed an unexpected potential benefit of severe COVID infection: it may help shrink cancer.

This surprising finding, based on research conducted in mice, opens up new possibilities for cancer treatment and sheds light on the complex interactions between the immune system and cancer cells – but it certainly doesn’t mean people should actively try to catch COVID.

The data outlining the importance of the immune system in cancer is considerable and many drugs target the immune system, unlocking its potential, an important focus of my own research.

The study here focused on a type of white blood cell called monocytes. These immune cells play a crucial role in the body’s defence against infections and other threats. However, in cancer patients, monocytes can sometimes be hijacked by tumour cells and transformed into cancer-friendly cells that protect the tumour from the immune system.

What the researchers discovered was that severe COVID infection causes the body to produce a special type of monocyte with unique anti-cancer properties. These “induced” monocytes are specifically trained to target the virus, but they also retain the ability to fight cancer cells.

To understand how this works, we need to look at the genetic material of the virus that causes COVID. The researchers found that these induced monocytes have a special receptor that binds well to a specific sequence of COVID RNA. Ankit Bharat, one of the scientists involved in this work from Northwestern University in Chicago explained this relationship using a lock-and-key analogy: “If the monocyte was a lock, and the COVID RNA was a key, then COVID RNA is the perfect fit.”

Remarkable

To test their theory, the research team conducted experiments on mice with various types of advanced (stage 4) cancers, including melanoma, lung, breast and colon cancer. They gave the mice a drug that mimicked the immune response to a severe COVID infection, inducing the production of these special monocytes. The results were remarkable. The tumours in the mice began to shrink across all four types of cancer studied.

Unlike regular monocytes, which can be converted by tumours into protective cells, these induced monocytes retained their cancer-fighting properties. They were able to migrate to the tumour sites – a feat that most immune cells cannot accomplish – and, once there, they activated natural killer cells. These killer cells then attacked the cancer cells, causing the tumours to shrink.

This mechanism is particularly exciting because it offers a new approach to fighting cancer that doesn’t rely on T cells, which are the focus of many current immunotherapy treatments.

While immunotherapy has shown promise, it only works in about 20% to 40% of cases, often failing when the body can’t produce enough functioning T cells. Indeed it’s thought that the reliance on T cell immunity is a major limitation of current immunotherapy approaches.

This new mechanism, by contrast, offers a way to selectively kill tumours that is independent of T cells, potentially providing a solution for patients who don’t respond to traditional immunotherapy.

It’s important to note that this study was conducted in mice, and clinical trials will be necessary to determine if the same effect occurs in humans.

Maybe aspects of this mechanism could work in humans and against other types of cancer as well, as it disrupts a common pathway that most cancers use to spread throughout the body.

While COVID vaccines are unlikely to trigger this mechanism (as they don’t use the full RNA sequence as the virus), this research opens up possibilities for developing new drugs and vaccines that could stimulate the production of these cancer-fighting monocytes.

Few would have imagined that there’d be an upside to COVID. Photo by Kelly Sikkema on Unsplash

Trained immunity

The implications of this study extend beyond COVID and cancer. It shows how our immune system can be trained by one type of threat to become more effective against another. This concept, known as “trained immunity”, is an exciting area of research that could lead to new approaches for treating a wide range of diseases.

However, it’s crucial again to emphasise that this doesn’t mean people should seek out COVID infection as a way to fight cancer, and this is especially dangerous as I have described. Severe COVID can be life-threatening and has many serious long-term health consequences.

Instead, this research provides valuable insights that could lead to the development of safer, more targeted treatments in the future. As we continue to grapple with the aftermath of the COVID pandemic, new infections and long COVID, studies like this remind us of the importance of basic scientific research.

Even in the face of a global health crisis, researchers are finding ways to advance our understanding of human biology and disease. This work not only helps us combat the immediate threat of COVID, but also paves the way for breakthroughs in treating other serious conditions such as cancer.

While there’s still much work to be done before these findings can be translated into treatments for human patients, this study represents an exciting step forward in our understanding of the complex relationship between viruses, the immune system and cancer. It offers hope for new therapeutic approaches and underscores the often unexpected ways in which scientific discoveries can lead to medical breakthroughs.

