One shot of the Sputnik V vaccine triggers strong antibody responses

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A single dose of the Sputnik V vaccine may elicit significant antibody responses against SARS-CoV-2, finds a study published July 13 in the journal Cell Reports Medicine.

“Due to limited vaccine supply and uneven vaccine distribution in many regions of the world, health authorities urgently need data on the immune response to vaccines to optimize vaccination strategies,” says senior author Andrea Gamarnik (@GamarnikLab) of the Fundación Instituto Leloir-CONICET in Buenos Aires, Argentina. “The peer-reviewed data we present provide information for guiding public health decisions in light of the current global health emergency.”

Past research has shown that two doses of Sputnik V results in 92% efficacy against coronavirus disease 2019 (COVID-19), which is caused by SARS-CoV-2. An important question is whether a single dose would achieve greater public health benefit than two doses by allowing protection of a larger population more quickly.

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Blood clots related to AstraZeneca/Oxford vaccine can be mitigated with early detection

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New research has shown that early testing for blood clots in patients who had received the AstraZeneca/Oxford vaccine led to them being treated successfully, highlighting the need for heightened awareness of the risk among doctors.

The work, led by researchers from RCSI University of Medicine and Health Sciences and the National Coagulation Centre at St James’s Hospital, is published in the British Journal of Haematology.

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Long COVID symptoms likely caused by Epstein-Barr virus reactivation

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Epstein-Barr virus (EBV) reactivation resulting from the inflammatory response to coronavirus infection may be the cause of previously unexplained long COVID symptoms — such as fatigue, brain fog, and rashes — that occur in approximately 30% of patients after recovery from initial COVID-19 infection. The first evidence linking EBV reactivation to long COVID, as well as an analysis of long COVID prevalence, is outlined in a new long COVID study published in the journal Pathogens.

“We ran EBV antibody tests on recovered COVID-19 patients, comparing EBV reactivation rates of those with long COVID symptoms to those without long COVID symptoms,” said lead study author Jeffrey E. Gold of World Organization. “The majority of those with long COVID symptoms were positive for EBV reactivation, yet only 10% of controls indicated reactivation.”

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COVID-19 reinfection rate less than 1% for those with severe illness

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A review of more than 9,000 U.S. patients with severe COVID-19 infection showed less than 1% contracted the illness again, with an average reinfection time of 3.5 months after an initial positive test. Those are the findings from a study conducted by researchers from the University of Missouri School of Medicine and MU Health Care.

The researchers teamed up with the MU Institute for Data Science and Informatics and the Tiger Institute for Health Innovation to review data from 62 U.S. health care facilities. They found 63 of the 9,119 patients (0.7%) with severe COVID-19 infection contracted the virus a second time, with a mean reinfection period of 116 days. Of the 63 who were reinfected, two (3.2%) died. Patients categorized as non-white were at greater risk of reinfection than white patients.

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Vitamin D may not protect against COVID-19, as previously suggested

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While previous research early in the pandemic suggested that vitamin D cuts the risk of contracting COVID-19, a new study from McGill University finds there is no genetic evidence that the vitamin works as a protective measure against the coronavirus.

“Vitamin D supplementation as a public health measure to improve outcomes is not supported by this study. Most importantly, our results suggest that investment in other therapeutic or preventative avenues should be prioritized for COVID-19 randomized clinical trials,” say the authors.

To assess the relationship between vitamin D levels and COVID-19 susceptibility and severity, the researchers conducted a Mendelian randomization study using genetic variants strongly associated with increased vitamin D levels. They looked at genetic variants of 14,134 individuals with COVID-19 and over 1.2 million individuals without the disease from 11 countries.

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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.

“Treatment with virus-specific siRNA reduces viral load by 99.9%. These stealth nanoparticles can be delivered to a wide range of lung cells and silence viral genes,” said co-lead researcher Nigel McMillan, Ph.D., professor and director of the Infectious Diseases & Immunology Program at MHIQ.

“Treatment with the therapy in SARS-Cov-2 infected mice improved survival and loss of disease. Remarkably, in treated survivors, no virus could be detected in the lungs,” McMillan said.

Kevin Morris, Ph.D., professor and associate director of the Center for Gene Therapy at City of Hope and co-lead researcher from both City of Hope and Griffith University said, “This treatment is designed to work on all betacoronaviruses such as the original SARS virus (SARS-CoV-1) as well as SARS-CoV-2 and any new variants that may arise in the future because it targets ultra-conserved regions in the virus’ genome.”

McMillan added, “We have also shown that these nanoparticles are stable at 4°C for 12 months and at room temperature for greater than one month, meaning this agent could be used in low-resource settings to treat infected patients.”

The results suggest that siRNA-nanoparticle formulations can be developed as a therapy to treat COVID-19 patients, as well as used for future coronavirus infections by targeting the virus’ genome directly.

“These nanoparticles are scalable and relatively cost-effective to produce in bulk,” Professor Morris said.

“This work was funded as an urgent call by Medical Research Futures Fund and is the type of RNA medicine that can be manufactured locally in Australia,” McMillan said.

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).