Category: Covid-19

LONDON, Nov 1 (Reuters) - The UK government has scrapped guarantees on nearly 1 billion pounds ($1.2 billion) of bank loans handed out to ailing businesses during the COVID-19 pandemic, leaving lenders on the hook for some of the borrowings that will not be repaid.

Previously unreported figures obtained by Reuters under a Freedom of Information (FOI) request show that the state-owned British Business Bank (BBB) - which administers the loan schemes - has removed state guarantees from 10,786 loans worth a combined 979 million pounds as of Oct. 11, shielding taxpayers from some losses.

While the amount is only a fraction so far of the 77 billion pounds of loans issued, the move follows pressure from lawmakers and Britain's public spending watchdog who criticised the programmes for being too lax. The figures could rise further - latest figures show just 17 billion pounds have been fully repaid by borrowers as of June 30.

Dozens of lenders took part in the government-backed schemes, including Britain's "Big Four" banks: Barclays (BARC.L), NatWest (NWG.L), Lloyds (LLOY.L) and HSBC (HSBA.L). Barclays and HSBC declined to comment, while the other two were not immediately available.

Britain's emergency lending schemes echoed government finance initiatives deployed worldwide to prop up companies during lengthy lockdowns, but the full costs and who will ultimately foot the various bills is only now becoming clearer.

Public officials have ratcheted up their scrutiny of the schemes to try to ensure better value for money, three sources familiar with the matter told Reuters, just as ministers review strained state finances ahead of a key budget update later this month.

"In unprecedented times, we stepped up to support the country," a spokesperson for the UK's business department said of the loan schemes, adding that where necessary it was working with lenders to remove guarantees to protect taxpayer money.

Bank lobby group UK Finance said lenders were in regular discussions with the BBB, with some removing loans from the guarantee at their own discretion.

Lenders who answered government calls to keep credit flowing to Britain's shell-shocked economy from 2020 did so via three main schemes. The largest and most controversial, the "Bounce Back Loan" (BBL) scheme, delivered 47 billion pounds and was specially designed to help Britain's smallest firms stay afloat.

Participants were requested to streamline their typical credit checks in order to lend up to 50,000 pounds within hours of an application. Under BBL terms, the government assumed 100% of the credit risk.

However, some lenders are finding they cannot claim on that guarantee, the FOI response shows. Following the removal, any financial loss is borne in full by the lender, BBB said.

The guarantees have been removed for a variety of reasons, the BBB said, including due to data corrections, application errors resulting in "duplicate" funds being sent to companies, as well as infringements of scheme rules.

Potential infringements could include evidence of poor treatment of borrowers, one of the sources said. The BBB has the power to offset a proportion of a lender's future claims for repeat infringements, but had not yet done so, the source added.

Mistakes had been identified voluntarily by the lenders themselves, or following discussions with the BBB, according to the FOI response.

All the lenders that participated in the emergency loan schemes have been subject to at least one audit, the BBB said.

Reuters requested a breakdown of state guarantee removals by lender, but this was rejected by the BBB on the grounds this could be "prejudicial to their commercial interests." Lender views were canvassed on potential disclosure and they agreed on this, the BBB said.

The lending schemes have been mired in controversy, as evidence mounts of widespread fraud. A junior government minister, Theodore Agnew, resigned last year in protest, saying efforts to stop fraudulent abuse were "woeful."

The latest overall scheme data, published in September, showed the value of suspected fraud across all the schemes had hit 1.7 billion pounds as of June 30, up 43% on the previous estimate in March.

The figures also showed the government had paid out 7.4 billion pounds to lenders under the state guarantees.

"Lenders are doing all they can to ensure loans are repaid as well as taking action to tackle fraud," a UK Finance spokesperson said.

Suspected fraud is not necessarily a reason for removing a guarantee, provided the lender is otherwise compliant with scheme rules, another source said.

A second source, who assisted in the design of the scheme and declined to be named, said it should not come as a surprise that loans that banks would ordinarily not consider were hitting problems, adding that lenders voiced reservations at the time.

The BBB had also raised concerns prior to the launch of the BBL scheme. In a letter to the government in May 2020, the BBB warned the scheme was "vulnerable to abuse by individuals and by participants in organized crime."

