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London, A team of Swedish researchers has revealed how different kinds of <keyword id="92416" type="PERSON" weightage="20" keywordseo="Immune-cells">immune cells</keyword>, called <keyword id="1323752" type="PERSON" weightage="20" keywordseo="macrophages">macrophages</keyword>, develop in the lungs, and which of them may be behind severe lung diseases, a discovery that may contribute to future treatments for Covid-19, among other diseases. To date, research on the development of <keyword id="10522711" type="UNKNOWN" weightage="20" keywordseo="human-lung-macrophages">human lung macrophages</keyword> has been limited. In a new study published in Immunity, researchers at Karolinska Institutet in <keyword id="23050" type="LOCATION" weightage="20" keywordseo="Sweden">Sweden</keyword> used a model to study the development of lung macrophages directly in a living lung. This has been combined with a method to study gene activity in individual cells, RNA sequencing, and thereby discovered how <keyword id="10522710" type="UNKNOWN" weightage="20" keywordseo="blood-monocytes">blood monocytes</keyword> become human lung macrophages. "In our study, we show that classical monocytes migrate into airways and lung tissue and are converted into macrophages that protect the health and function of the lungs," said Tim Willinger, Associate Professor at the <keyword id="199625" type="COMPANY" weightage="20" keywordseo="Department-of-Medicine">Department of Medicine</keyword> who led the study. "We have also identified a special kind of monocyte, HLA-DRhi, which is an intermediate immune cell between a blood monocyte and an airway macrophage." These HLA-DRhi monocytes can leave the blood circulation and migrate into the lung tissue. Macrophages are immune cells that, among other things, protect the lungs from such attacks. But under certain conditions, lung macrophages can also contribute to severe lung diseases, such as chronic obstructive pulmonary disease (COPD) and Covid-19. The non-classical monocytes, however, develop into macrophages in the many blood vessels of the lungs and do not migrate into the lung tissue. In an infection with the novel coronavirus, SARS-COV-2, which causes Covid-19, researchers believe that protective, anti-inflammatory macrophages are replaced by pro-inflammatory lung macrophages from blood monocytes. "Given their important role in rapid inflammatory responses, our results indicate that future treatments should focus on inflammatory macrophages and monocytes to reduce lung damage and mortality from severe Covid-19," said Willinger. SEE ALSO: <a href="https://www.businessinsider.in/stock-market/news/top-stocks-to-watch-tata-steel-vedanta-adani-green-tata-motors-maruti-mm-dhfl-v-mart-indian-bank-and-others/articleshow/80038635.cms">Top stocks to watch — Tata Steel, Vedanta, Adani Green, Tata Motors, Maruti, M&amp;M, DHFL, V-Mart, Indian Bank, and others</a> <a href="https://www.businessinsider.in/tech/mobile/news/checkout-the-list-of-upcoming-new-mobiles-in-january-2021-with-expected-price/articleshow/80039794.cms">Upcoming smartphones in India in January 2021</a> <a href="https://www.businessinsider.in/international/news/ten-of-the-most-outrageous-predictions-for-2021-according-to-saxo-bank/slidelist/80040045.cms">From Amazon buying Cyprus to Germany bailing out France — here are ten of the most ‘outrageous’ predictions for 2021</a> <a href="https://www.businessinsider.in/business/startups/news/india-edtech-in-charts-how-the-shi[%E2%80%A6]es-of-byjus-unacademy-and-others/articleshow/80040270.cms">India’s edtech in charts – How the shift to online learning meant money, valuation and users for the likes of BYJU’S, Unacademy, and others</a>

