Researchers uncover mechanism related to severe post-COVID-19 disease in children

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A multidisciplinary team from MassGeneral Hospital for Children (MGHfC), Brigham and Women’s Hospital and other institutions have identified the mechanism of how an extremely rare but serious post-COVID-19 complication develops in children and adolescents. Led by MGHfC pediatric pulmonologist Lael Yonker, MD, researchers determined that viral particles remaining in the gut long after an initial COVID-19 infection can travel into the bloodstream, instigating the condition called Multisystem Inflammatory Syndrome in Children (MIS-C).

The syndrome can occur several weeks after an initial infection; symptoms include high fever, abdominal pain, vomiting, diarrhea, rash and extreme fatigue. The hyperinflammatory response and “cytokine storm” seen in MIS-C can lead to extensive damage in the heart, liver and other organs.

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Direct-acting antiviral to treat COVID-19

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An international team of scientists from the Menzies Health Institute Queensland (MHIQ) at Griffith University and from City of Hope, a research and treatment center for cancer, diabetes and other life-threatening diseases in the U.S., have developed an experimental direct-acting antiviral therapy to treat COVID-19.

Traditional antivirals reduce symptoms and help people recover earlier. Examples include Tamiflu®, zanamivir and remdesivir.

This next-generation antiviral approach used gene-silencing RNA technology called siRNA (small-interfering RNA) to attack the virus’ genome directly, which stops the virus from replicating, as well as lipid nanoparticles designed at Griffith University and City of Hope to deliver the siRNA to the lungs, the critical site of infection.

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COVID-19 vaccination: Thrombosis can be prevented by prompt treatment

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A rare syndrome has been observed in people following vaccination against Covid-19. This involves thrombosis at unusual sites in the body, associated with a low thrombocyte (blood platelet) count and a clotting disorder. In medical jargon, this syndrome is referred to as VITT (vaccine-induced thrombotic thrombocytopenia). Doctors at the Department of Medicine I of MedUni Vienna and Vienna General Hospital (Division of Hematology and Hemastaseology) have now successfully treated an acute instance of this syndrome.

VITT is most probably caused by a defective immune response, whereby thrombocyte-activating antibodies are produced resulting in thrombocytopenia (low platelet count) and thrombosis. The mortality rate in VITT is high (40-50 %) and the syndrome requires immediate and appropriate treatment. However, the current recommendations are only empirical and are based on in-vitro data.

A team of doctors at the Department of Medicine I of MedUni Vienna and Vienna General Hospital, led by coagulation specialist Paul Knöbl, has now successfully treated a patient suffering from vaccine-induced prothrombotic immune thrombocytopenia (VIPIT). The female patient was admitted to the Department with a low platelet count and low fibrinogen levels. Fibrinogen is a protein that plays a major role in blood clotting. Knöbl reports: “Apart from that, her D-dimer values, which indicate thrombosis, were very high and an ELISA assay produced a clear positive result for heparin-PF4 antibodies – all signs of incipient thrombosis.”

The doctors acted quickly, and the patient responded immediately to treatment with a high dose of intravenous immunoglobulin concentrates, cortisone and specific anticoagulants, so that thrombosis was prevented. Immunoglobulin concentrates contain antibodies that can block the misdirected immune response. The usual heparin preparations must not be used to prevent clotting, since they can trigger thrombosis, or aggravate it.

“In this case we were able to describe, for the first time, the efficacy of a potentially life-saving treatment strategy for vaccine-induced thrombosis,” says Knöbl. These new findings have been published in the Journal of Thrombosis and Haemostasis. On the one hand, the findings support the current treatment recommendations, but they also show that prompt diagnosis and immediate initiation of treatment are necessary in order to prevent a life-threatening thrombosis. “This experience could be of great help in treating other patients with similar conditions.”

Why is COVID-19 so hard to treat? Growing evidence points to unique infectious profile

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A comprehensive review into what we know about COVID-19 and the way it functions suggests the virus has a unique infectious profile, which explains why it can be so hard to treat and why some people experience so-called “long-COVID”, struggling with significant health issues months after infection.

There is growing evidence that the virus infects both the upper and lower respiratory tracts – unlike “low pathogenic” human coronavirus sub-species, which typically settle in the upper respiratory tract and cause cold-like symptoms, or “high pathogenic” viruses such as those that cause SARS and ARDS, which typically settle in the lower respiratory tract.

Additionally, more frequent multi-organ impacts, and blood clots, and an unusual immune-inflammatory response not commonly associated with other, similar viruses, mean that COVID-19 has evolved a uniquely challenging set of characteristics.