In a response that month, the government said it had assessed the risks but decided to proceed with its launch, citing "the unprecedented situation facing the country."

($1 = 0.8235 pound)

Reporting by Sinead Cruise and Iain Withers in London Editing by Matthew Lewis

Our Standards: The Thomson Reuters Trust Principles.

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Exclusive: UK rips up state guarantees on nearly 1 billion pounds of COVID loans - Reuters UK

The lungs were once at the forefront of SARS-Cov-2 research, but as reports of organ failure and other serious complications poured in, scientists set out to discover how and why the respiratory virus was causing serious damage to the body's major organs, including the lungs.

An interdisciplinary COVID-19 International Research Team (COV-IRT), which includes UNC School of Medicine's Jonathan C. Schisler, PhD, found that SARS-CoV-2 alters mitochondria on a genetic level, leading to widespread "energy outages" throughout the body and its major organs. Their findings, published in Science Translational Medicine, explain how these effects contribute to long COVID symptoms and point to new therapeutic targets.

We found that at peak infection time, there are distinct changes in different regions of the brain, including is a large decrease in mitochondrial genes in the cerebellum, the part of the brain that controls our muscles, balance, cognition, and emotion. The lung is the primary site of infection, but molecular signals are being transmitted affecting the entire body, with the heart, kidney, and liver being more affected than others, even long after the virus is gone."

Jonathan C. Schisler, PhD, assistant professor of pharmacology and member of the UNC McAllister Heart Institute

Every cell in our bodies is equipped with biological power stations known as mitochondria, which are especially important for maintaining the function of energy-demanding organs, such as the heart, brain, and lungs. Mitochondria require genes from their own genome (mitochondrial DNA) and nuclear DNA (nDNA) to create energy. Together, they instruct the mitochondria to convert oxygen molecules into cellular energy called adenosine triphosphate (ATP).

Using nasal swabs and autopsy tissues from affected patients and animal models, researchers found that the virus blocks specific genes that use oxygen to create ATP, forcing the body to deplete finite energy reserves in the body. Without an energy source, cells throughout the body begin to starve, with the cells powering the brain and the heart suffering the most.

To keep the body functioning, cardiac and neural cells can resort to consuming their cellular parts, including their mitochondria. Eventually, the cells are deprived of their vital elements and initiate a form of programmed cell death called necroptosis. Unlike other forms of cellular death, necroptosis causes a cascade of ill effects, including a robust inflammatory response, which releases pro-inflammatory cells called cytokines throughout the body as the cells rupture. Uncontrolled necroptosis further enhances sepsis and organ failure.

Schisler says the ensuing cell death and inflammation may explain why patients with long COVID are likely to have persisting cardiovascular, cognitive, and inflammatory side effects after the initial infection has run its course.

"If we can start to appreciate and understand how each organ system adapts in the long-term to viral infection, and if we can discover the biology behind why people respond differently to SARS-CoV-2, we will be better positioned to combat chronic, long COVID symptoms that might be affecting cells in the heart, or the immune cells, or the neurons in our brain," said Schisler.

Drawing on past research, the scientists know that a specific microRNA, a small piece of RNA that circulates throughout the body, increases in number during severe respiratory infections. This particular microRNA, which can affect mitochondrial gene expression in numerous cells and tissues, could be a new therapeutic target against SARS-CoV-2.

The new findings also highlight new ways to address the mitochondrial dysfunction that occurs during COVID infection. Diet, exercise, natural compounds, or a combination of the three, may be able to stimulate mitochondrial function, but whether or not they are effective for patients with long COVID is yet to be known. Moving forward, the research team will explore how long mitochondrial dysfunction lasts in the body, especially in cases of long-COVID, and how mitochondrial function can be restored.

Source:

Journal reference:

Guarnieri, J. W., et al. (2023) Core mitochondrial genes are down-regulated during SARS-CoV-2 infection of rodent and human hosts. Science Translational Medicine. doi.org/10.1126/scitranslmed.abq1533.

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Study reveals how SARS-CoV-2 alters mitochondria, leading to energy outages and organ failure - News-Medical.Net

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More than 50% of long-COVID patients failed to improve 1.5 years after their initial diagnosis, according to a new study based on cases seen at a Danish post-COVID clinic, both before and after the Omicron variant period. The study was published yesterday in the International Journal of Infectious Diseases.