Justin Stebbing, Professor of Biomedical Sciences, Anglia Ruskin University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Categories : COVID General InterestTags :

How COVID Transformed Family Dinners for the Better

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Photo by Vanessa Loring on Pexels

While the lockdowns associated with the COVID pandemic led many families to eat more meals at home, they had an additional benefit: an increase in the quality of family time during those dinners, according to research published by the American Psychological Association.

The study, published in the journal Couple and Family Psychology: Research and Practice, found that families who ate together more often during the pandemic also had more positive interactions, shared news and information, and even embraced technology such as videoconferencing to connect with distant family members.

“The predominance of past research on family dinners has focused on frequency as the key predictor of benefits for children and adolescents,” said lead author Anne Fishel, PhD, a clinician and researcher in family therapy at Massachusetts General Hospital. “This study highlights the importance of examining both frequency and quality to understand the full picture of how shared meals can impact families.”

Researchers examined data from a survey of 517 ethnically and socioeconomically diverse parents across the United States, administered in May 2021. Their aim was to investigate changes in family dinner frequency and quality during the COVID pandemic.

Participants were asked about dinner frequency, quality and post-pandemic expectations. The survey included questions about positive and negative interactions, family support and incorporation of the outside world. They were asked questions such as, “During the pandemic, did all or most of the people living in your home eat dinner together less, about the same, or more than compared to before the pandemic?” Participants then provided answers ranging on a scale of 1–5, 1 being “much less” and 5 being “much more.”

Over 60% of respondents reported eating dinner together more often during the pandemic compared with pre-pandemic times. There was also a significant increase in positive interactions (e.g, expressing gratitude, laughing or feeling connected) during family meals.

“Specifically, 56% said they increased talking about their days during dinner, 60% said they increased talking about their identity as a family, 60% said they increased expressing gratitude, 67% said they increased laughing together and 59% said they felt more connected to each other around the dinner table,” said Fishel. This positive association was evident across income levels, education, age, gender and race.

The pandemic introduced new aspects to family dinners, including remote dining with extended family members and more discussions about current events, according to Fishel. Many families turned to videoconferencing to connect with extended family, potentially strengthening a sense of belonging to a larger family unit. Most parents who increased the use of technology for remote dinners during the pandemic reported that they plan to continue this practice as the pandemic subsides.

The researchers also found an increase in families incorporating news and information from the outside world into their dinner conversations, potentially offering a safe space for children to discuss anxieties and questions with their parents.

Overall, this study suggests that the increased frequency of family dinners during the pandemic may have had lasting positive effects on family dynamics, according to Fishel.

Source: American Psychological Association

Categories : COVID Immune SystemTags :

SARS-CoV-2 Hijacks Three Key Proteins in the Complement System

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SARS-CoV-2 viruses (yellow) infecting a human cell (blue). Photo by CDC on Pexels

Researchers at the Medical University of Vienna and the Medical University of Innsbruck discovered that SARS-CoV-2 hijacks three important host proteins that dampen the activity of the complement system, a key component of early antiviral immunity. This significantly impairs viral clearance which may affect the course of both acute COVID infections and post-COVID sequelae. The study was recently published in the journal Emerging Microbes & Infections.

An early and effective immune response is crucial for resolving viral infections and preventing post-infectious complications. The complement system, a pivotal element of antiviral immunity, is a cascade of proteins found in the bloodstream and at mucosal sites, such as the respiratory tract. Activated through three different pathways, complement facilitates the clearance of virus particles by directly inducing their destruction (lysis). To prevent bystander damage to host cells, complement is rapidly inactivated by a set of host molecules referred to as complement regulatory proteins. The new study led by Anna Ohradanova-Repic and colleagues from the Center for Pathophysiology, Infectiology and Immunology at the Medical University of Vienna in collaboration with the team of Heribert Stoiber from the Institute of Virology at the Medical University of Innsbruck shows that SARS-CoV-2 hijacks three of these regulatory proteins, CD55, CD59 and Factor H, and thereby successfully shields itself from complement-mediated lysis.