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Rare neurological condition linked to COVID-19 cases in 21 countries

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As researchers continue to study the neurological impacts of COVID-19, a Houston Methodist international collaboration has documented an unexpectedly frequent occurrence of acute transverse myelitis (ATM) – inflammation of the spinal cord – in 43 COVID-19 patients. Led by Houston Methodist neurologist Dr. Gustavo Roman, the study of existing scientific literature found that patients from 21 countries developed spinal cord lesions after contracting the virus. Symptoms included paralysis and sphincter/bowel dysfunction. The patients ages ranged from 21 to 73 and included about half-and-half women and men. ATM, a rare neurological condition, affects between 1.34 and 4.6 cases per million per year, and researchers believe the unusually high rate in post-COVID-19 patients merits additional investigation. Moreover, 3 ATM cases were reported during the trials of the Oxford AstraZeneca vaccine. The study is published in Frontiers in Immunology. Dr. Roman collaborated with researchers from Hospital Paitilla, Interamerican University of Panama and Hospital Santo Tomas (Drs. Fernando Gracia, Antonio Torres, Alexis Palacios, Karla Gracia and Diogenes Harris).

New AI tool tracks evolution of COVID-19 conspiracy theories on social media

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A new machine-learning program accurately identifies COVID-19-related conspiracy theories on social media and models how they evolved over time–a tool that could someday help public health officials combat misinformation online.

“A lot of machine-learning studies related to misinformation on social media focus on identifying different kinds of conspiracy theories,” said Courtney Shelley, a postdoctoral researcher in the Information Systems and Modeling Group at Los Alamos National Laboratory and co-author of the study that was published last week in the Journal of Medical Internet Research. “Instead, we wanted to create a more cohesive understanding of how misinformation changes as it spreads. Because people tend to believe the first message they encounter, public health officials could someday monitor which conspiracy theories are gaining traction on social media and craft factual public information campaigns to preempt widespread acceptance of falsehoods.”

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Evolution of outcomes for patients hospitalized during the COVID pandemic

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As SARS-CoV-2 continues to spread in France, a thorough characterization of hospital care needs and of the trajectories of hospital patients, as well as how they have changed over time, is essential to support planning. This led scientists from the Mathematical Modeling of Infectious Diseases Unit at the Institut Pasteur and the University of Cambridge to develop a probabilistic model that can be used to analyze detailed patient trajectories based on 198,846 hospitalizations in France during the first nine months of the pandemic (from March to No-vember 2020). These findings were published in The Lancet Regional Health Europe on March 20, 2021.

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B.1.1.7 variant of COVID-19 spreading rapidly in United States

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The faster-spreading B.1.1.7 variant of SARS-CoV-2 first detected in the United Kingdom, the coronavirus that causes COVID-19, is quickly on its way to becoming the dominant variant of the virus in the United States, according to a study from scientists at Scripps Research and the COVID-19 test maker Helix.

The findings, which appear today in Cell, suggest that future COVID-19 case numbers and mortality rates in the United States will be higher than would have been otherwise. The analysis suggests that the variant, which has been detectable in an increasing proportion of SARS-CoV-2 samples, is 40-50 percent more transmissible than SARS-CoV-2 lineages that were previously dominant. Other studies have found evidence that the B.1.1.7 variant may be about 50 percent more likely to cause fatal COVID-19.

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Evidence for reduced antibody protection against SARS-CoV-2 variants

Testing and vaccination – these are the pillars on which humanity is trying to get a grip on the Coronavirus pandemic. Although it is taking longer than many had expected, it is believed that it is only a matter of time before we are all vaccinated and thus protected. However, time is also working for the virus, which has now mutated several times, with variants B.1.1.7 from the United Kingdom, B.1.351 from South Africa and P.1 from Brazil spreading rapidly. These viruses have mutations in the so-called spike protein, the structure on the surface of the virus that is responsible for attachment to host cells. At the same time, the spike protein is also the major target of the immune response. Antibodies generated in response to SARS-CoV-2 infection or vaccination bind to the spike protein, thereby blocking the virus. A team led by Markus Hoffmann and Stefan Pöhlmann of the German Primate Center – Leibniz Institute for Primate Research and Jan Münch of the Ulm University Medical Centre has found that the SARS-CoV-2 variants B.1.351 and P.1 are no longer inhibited by an antibody used for COVID-19 therapy. In addition, these variants are less efficiently inhibited by antibodies from recovered patients and vaccinated individuals. Thus, convalescence from COVID-19 as well as vaccination may offer only incomplete protection against these mutant viruses (Cell).

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Investigational AstraZeneca vaccine prevents COVID-19

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Results from a large clinical trial in the United States and South America indicate that AstraZeneca’s COVID-19 vaccine, AZD1222, is well-tolerated and protects against symptomatic COVID-19 disease, including severe disease or hospitalization. The independent Data and Safety Monitoring Board (DSMB) overseeing the trial identified no safety concerns related to the vaccine. The United Kingdom-based global biopharmaceutical company AstraZeneca developed the vaccine and led the trial as regulatory sponsor.

The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and the Biomedical Advanced Research and Development Authority (BARDA), part of the U.S. Department of Health and Human Services’ Office of the Assistant Secretary for Preparedness and Response, provided funding support for the trial through the federal COVID-19 response.

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