New research explains severe virus attacks on lungs

Scientists have discovered details about the genetic predispositions of children who tended to fall ill suddenly and dramatically during the Covid pandemic. "The patients are sick not because of the virus," said Jean-Laurent <keyword id="5223" type="General" weightage="80" keywordseo="casanova" source="Orion">Casanova</keyword>, a geneticist at <keyword id="120084" type="General" weightage="50" keywordseo="rockefeller-university" source="Orion">Rockefeller University</keyword>, US. "They're sick because they excessively respond to the virus." <keyword id="707693" type="General" weightage="50" keywordseo="rockefeller" source="Orion">Rockefeller</keyword> scientists and affiliates of the COVID Human Genetic Effort (CHGE) described how a trio of faulty genes fail to put the brakes on the immune system's all-out assault on SARS-CoV-2, leading to the inflammatory overload characteristic of multisystem inflammatory syndrome in children, or MIS-C. Children with MIS-C, who end up in the hospital, are characterised by inflamed hearts, lungs, kidneys, and brains, spiked temperatures, skin rashes, and abdominal pain. The CHGE is an international consortium of researchers seeking the human genetic and immunological bases of all the different ways a SARS-CoV-2 infection can manifest. The study said that the findings constituted the first mechanistic explanation of any Kawasaki disease and that they were reported in a paper published in the journal Science. According to the study, in February 2020, Casanova and his collaborators in the CHGE began searching for inborn errors, or genetic mutations, of immunity among healthy people who had severe forms of COVID. Among their targets were children with MIS-C, the study said. Casanova and his team assembled an ever-growing database of hundreds of fully sequenced genomes of COVID victims from hospitals across North America, Asia, Europe, Latin America, Oceania, and the Middle East, the study said. They have since made several discoveries about the genetic predispositions of individuals who develop severe COVID, the study said. For the current study, the researchers hypothesized that in some children, MIS-C could be caused by a gene defect that rendered them vulnerable to an inflammatory condition provoked by a SARS-CoV-2 infection, said Casanova. To find out, they analyzed the genomes of 558 children who had had MIS-C, the study said. Five unrelated kids from four countries - Turkey, Spain, the Philippines, and Canada - shared mutations in three closely related genes controlling the OAS-RNase L pathway, which is involved in viral response, the study said. Normally, this pathway is induced by type 1 interferons and activated by viral infection, which induce OAS1, OAS2 and OAS3 molecules. These in turn activate <keyword id="16459356" type="General" weightage="80" keywordseo="rnase-l" source="Orion">RNase L</keyword>, an antiviral enzyme that chops up single-strand viral and cellular RNA, shutting down the cell. When a cell goes dark, the virus cannot hijack its replication machinery to spread disease. But in the five children with these mutations, the pathway failed to activate in response to the presence of SARS-CoV-2, the study said. According to the study, the cell instead sensed the viral RNA using another pathway known as MAVS, which provokes an army of dendritic cells, <keyword id="16459355" type="General" weightage="80" keywordseo="phagocytes" source="Orion">phagocytes</keyword>, monocytes, and macrophages to attack the viral invaders en masse. The MAVS pathway acts as a sort of accelerator of the immunological response. The OAS-RNase L pathway, on the other hand, is supposed to act as the brake. But in MIS-C, the brake fails, and the response careens out of control. "Phagocytes produce excessive levels of inflammatory cytokines and chemokines and growth factors and interferons - you name it," said Casanova. Massive inflammation ensues. Because MIS-C is clinically and immunologically so aligned with other examples of Kawasaki disease, the researchers believe that MIS-C is a variety of the disease driven by a SARS-CoV-2 infection - the first such provocateur of Kawasaki to be pinpointed. One of the most terrifying aspects of the COVID pandemic has been its unpredictably severe impact on some children. While most infected kids have few or no symptoms, one in 10,000 fall suddenly and dramatically ill about a month after a mild infection and land in the hospital with what researchers call MIS-C. Why this reaction only takes place about a month after infection remains unknown, the study said. "We now understand the molecular and cellular basis of the disease, but we don't understand the timing," said Casanova. SEE ALSO: <a target="_blank" class="c-link c-message_attachment__title_link" href="https://www.businessinsider.in/international/news/pakistan-pumps-run-out-of-petrol-disrupts-routine-life-of-people-says-a-dawn-report/articleshow/97795433.cms">Pakistan pumps run out of petrol, disrupts routine life of people says a Dawn report</a> <a target="_blank" class="c-link c-message_attachment__title_link" href="https://www.businessinsider.in/business/news/game-of-thrones-spider-man-no-way-home-among-most-pirated-content-in-india-in-2022/articleshow/97795322.cms">Game of Thrones, Spider-Man: No Way Home among most-pirated content in India in 2022</a>