Hijacking host proteins for effective complement resistance

By propagating SARS-CoV-2 in human cells the researchers discovered that the virus particles acquire the cellular proteins CD55 and CD59. Further experiments showed that SARS-CoV-2 also binds to Factor H, another complement regulatory protein that is primarily found in the bloodstream. Confronting the virus particles with active complement revealed that they are partially resistant to complement-mediated lysis. By removing CD55, CD59 and Factor H from the virus surface or inhibiting their biological functions, the researchers could successfully restore complement-mediated clearance of SARS-CoV-2.

“Through hijacking these three proteins, SARS-CoV-2 can evade all three complement pathways, resulting in reduced or delayed viral clearance by the infected host,” Anna Ohradanova-Repic, the leader of the study explains. Because complement is intricately linked with other components of the immune system, this not only affects virus elimination but can also cause significant inflammation, a core feature of both severe COVID-19 and Long COVID. “Uncovering immune evasion mechanisms that allow the virus to linger within the host for longer, deepen our understanding of the acute and long-term impacts of SARS-CoV-2 infection,” says first author Laura Gebetsberger.

Source: Medical University of Vienna

Categories : COVID Immune SystemTags :

New Discovery Explains How SARS-CoV-2 Evades Anti-viral Immunity

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The novel coronavirus SARS-CoV-2 has an enzyme that can counteract a cell’s innate defence mechanism against viruses, explaining why it is more infectious than the previous SARS and MERS-causing viruses. This discovery, from Kobe University, may point the way to the development of more effective drugs against this and possibly similar, future diseases.

When a virus attacks, the body’s immune response has two basic layers of defence: the innate and the adaptive immune systems. While the adaptive immune system grows stronger against a specific pathogen as the body is exposed to it multiple times and which forms the basis of vaccinations, the innate immune system is an assortment of molecular mechanisms that work against a broad range of pathogens at a basic level. The Kobe University virologist SHOJI Ikuo says, “The new coronavirus, however, is so infectious that we wondered what clever mechanisms the virus employs to evade the innate immune system so effectively.”

Shoji’s team previously worked on the immune response to hepatitis viruses and investigated the role of a molecular tag called “ISG15” the innate immune system attaches to the virus’s building blocks. Having learned that the novel coronavirus has an enzyme that is especially effective in removing this tag, he decided to use his team’s expertise to elucidate the effect of the ISG15 tag on the coronavirus and the mechanism of the virus’s countermeasures.

In a paper in the Journal of Virology, the Kobe University-led team is now the first to report that the ISG15 tag gets attached to a specific location on the virus’s nucleocapsid protein, the scaffold that packages the pathogen’s genetic material. For the virus to assemble, many copies of the nucleocapsid protein need to attach to each other, but the ISG15 tag prevents this, which is the mechanism behind the tag’s antiviral action. “However, the novel coronavirus also has an enzyme that can remove the tags from its nucleocapsid, recovering its ability to assemble new viruses and thus overcoming the innate immune response,” explains Shoji.

The novel coronavirus shares many traits with the SARS and MERS viruses, which all belong to the same family of viruses – which also have an enzyme that can remove the ISG15 tag. But their versions are less efficient at it than the one in the novel coronavirus, Shoji’s team found. And in fact, it has been reported recently that the previous viruses’ enzymes have a different primary target. “These results suggest that the novel coronavirus is simply better at evading this aspect of the innate immune system’s defence mechanism, which explains why it is so infectious,” says Shoji.

But understanding just why the novel coronavirus is so effective also points the way to developing more effective treatments. The Kobe University researcher explains: “We may be able to develop new antiviral drugs if we can inhibit the function of the viral enzyme that removes the ISG15 tag. Future therapeutic strategies may also include antiviral agents that directly target the nucleocapsid protein, or a combination of these two approaches.”

Source: Kobe University

Categories : COVIDTags :

Persistent Infection could Explain Some Long COVID Cases

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A persistent infection could explain why some people experience long COVID symptoms, according to a new study led by researchers at Brigham and Women’s Hospital. The team found evidence of persistent infection in 43% of participants with cardiopulmonary, musculoskeletal or neurologic symptoms of long COVID. The results are published in Clinical Microbiology and Infection.