The analysis included 806 patients who were infected with the wild-type strain, Alpha, Delta, or Omicron strain. All case-patients had been referred to a long COVID clinic with symptoms persisting at least 12 weeks from onset of COVID-19. Seventy percent of participants were female, with a median age of 48.

Patients were given a post-COVID symptom questionnaire (PCQ), and standard health scores, four times between enrollment and 18 months of follow-up. The first clinic visit for long COVID occurred an average of 7 months after acute infection. Patients were grouped according to the period of transmission of predominant SARS-CoV-2 variants, with 69% of patients infected during the wild-type period and 9%, 7%, and 15% infected in the Alpha, Delta, and Omicron periods, respectively.

The authors found that patients infected in the Delta period had significantly more severe long COVID initially, with a mean PCQ score of 43, compared with 38 for patients infected in the wild-type period.

Patients infected in the Omicron period did not differ in PCQ score (median 40) compared to wild-type patients (median 38) or to pre-Omicron patients (median 38). However, patients infected with Omicron had a lower health-related quality of life compared to patients infected with wild-type strain.

At 1.5 year after infection, patients had no clinically meaningful decline in severity of long COVID.

"At 1.5 year after infection, patients had no clinically meaningful decline in severity of long COVID, and 57% (245/429) of patients failed to improve 1.5 years after infection, with no differences between variants," the authors wrote.

Overall, PCQ scores fell 7 to 10 months post-infection, then plateaued between 10 and 18 months, Overall median PCQ score declined from 38 at 7 months to 33 at 18-month follow-up.

"In some patients, long COVID may last for more than 2 years after infection, which is supported by our data," the authors concluded.

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Study: Regardless of variant, half of long-COVID patients fail to improve after 18 months - University of Minnesota Twin Cities

Superspreading is known to have played an important role in the transmission dynamics of SARS-CoV-2. In this Comment, the authors discuss how knowledge of the extent and cause of superspreading is important for designing appropriate control measures for emerging infectious diseases.

As SARS-CoV-2 swept the globe, two major features of its transmission became apparent: its tendency towards superspreading and its airborne nature. In fact, the superspreading tendency was established early on, even before COVID-19 was declared a pandemic in March 20201. The dispersion parameter k, which quantifies the degree of heterogeneity in transmission2, was determined to be in the range of 0.10.2, indicating that a minority (1020%) of SARS-CoV-2 infected individuals accounted for the majority (80%) of new infections3. The numerous well-documented superspreading events where single individuals infected dozens of others without close contact should have been a red flag, strongly suggesting spread by aerosols. The realization that COVID-19 transmission was characterized by airborne transmission was only acknowledged by WHO and the CDC much later, in mid-to-late 2021.

Influenza, the main culprit during the last 150 years of respiratory pandemics, does not exhibit a strong superspreading potential and, while data is scarce, values of k close to or exceeding 1 have generally been reported4,5. For coronaviruses, the superspreading characteristic was already noted during the 2003 SARS outbreak where the need for a theoretical understanding of its implications for outbreak control was noted6. The spread of SARS involved several nosocomial superspreading events as well as an iconic outbreak in a private apartment complex in Hong Kong attributed to spread via aerosols suspended in the buildings plumbing7. However, a thorough theoretical understanding of how superspreading impacts mitigation did not arise and interest seemingly faded after the outbreak was contained later that year. MERS, a looming threat since 2012, was also characterized by superspreading, with notable nosocomial superspreading events in South Korea in 2015; again, few theoretical insights were gained about the phenomenon. In the early months of the COVID-19 pandemic, epidemiological evidence of superspreading began piling up once again, reaffirming the need for a theoretical understanding of its mechanisms and implications for outbreak control.