US scientists discover genetic mechanism behind some children falling extremely ill

London, June 11 () Two drugs companies in the UK are collaborating with the universities of Birmingham and Oxford as part of a major trial to test potential therapeutics to treat patients hospitalised with COVID-19, according to a statement. The CATALYST trial, a collaboration with University Hospitals Birmingham NHS Foundation Trust (UHB), will test a series of new drugs, including those already in use for patients with cancer and inflammatory diseases such as rheumatoid arthritis. Oxford based biopharmaceutical company Izana Bioscience will provide the first of four potential treatments to be tested, according to the statement by the University of Birmingham. Namilumab is a fully human monoclonal antibody already in late-stage trials to treat rheumatoid arthritis, and an inflammatory disease called ankylosing spondylitis, it said. The drug targets a 'cytokine' called GM-CSF (granulocyte-macrophage colony stimulating factor), which is naturally secreted by immune cells in the body but, in uncontrolled levels. The cytokine is believed to be a key driver of the excessive and dangerous lung inflammation seen in COVID-19 patients, the university said. The second drug, Infliximab developed by Slough based Celltrion Healthcare UK, is an anti-tumour necrosis factor (TNF) therapy that is designed to attach to a protein involved in inflammation, according to the statement. It is currently used as a treatment for other inflammatory conditions including eight autoimmune diseases including rheumatoid arthritis and irritable bowel syndrome under the trade name Remsima. It is hoped that by using drugs that target the most serious symptoms of the virus, the severity of the disease could be reduced leading to a reduction in the number of patients needing to be admitted to intensive care and ultimately, a reduction in virus related deaths, the university said. "There has been a tremendous effort to pull together this initiative so rapidly. Emerging evidence is demonstrating a critical role for anti-inflammatory drugs in the cytokine storm associated with severe COVID-19 infection," said Ben Fisher, co-clinical investigator of the CATALYST trial from the University of Birmingham's Institute of Inflammation and Ageing. "In the CATALYST study we hope to show with a single dose of these kinds of drugs in hospitalised patients, that we are able to delay or prevent the rapid deterioration into intensive care and requirement for invasive ventilation in this critical patient group," Fisher said. "We hope that by using a treatment that is already used to treat inflammation in other autoimmune conditions we may be able to manage inflammation associated with COVID-19 early," said Marc Feldmann, Professor of Immunology, University of Oxford. "If, when people are initially admitted to hospital, we are able to keep symptoms within manageable levels, this may reduce the number of patients who need to be admitted to intensive care," said Feldmann. HSR SAR SAR

'Major UK drug trial to test potential therapeutics for COVID-19'