“If we can identify a subset of people who have persistent viral symptoms because of a reservoir of virus in the body, we may be able to treat them with antivirals to alleviate their symptoms,” said lead author Zoe Swank, PhD, a postdoctoral research fellow in the Department of Pathology at Brigham and Women’s Hospital.

The study analysed 1569 blood samples collected from 706 people, including 392 participants from the National Institutes of Health-supported Researching COVID to Enhance Recovery (RECOVER) Initiative,  who had previously tested positive for a COVID infection. With a highly sensitive test they developed, researchers looked for whole and partial proteins from the SARS-CoV-2 virus. They also analysed data from the participants’ long COVID symptoms, using electronic medical chart information or surveys that were gathered at the same time as the blood samples were taken.

Compared to people who didn’t report long COVID symptoms, those who reported persisting symptoms many organ systems were approximately twice as likely to have SARS-CoV-2 proteins circulating in their blood. The research team was able to detect the spike protein and other components of the SARS-CoV-2 virus using Simoa, an ultrasensitive test for detecting single molecules. Commonly reported long COVID symptoms included fatigue, brain fog, muscle pain, joint pain, back pain, headache, sleep disturbance, loss of smell or taste, and gastrointestinal symptoms.

Specifically, 43% of those with long COVID symptoms affecting three major systems in the body, including cardiopulmonary, musculoskeletal, and neurologic systems, tested positive for viral proteins within 1 to 14 months of their positive COVID test. But only 21% of those who didn’t report any long COVID symptoms tested positive for the SARS-CoV-2 biomarkers in this same period.

It’s possible that a persistent infection explains some – but not all – of the long COVID sufferers’ symptoms. If this is the case, testing and treatment could aid in identifying patients who may benefit from treatments such as antiviral medications.

A Condition with More Than One Cause

One of the questions raised by the study is why more than half of patients with wide-ranging long COVID symptoms tested negative for persistent viral proteins.

“This finding suggests there is likely more than one cause of long COVID,” said David Walt, PhD, a professor of Pathology at Brigham and Women’s Hospital and Principal Investigator on the study. “For example, another possible cause of long-COVID symptoms could be that the virus harms the immune system, causing immune dysfunction to continue after the virus is cleared.”

To better understand whether an ongoing infection is behind some people’s long COVID symptoms, Swank, Walt and other researchers are currently conducting follow-up studies. They’re analyzing blood samples and symptom data in larger groups of patients, including people of wide age ranges and those with compromised immune symptoms. This way, they can also see if some people are more likely to have persistent virus in the body.

“There is still a lot that we don’t know about how this virus affects people,” said David C. Goff, MD, PhD, a senior scientific program director for the RECOVER Observational Consortium Steering Committee and director of the Division of Cardiovascular Sciences at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “These types of studies are critical to help investigators better understand the mechanisms underlying long COVID – which will help bring us closer to identifying the right targets for treatment.”

Goff added that these results also support ongoing efforts to study antiviral treatments.  

The SARS-CoV-2 blood test developed by Brigham and Women’s researchers is also currently being used in a national study, called RECOVER-VITAL, that is testing whether an antiviral drug helps patients recover from long COVID. The RECOVER-VITAL trial will test the patients’ blood before and after treatment with an antiviral to see if treatment eliminates persistent viral proteins in the blood.

The idea that a virus can stay in the body and cause ongoing symptoms months after an infection isn’t unique to COVID. “Other viruses are associated with similar post-acute syndromes,” said Swank. She noted animal studies have found Ebola and Zika proteins in tissues post-infection, and these viruses have also been associated with post-infection illness.

Source: Brigham and Women’s Hospital

Categories : Cardiovascular Disease COVIDTags :

COVID Infection Linked to MI & Stroke Risk Increases up to 3 Years Later

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Photo: CC0

An analysis of data in the UK Biobank has found that COVID infection may increase the risk of myocardial infarction (MI), stroke and death from any cause for up to three years for people with and without cardiovascular disease, according to new research published in the American Heart Association’s peer-reviewed journal Arteriosclerosis, Thrombosis and Vascular Biology (ATVB).