Our recent theoretical studies have shown that superspreading plays a profound role in determining the most effective strategies to curb a disease outbreak. At the same average transmissibility (same R0), an outbreak of a more superspreading disease can be more readily controlled8, as illustrated in Fig.1. Specifically, we found that mitigation strategies that reduce contacts in public spaces are vastly more effective when superspreading is a key driver of high average transmissibility (R0). Consequently, the closing of venues such as concert halls and bars can significantly curb the spread of a superspreading respiratory pathogen, while the same measures may do little to halt a non-superspreading pathogen with the same basic reproductive number. The origin of this effect lies in the statistics of superspreading, which somewhat counterintuitively imply that most infected individuals do not become very infectious. Thus, mitigation of a superspreading disease relies on either a) directly targeting interventions at superspreaders or b) limiting the number of contacts that the typical infected individual has. The former strategy depends on being able to a priori identify the superspreaderoften practically impossiblewhile the latter does not. Model simulations confirm this logic, showing that effective mitigation of a superspreading disease can be achieved by moderate interventions, such as the closure of large events. No such effect was seen for this scenario with an otherwise comparable disease with homogeneous transmission. Thus, it appears that superspreading is an Achilles heel for a pathogen like SARS-CoV-2. The transmission statistics of superspreading can be leveraged to drastically improve the effectiveness of contact tracing programmes as well9.

Superspreading diseases exhibit a skewed distribution of infectiousness, where most infected individuals transmit to very few or none at all, while a minority spread the disease to large numbers of people (left panel). In this case, limiting gatherings and situations where many people meet (even briefly) has an outsized mitigating effect, as shown by the epidemic curves at the bottom of the left panel, which result from agent-based simulations of a superspreading disease. In diseases where transmission is more evenly distributed (non-superspreading, right panel), such interventions do not hold the same potential for outbreak control. Data from Sneppen et al.8. ProPublicas Wee People font used for human silhouettes.

Crucially, the interactions between superspreading and mitigation strategies are not readily captured by typical compartmental transmission models, necessitating the use of e.g. agent based models. The limitations of traditional compartment models and some network models have also fueled the misconception that the impact of superspreading is largely confined to the early stages of an epidemic. One viewpoint is that superspreading events merely serve as stochastic sparks that ignite the initial outbreak, but whose influence is quickly drowned out as the incidence increases. This has been shown not to be the case when imperfect social mixing is taken into account, it becomes clear that superspreading has a significant impact throughout an epidemic8,10.

Adding another layer of complexity is the commonly held belief that superspreaders fuel the rapid initial growth of an outbreak but are subsequently depleted, leading to a decline in the growth rate. This belief often rests on the assumption that superspreading is a function of hypersocial individuals who both spread and contract the infection at higher rates11. While this pattern describes some instances of superspreading well, such as the recent mpox outbreak12 and some sexually transmitted infections (related to the concept of Core Groups13), it does not apply universally. Particularly for diseases where superspreading has a biological basis rendering some individuals inherently more infectious the picture changes. In this case, superspreaders are not necessarily super-receivers, and their influence may persist throughout the outbreak10. In other words, the impact of superspreading depends strongly on the degree of correlation between susceptibility and infectiousness. Therefore, it is critical to distinguish between superspreading as a consequence of social behavior/contact rate heterogeneity, and superspreading rooted in biological factors, all of which may affect susceptibility as well as infectiousness.

At present, the exact etiology of the superspreading phenomenon remains incompletely understood. The fact that some respiratory pathogens are highly superspreading, while others are not, likely depends on several behavioral as well biological factors, including aerosolized spread, the degree of pre- and asymptomatic transmission, the minimal infective dose, as well as person-to-person variability in respiratory viral load and aerosolization5,14. Infections that have a high degree of pre- and asymptomatic transmission, and those with a low minimum infective dose, are likely to have a greater superspreading potential; asymptomatic transmission increases the risk of (unknowingly) infectious individuals participating in public life, while a low minimum infective dose increases the range of transmission and decreases the necessary exposure time. High person-to-person variability in respiratory viral load is another factor that may contribute significantly to superspreading. In infections such as COVID-19, where viral loads vary enormously from person to person, a pronounced degree of superspreading is observed, pointing to superspreading as an intrinsic feature of the pathogen and its interaction with the human host5,15. Understanding these factors is crucial in developing effective mitigation and containment strategies for future pandemics. Thus, there is a need for research into the mechanisms behind superspreading, and potentially to differentiate between different types of heterogeneous spread.