By Shakoor Rather New Delhi, Jul 10 () As dengue season sets in across large parts of India with the onset of the monsoon, scientists warn that COVID-19 and the mosquito-borne disease have overlapping symptoms and worry the country's healthcare infrastructure won't be able to cope with this double whammy. The impact of a 'dengue-COVID-19' season would entail two different diagnostic tests and extract a huge toll on patients too, each disease making the other more complicated to deal with and perhaps more fatal. While the number of COVID-19 cases races towards the 8,00,000 mark with 7,93,802 cases on Friday and 21,604 fatalities, the incidence of dengue is also high. Based on 2016-2019 data, virologist Shahid Jameel estimated that India gets about 100,000 to 200,000 confirmed cases of dengue each year. According to the National Vector Borne Disease Control Programme (NVBDCP), 1,36,422 dengue cases were diagnosed in 2019 and an estimated 132 people died. "The virus is endemic and present around the year in southern India, and in monsoon and early winter in northern India," Jameel, CEO at DBT/Wellcome Trust India Alliance, a public charity that invests in building biomedical sciences and health research framework, told . Both COVID-19 and have symptoms such as high fever, headache and body pain. The dengue season may aggravate the COVID-19 situation as both viruses may supplement each other, warned Dhrubjyoti Chattopadhyay, virologist and vice chancellor of the Amity University in Kolkata. "This situation is not yet well studied. But the information available from South America is dangerous and found to create a major challenge to their medical infrastructure," he said. "The effect will be very critical. As major symptoms are overlapping, simultaneous infection will be much more fatal. Weakened immune systems will help the other to be more fatal." Once the dengue season starts, added virologist Upasana Ray, the infection spreads aggressively due to high prevalence of its mosquito vector, aedes aegypti. "Each season, we experience heavy loads in the hospital wards due to dengue outbreak and those times it gets almost unmanageable. So, have we thought about what will happen when we have two menaces to handle together? Both of them have overlapping symptoms. Are we geared to distinguish if a person has dengue or COVID 19?" asked the senior scientist, CSIR-IICB, Kolkata. The challenges are many. Almost each patient with a three-day fever would need to undergo a test for dengue and another for the SARS-CoV-2 virus which causes COVID-19. "Considering the current numbers of COVID-19 patients, will our hospitals have beds available for dengue patients? Or will only severe dengue cases be handled at hospitals?" she asked. Explaining how the viruses manifest in the human body, Jameel said the dengue virus enters via a mosquito bite through the subcutaneous layer of the skin from where it reaches the lymph nodes that are rich in types of blood cells called monocytes, macrophages and dendritic cells. The virus, he said, primarily reproduces in these cells and can severely alter cytokine production by these cells, a fundamental response to injury and infection in the body. On the other hand, SARS-CoV-2 enters the cells primarily through mucosal membranes of the mouth and nasal cavity and initially replicates in the epithelial cells of the upper respiratory tract. "In some cases, however, the infection moves down the trachea into the lungs, where it infects the air sacs that exchange oxygen with blood. This causes inflammation as the immune system tries to fight the virus and leads to fluid accumulation in the lungs, which results in respiratory distress and oxygen demand. "So, you see, both viruses infect via different pathways and different cell types. There would of course be overlaps in physiological effects and immunological responses. They would most likely make each disease worse than either infection alone," Jameel noted. The most likely effect, he said, would be on healthcare capacity. "Since initial clinical presentation is similar -- high fever -- one would be ignored at the expense of the other. With hospitals mainly in COVID-19 mode, they may also refuse dengue patients," Jameel said. He said this has been already seen in connection with pregnancy care and deliveries, dialysis and tuberculosis treatment. "We need to be careful and deploy tests for dengue also for febrile illness. Thankfully, India makes some very good tests for dengue virus, e.g. NS1 antigen test that is positive on the first day of fever," said Jameel. Ray pointed out that there is no vaccine available clinically for either and no specific antiviral to treat them. "This infection may show low to severe forms of infection including simple dengue fever, severe dengue and the haemorrhagic fever," said Ray. "We are already amidst the SARS-CoV2 pandemic and hospitals are running out of beds although the government is trying its level best. We are yet to attain enough facility to handle the increasing coronavirus cases every day in India," she said. According to Ray, careful preparation is needed as the country has very little time before a full-blown dengue season starts. "While many dengue patients don't end up in critical care units (CCUs), a good fraction do. Do we have enough ICUs and CCUs to tackle dengue and COVID 19 together? Do we have enough trained manpower?" Healthcare and research, she said, need to gear up to fight this "upcoming very realistic situation". SAR MIN MIN MIN

Season of two viruses? Scientists worried that dengue outbreak may aggravate COVID-19 crisis

Unlicensed medical 'cures' are flourishing in closed Facebook groups, where cancer treatments - and even surgery - are sold beyond the reach of the law

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New research explains severe virus attacks on lungs

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US scientists discover genetic mechanism behind some children falling extremely ill

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'Major UK drug trial to test potential therapeutics for COVID-19'

PTI

Season of two viruses? Scientists worried that dengue outbreak may aggravate COVID-19 crisis

PTI

Unlicensed medical 'cures' are flourishing in closed Facebook groups, where cancer treatments - and even surgery - are sold beyond the reach of the law

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