“We found a long-term cardiovascular health risk associated with COVID, especially among people with more severe COVID cases that required hospitalisation,” said lead study author James Hilser, M.P.H., Ph.D.-candidate at the University of Southern California Keck School of Medicine in Los Angeles. “This increased risk of heart attack and stroke continued three years after COVID infection. Remarkably, in some cases, the increased risk was almost as high as having a known cardiovascular risk factor such as Type 2 diabetes or peripheral artery disease.”

Previous research has shown that COVID increases the risk of serious cardiovascular complications within the first month after infection. This study examined how long the increased risk lasted and whether it subsided after recovering from COVID infection.

Researchers reviewed health and genetic data in the UK Biobank for more than 10 000 adults, including approximately 8000 who had tested positive for SARS-CoV-2 from February 1 to December 31, 2020 and about 2000 who tested positive for the virus in a hospital setting in 2020. A group of more than 200,000 adults who had no history of COVID infection during the same time frame in the UK Biobank were also reviewed for comparison. None of the participants were vaccinated at the time of infection because COVID vaccines were not yet available in 2020.

The analysis found:

  • During the nearly 3-year follow-up period, the risk of heart attack, stroke and death was more than two times higher among adults who had COVID, and nearly four times greater among adults hospitalized with COVID, compared with the group with no history of COVID infection.
  • People hospitalized with COVID, without cardiovascular disease or without Type 2 diabetes, had a 21% greater risk of heart attack, stroke and death compared to people with cardiovascular disease and without COVID infection.
  • There was a significant genetic interaction among the non-O blood types and hospitalisation for COVID. People with severe COVID infections had an increased risk of heart attack and stroke, however, that risk was even higher in people who had non-O blood types (those with blood types A, B or AB).
  • The risk of heart attack and stroke was about 65% higher in adults with non-O blood types compared to those who had type O blood. A preliminary analysis did not show that Rh (positive or negative) blood type interacted with severe COVID, the authors noted.

“Worldwide, over a billion people have already experienced COVID infection. The findings reported are not a small effect in a small subgroup,” said co-senior study author Stanley Hazen, M.D., Ph.D., chair of cardiovascular and metabolic sciences in Cleveland Clinic’s Lerner Research Institute and co-section head of preventive cardiology. “The results included nearly a quarter million people and point to a finding of global health care importance that may translate into an explanation for a rise in cardiovascular disease around the world.” 

Study details, background and design:

  • Health data was from the UK Biobank, a large-scale study of 503,325 adults living in the United Kingdom who were 40 to 69 years of age at enrollment between 2006 and 2010. The in-depth health and biomedical information was collected for participants registered in the UK National Health Service with a UK general practitioner (similar to a primary care physician in the U.S.).
  • This analysis included health data for 10,005 adults who tested positive for the COVID virus or were hospitalized with COVID between February 1, 2020, and December 31, 2020. An additional 217,730 peers enrolled in the UK Biobank who did not have COVID during the same time period were included. In the analysis, all participants were matched as closely as possible for demographics and similar health conditions.
  • Major adverse cardiovascular events (heart attack, stroke and all-cause death) were evaluated for long-term risk, through October 31, 2022, approximately 3 years later.

“This interesting paper is really two studies in one,” said Sandeep R. Das, M.D., M.P.H., MBA, FAHA, co-chair of the American Heart Association’s COVID-19 CVD Registry committee and director for quality and value in the cardiology division for UT Southwestern Medical Center in Dallas. “First, the authors show that having been hospitalized with COVID is a marker of increased cardiovascular risk, on par with having a pre-existing diagnosis of cardiovascular disease. Although proving direct cause and effect is very difficult to tease out in a study that only analyses past data collected for other purposes, this finding is important because it suggests a history of prior COVID hospitalization, even without a history of CVD, should be considered to initiate and possibly accelerate CVD prevention efforts. Whether severe COVID infection has a direct impact on the vascular system is an interesting area for study as well,” Das said.

“The second ‘study’ in this paper looks at the relationship between ABO blood type and COVID outcomes. They show that something located close to the genetic home of ABO blood type is associated with different degrees of susceptibility to COVID. This is really fascinating, and I look forward to seeing scientists tease out what the specific pathway may be.”