Even in the absence of a clear etiology, our research shows that knowledge of the bare transmission statistics is a powerful thing which can enable the design of improved control strategies. In general, this highlights the importance of getting the intricacies of transmission right when the next pandemic threat emerges. COVID-19 has shown that the dispersion factor k can be rapidly ascertained for an emerging pathogen. This suggests that k should join the basic reproductive number (R0), the generation time and the infection and case fatality ratios (IFR and CFR) as critical parameters needed for initial response to an emerging pandemic. Crucially, knowing k can not only aid the design of interventions but may also provide early indications of airborne transmission potential. However, this rapid quantification of superspreading depends on the timely availability of high-quality data, including detailed low-bias spatiotemporal incidence data and representative viral sequencing, highlighting the importance of rapidly scalable epidemiological and genomic surveillance.

With pandemic preparedness historically geared towards influenza A, we had not anticipated a superspreading disease like COVID-19, nor were the implications for control understood. Coronaviruses, however, have repeatedly emerged as significant pandemic threats over the last two decades, each one exhibiting considerable superspreading potential. As we move forward, it is crucial that mathematical models of Disease X scenarios take this phenomenon into account.

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The counterintuitive implications of superspreading diseases - Nature.com

LONDON (AP) The former top aide to ex-British Prime Minister Boris Johnson on Tuesday painted a picture of widespread chaos and dysfunction in the U.K. government during the coronavirus pandemic.

In keenly awaited testimony to the countrys public inquiry into the COVID-19 pandemic, Dominic Cummings was withering about many of the people dealing with the situation, including his former boss, describing a culture of toxic relations and lack of trust but denied that he had broken any rules.

I would say, overall, its widespread failure, but pockets of excellent people and pockets of excellent teams doing excellent work within an overall dysfunctional system, said Cummings, a self-styled political disruptor.

In emails and WhatsApp messages that were handed to the inquiry and read out by the lead counsel, Cummings also slammed many in Johnsons Cabinet and other top officials in expletive-ridden terms.

While apologizing repeatedly for his deplorable language that was aired live across British media, Cummings denied he was a misogynist and said the exchanges took place in the midst of the underlying insanity that was in place at Johnsons Downing Street offices.

My appalling language has always been my own but my judgment of a lot of senior people was widespread, said Cummings, who was the prime ministers chief adviser during the first months of the pandemic in 2020 and at the heart of the U.K.'s response.

Cummings also said Johnson, who was hospitalized for several days with the virus in April 2020, lacked focus and discipline, constantly changing his mind during the pandemic which made it difficult to set policy.

Pretty much everyone called him the trolley, he said, using the British term for a shopping cart.

Cummings was hired by Johnson after helping to mastermind the victorious leave campaign in Britains 2016 European Union membership referendum. He went to work in Downing Street when Johnson became prime minister in 2019, filling a loosely defined but powerful role that saw him dubbed Boris brain.

At one point in May 2020, Cummings became the focal point of the pandemic when it emerged that he had driven 250 miles (400 km) across England to his parents house while the country was under a stay-at-home order and while he was ill with coronavirus. Cummings made a later journey to a scenic town 30 miles (50 km) away.

At the time Johnson resisted calls to fire him, but Cummings left his job in November 2020 and has fired broadsides at Johnson ever since. He conceded to the inquiry that he left government with someone unfit for office at its helm.

During his testimony, he also took a swipe at many of the formal structures of government during the pandemic and how a lack a planning hobbled the immediate response to the virus after it first emerged in China in late 2019.

The Cabinet Office, which coordinates policy around departments, bore the brunt of Cummings scorn. Describing it as a dumpster fire, he accused it of trying to block a shielding plan for the vulnerable in the days and weeks before Johnson eventually announced a national lockdown on March 23, 2020.

Cummings follows other aides who have painted a picture of Johnson as a leader who was distracted and indecisive during the countrys biggest peacetime crisis.

Also on Tuesday, former top communications director Lee Cain, said Johnsons erratic decision-making was rather exhausting and indicated that the pandemic did not suit his temperament.

Cain said COVID was the wrong crisis for this prime ministers skillset and that Johnson, in the early days of the pandemic, often referred to the mayor in the 1975 Stephen Spielberg movie Jaws, who wanted to keep the beaches open despite mounting evidence of a deadly shark in its waters.

Cain also said that Johnson considered allowing the pandemic to let rip through the elderly population in order to protect the economy and allow younger people to live their lives, but that he eventually took the moral and responsible action of imposing lockdowns, though admittedly later than they should have been.

The U.K. has one of the highest COVID-19 death tolls in Europe, with the virus recorded as a cause of death for around 230,000 people.

Johnson, who was forced to step down as prime minister in September 2022 following revelations of rule-breaking parties at his Downing Street residence during the pandemic, is due to address the inquiry before Christmas. Current Prime Minister Rishi Sunak is also expected to give evidence this year as he was Johnsons Treasury chief during the pandemic.

The inquiry is divided into four so-called modules, with the current phase focusing on political decision-making around major developments, such as the timing of lockdowns. The first stage, which concluded in July, looked at the countrys preparedness for the pandemic.

Overall, the probe, which is being led by retired judge Heather Hallett, is expected to take three years to complete, though it will be publishing interim reports in the meantime in the hope of bolstering Britains response in the event of another pandemic.

Johnson agreed in late 2021 to hold a public inquiry after heavy pressure from bereaved families, who have hit out at the evidence emerging about his actions.

The nastiness, arrogance and misogyny at the heart of government during the pandemic is core to the awful decision-making that led to thousands of unnecessary deaths and tore families like mine apart, said Susie Flintham, spokesperson for COVID-19 Bereaved Families for Justice U.K.

When you see that these figures had such a shocking disregard for each other, you can only imagine the disregard they had for families like mine, she added.

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Boris Johnson's former top aide is withering about UK government during COVID-19 pandemic inquiry - The Associated Press

New research has identified 38 direct-to-consumer businesses marketing stem-cell treatments and exosome therapies for COVID-19 infections and, especially, long COVID, despite lacking approval by US Food and Drug Administration and other regulatory body in the United States. Descriptions of the businesses and an analysis of their marketing strategies are published in Stem Cell Reports.

The 38 businesses operated or facilitated access to 60 clinics, almost all in the United States and Mexico, the authors said. The businesses were identified via web-based searches including "stem cell COVID treatments," "stem cell clinic treating COVID-19," and "exosome therapy for COVID-19."

Once businesses were identified, the researchers, from the University of California, Irvine, tracked how many clinics the companies operated, and they searched social media sites and platforms for the businesses.

Twenty-four of the 60 clinics (40%) listed on websites of theidentified businesses were in theUnited States, 22 (37%) were in Mexico, four (7%) were in Ukraine, and two (3%) were in the Cayman Islands. Guatemala, Malaysia, Panama, Philippines, Poland, Spain, Thailand, and the United Arab Emirates had one clinic each (around 2% per country).

Thirty-six of the 38 marketed their stem cell and exosome products as treatments for long COVID, six advertised them as "immune boosters," five claimed to treat patients in the acute infection phase, and two claimed their products were preventive.

Twenty businesses (53%) sold umbilical cord blood or umbilical cord tissuederived mesenchymal stem cells, and 16 (42%) marketed exosomes. Methods for treatment delivery varied, with 58% reportedly using intravenous infusions, and 21% claimed they nebulized their product. Eleven businesses (29%) did not specify how they administered their products, the authors said.

Only nine of the businesses clearly advertised how much services cost, with the lowest treatment available at $2,950. The most expensive was $25,000, and the average listed cost for patients was $11,322.

Almost all online and social media advertising was aimed toward relieving symptoms of long COVID, including brain fog and fatigue.

The patients being targeted by such marketing claims are particularly vulnerable.

"The patients being targeted by such marketing claims are particularly vulnerable, " said Leigh Turner, PhD, lead author and a bioethics professor in the University of California, Irvine Department of Health, Society, and Behavior in a press release from Cell Press, the journal's publisher.

"They're suffering, and in some cases, they've been suffering for a long time, making them highly susceptible to misleading marketing representations and persuasive marketing pitches.

In a conclusion on the study, the authors wrote that, until evidence of efficacy is studied and approved by regulatory bodies, vulnerable patients will be exploited by online businesses.

"Further clinical research should provide insight into whether specific stem cell-based interventions or exosome products are backed by sufficient evidence of safety and efficacy related to treating or preventing COVID-19 to warrant premarketing approval or emergency use authorization by national regulators," the authors wrote. "Absent such evidence, patients are vulnerable to being exploited by businesses using direct-to-consumer online advertising to make persuasive but unjustified claims about treating or preventing COVID-19."