The study had several limitations, including that the data was from patients who had the original strain of the COVID virus before vaccines were widely available in 2021. Additionally, the researchers noted that UK Biobank information on medication use was not specific to the beginning of the pandemic in 2020 or the date that patients were infected with SARS-CoV-2. Also, because the majority of participants in the UK Biobank are white, additional research is needed to confirm that these results apply to people with diverse racial and ethnic backgrounds.

“The results of our study highlight the long-term cardiovascular effects of COVID infection. Given the increased risk of heart attack, stroke and death, the question is whether or not severe COVID should be considered as another risk factor for CVD, much like Type 2 diabetes or peripheral artery disease, where treatment focused on CVD prevention may be valuable,” said co-senior study author Hooman Allayee, Ph.D., a professor of population and public health sciences at the University of Southern California Keck School of Medicine in Los Angeles. “The results suggest that people with prior COVID infection may benefit from preventive care for cardiovascular disease.”

Source: American Heart Association

Categories : COVID NeurologyTags :

Higher Doses of Lithium might Relieve Long COVID, Research Suggests

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Photo by Andrea Piacquadio

A small University at Buffalo clinical trial has found that at low doses, lithium aspartate is ineffective in treating the fatigue and brain fog that is often a persistent feature of long COVID; however, a supplemental dose-finding study found some evidence that higher doses may be effective.

Published in JAMA Network Open, the study was led by Thomas J. Guttuso, Jr., MD, professor of neurology in the Jacobs School of Medicine and Biomedical Sciences at UB and a physician with UBMD Neurology.

“It’s a negative study with a positive twist,” Guttuso concludes.

Because long COVID is believed to stem from chronic inflammation and lithium has known anti-inflammatory actions, Guttuso had recommended that a patient of his try low-dose lithium for persistent long COVID symptoms. He was surprised when this patient reported a near full resolution of fatigue and brain fog within a few days of initiating lithium aspartate at 5mg a day.

Relief from symptoms

Based on this single case, Guttuso became interested in lithium aspartate as a potential treatment for long COVID and recommended it to other such patients.

According to Guttuso, 9 of 10 long COVID patients he treated with lithium aspartate 5-15mg a day saw very good benefit in terms of improvements to their fatigue and brain fog symptoms.

“Based on those nine patients, I had high hopes that we would see an effect from this randomized controlled trial,” says Guttuso. “But that’s the nature of research. Sometimes you are unpleasantly surprised.”

The randomised controlled trial showed no benefit from 10-15mg a day of lithium aspartate compared to patients receiving a placebo.

After one patient from the study subsequently increased the lithium aspartate dosage to 40mg a day and experienced a marked reduction in fatigue and brain fog symptoms, Guttuso decided to then conduct a dose-finding study designed to explore if a higher dose of lithium aspartate may be effective.

The three participants who completed the dose-finding study reported greater declines in fatigue and brain fog with the higher dose of 40-45mg per day. This was especially true in the two patients with blood lithium concentrations of 0.18 and 0.49mmol/L compared to one patient with a level of 0.10mmol/L who saw partial improvements.

“This is a very small number of patients, so these findings can only be seen as preliminary,” says Guttuso. “Perhaps achieving higher blood levels of lithium may provide improvements to fatigue and brain fog in long COVID.”

Dosage may be too low

He notes that it is possible the randomized controlled trial was ineffective because the dose of lithium aspartate that was used was too low.

“The take-home message is that very low dose lithium aspartate, 10-15 milligrams a day, is ineffective in treating the fatigue and brain fog of long COVID,” says Guttuso. “Perhaps we need to do another randomised controlled trial that uses higher lithium aspartate dosages that achieve blood lithium levels of 0.18-0.50mmol/L to determine if they could be effective.”

An estimated 17 million people have long COVID in the US, and worldwide the number is estimated at 65 million.

“There currently are no evidence-based therapies for long COVID,” says Guttuso. He hopes that the National Institutes of Health will view lithium as worth studying through a trial with higher dosages; the NIH is allocating an additional $500 million to study long COVID therapies that appear to be promising.

Guttuso adds that if a subsequent randomised controlled trial finds that higher dosages of lithium aspartate are effective, long COVID patients would still need to discuss taking it with their health care providers; in addition, he says, if they do begin taking it at higher dosages, blood lithium levels should be monitored.

Source: University at Buffalo