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Unapproved stem-cell therapies marketed to people with long COVID - University of Minnesota Twin Cities

TOPLINE:

Severe mental illness (SMI) has been linked to a 50% increased risk for all-cause mortality risk after COVID-19, a large population-based study suggests.

Investigators analyzed data from the Clinical Practice Research Datalink database, which contains health information on 13.5 million patients receiving care from family practices in England and Northern Ireland.

The study included participants with SMI, including schizophrenia, schizoaffective disorder, and bipolar disorder.

Participants were aged 5 years or older with a SARS-CoV-2 infection recorded between February 1, 2020, and March 31, 2021, spanning two waves of the pandemic.

Death rates among participants with SMI and COVID-19 (n = 7150; 56% female) were compared with those in a control group of participants without SMI who had been diagnosed with COVID-19 (n = 650,000; 55% female).

Participants with SMI and COVID-19 had a 53% higher risk for death than those in the non-SMI control group (adjusted hazard ratio [aHR], 1.53; 95% CI, 1.39-1.68).

Black Caribbean/Black African participants were more likely than White people to die of COVID-19 (aHR, 1.22; 95% CI, 1.12-1.34), although ethnicity was not recorded in 30% of participants.

After SARS-CoV-2 infection, for every additional multimorbid condition, the aHR for death increased by 6% in the SMI group and 16% in the non-SMI group (P = .001). Some of these conditions included hypertension, heart disease, diabetes, kidney disease, depression, and anxiety.

"From a public health perspective, our study has emphasised the need for early and timely preventative interventions (e.g. vaccination) for the SMI population. Future studies are needed to disentangle the complex biological and psychosocial factors, and healthcare pathways, that have led to the greater mortality rates in the SMI population," the authors write.

Jayati Das-Munshi, MD, of Kings College London, led the study, which was published online October 25 in the British Journal of Psychiatry. The study was funded by the Health Foundation.

COVID-19 may have been underdiagnosed or underreported in the records studied. Also, investigators did not have information about cause of death.

As reported in the original article, one author received funding from Janssen, GSK and Takeda. All other authors declared no conflicts of interest.

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Cite this: Serious Mental Illness Tied to 50% Higher All-Cause Mortality Risk After COVID-Medscape-Nov01,2023.

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SMI Linked to Higher All-Cause Mortality Risk After COVID - Medscape

[1/3]A woman receives a booster dose of Pfizer-BioNTech vaccine against the coronavirus disease (COVID-19) in Bangkok, Thailand, January 5, 2023. REUTERS/Athit Perawongmetha/File Photo Acquire Licensing Rights

Oct 26 (Reuters) - Pfizer (PFE.N) and German partner BioNTech said on Thursday that their vaccine to prevent flu and COVID-19 generated a strong immune response against strains of the viruses in an early- to mid-stage trial.

The companies said they plan to start a late-stage trial in the coming months.

"This vaccine has the potential to lessen the impact of two respiratory diseases with a single injection and may simplify immunization practices," Annaliesa Anderson, Pfizer's head of vaccine research and development, said in a statement.

In the trial, the vaccine candidates were compared to a licensed influenza vaccine and the companies' updated COVID-19 vaccine given at the same visit.

The data from the trial showed that the flu-COVID vaccine demonstrated robust immune responses to influenza A, influenza B and SARS-CoV-2 strains, the companies said.

(This story has been refiled to fix syntax in the headline)

Reporting by Manas Mishra in Bengaluru; Editing by Savio D'Souza

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Pfizer, BioNtech say flu-COVID shot generates strong immune response in trial - Reuters

According to a new study led by Weill Cornell Medicine and New York-Presbyterian, specific gut-dwelling fungi thrive in severe cases of COVID-19, exacerbating the disease's extreme inflammation while also causing long-term immune system changes.

This research indicates a subset of individuals who could benefit from specialised, yet-to-be-determined treatments.

ALSO READ: Specific gut bacteria raise risk of severe malaria: Research

Using patient samples and preclinical models, the researchers discovered that the proliferation of fungus in the intestine, particularly Candida albicans yeast strains, causes an increase in immune cells whose actions can exacerbate lung injury.Their findings, published in Nature Immunology on Oct 23, also elucidate that patients retain a heightened immune response and immune memory against these fungi for up to a year after the resolution of SARS-CoV-2 infection.

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The research reveals a new dimension of the complex pathology unleashed by severe COVID-19, according to senior author Dr Iliyan Iliev, an associate professor of immunology in medicine in the Department of Medicine, co-director of the Microbiome Core Lab and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine.

"Severe and long COVID-19 were not thought to involve fungal blooms in the intestines that, in addition to the virus, can impact patient's immunity," he said.

Dr Iliev, an immunologist who studies the microbiome and the chronic inflammatory conditions targeting the gastrointestinal tract, pivoted to COVID-19 during the pandemic. As researchers gained a better handle on the new viral infections, it became clear that in COVID-19 as in inflammatory bowel disease, the body's own inflammatory immune response causes harm.

To investigate this errant immune response, Dr Iliev and Dr Takato Kusakabe, a postdoctoral fellow and the first author in the study, worked with numerous colleagues to acquire three large clinical cohorts of COVID-19 patients and develop a mouse model to study the disease.They collaborated with members of the Weill Department of Medicine and the Department of Pathology and Laboratory Medicine at Weill Cornell Medicine, including Dr Stephen Josefowitz, Dr Mirella Salvatore, Dr Melissa Cushing, Dr Lars Westblade, and Dr Adolfo Garcia-Sastre, a professor of microbiology and director of the Global Health and Emerging Pathogens Institute of the Icahn School of Medicine at Mount Sinai.

The team first made the connection when analysis of blood samples from patients at New York-Presbyterian/Weill Cornell Medical Center diagnosed with severe COVID-19 unveiled the presence of antibodies tuned to attack fungi common to the gut.The researchers then found that populations of yeast, and one species in particular, Candida albicans, increased in the intestines of the patients during the course of severe COVID-19.

When they looked at the patient's immune systems, the researchers found a parallel increase in immune cells called neutrophils. In severe COVID-19, excessive numbers of neutrophils appear in the lungs, where their activity worsens the inflammatory response already damaging these organs.

Turning to preclinical models, the investigators found that mice bearing fungi from patients with severe COVID-19 produced more neutrophils in their blood and lungs, and had signs of heightened inflammation when infected with SARS-CoV-2. However, giving them an antifungal drug reduced these effects.

From within patients' blood samples, researchers also uncovered evidence of persistent changes to the immune system they believe are related to a condition known as long COVID-19, in which symptoms linger, or new ones develop after an infection has cleared.When the team examined patients' blood up to a year afterwards, they found it still contained anti-fungal antibodies. In addition, when they looked at the stem cells that give rise to neutrophils, the researchers found that these progenitors are primed to respond to fungi.They found that an immune protein called IL-6 that these fungi induce, appears to bolster both the neutrophils and the antibodies.

Original post:

Gut fungus has long-term impact on the immunological response to severe COVID-19 - Hindustan Times

WASHINGTON The University of Maryland (UMD) reversed its coercive COVID-19 directive after Select Subcommittee on the Coronavirus Pandemic Chairman Brad Wenstrup (R-Ohio) and all Majority Members opened an investigation into the Universitys policy earlier this month. Under the previous directive, COVID-19 positive students were forced to immediately leave campus and isolate presumably at their own expense at a nearby hotel or by boarding a flight home. Effective November 1, University of Maryland students who test positive for COVID-19 will be allowed to isolate in-place within their residence halls.

Chairman Wenstrup released the following statement on the Universitys policy reversal:

Reinstituting an outdated COVID-19 policy that threatened the well-being of Maryland students was not only counterproductive, but also unscientific. The Select Subcommittee wrote to UMD President Pines to highlight the negative impact of similar, pandemic-era education policies on Americas youth and encourage the University to reconsider its destructive directive. Thankfully the University, within days of receiving the Select Subcommittees letter, changed its quarantine policy to follow science, data, and common sense. The Majority members of the Select Subcommittee appreciate UMDs prompt response to our letter and will continue to investigate any potentially harmful COVID-19 policies reemerging at universities across the country.

Read the University of Marylands response letter here.

Read the Select Subcommittees October 13, 2023 letter to the University of Maryland here.

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Wenstrup Releases Statement After University of Maryland ... - House Committee on Oversight and Reform |