Category Archives: Immunology

High-throughput production of tetramer assay probes used for COVID-19 – Drug Target Review

The developers of a novel method to create immunological assay probes for screening T cells has leveraged their new protocol against COVID-19.

Researchers have developed a method that enables them to create libraries containing hundreds of molecular probes for tetramer assays in only days, whereas previous protocols required a week to produce a single probe. The team suggest their process opens up new opportunities for immunological research, development of cancer immunotherapies and assessment of immune responses from patients with COVID-19.

Tetramer assays are an immunological test used to detect and analyse the T cells in a blood sample. T cells each recognise and bind to a specific antigen like a viral protein and bind to them, identifying them to the immune system. However, where antibodies bind directly to antigens on the surface of a pathogen, T cells only bind to antigens expressed on the surface of antigen presenting cells, like macrophages and dendritic cells.

As a result, antibody assays are relatively simple and T-cell assays are more complex; requiring the probes for the latter to be formed of antigens incorporated into a molecular complex that mimics how they are presented in vivo, where they are bound to tetramers of major histocompatibility complex (MHC) proteins.

This diagram outlines a workflow for preparing and using a library of peptide-loaded MHC multimers for assessment of T cell repertoires in patient blood samples [credit: Overall et al., Nature Communications, 2020].

Corresponding author of the study published in Nature Communications, Nikolaos Sgourakis, assistant professor of chemistry and biochemistry at the University of California (UC) Santa Cruz has been studying how protein fragments are selected and bound to MHC proteins in cells for years, a process which requires molecular chaperones. The new protocol is based on his research which indicates that molecular chaperones can eject antigens that have low affinity for the MHC protein tetramers, in favour of antigens with higher affinity.

Sgourakis designed a placeholder peptide for use in preparing large quantities of pre-loaded MHC complexes. When incubated with a high-affinity antigen, the placeholder is displaced, a reaction that can be performed in a high-throughput system with large numbers of antigens.

Its a force multiplier, enabling us to perform these reactions at high throughput, Sgourakis said. A lot of groups are working on similar methodologies, all of which have their pros and cons. This technology has the advantage of using the same system that cells use naturally and we can combine it very elegantly with existing single-cell analytical tools.

The researchers originally used the new method to develop libraries of probes for assessing T-cell responses to neuroblastoma and designing cancer immunotherapies. However, since the emergence of COVID-19, the team have been exploring ways to apply the technology to address the challenges of the novel coronavirus. With a viral infection, there are many different fragments of the viral proteins that an infected cell can display and the researchers say it is important for drug design to determine which of these peptides elicit a strong immune response.

Based on the coronavirus genome, we can predict all the possible peptides, synthesise them, load them onto MHC tetramers and do a fishing expedition to find which ones are recognised by the T cells in blood samples from patients, Sgourakis explained. Certain peptides are immunodominant, ie, they steer the immune response and those are the ones we want to discover so we can potentially use them in a vaccine.

Sgourakis explained that the tetramer assays could also answer one of the biggest questions surrounding COVID-19: why is there so much variability in the severity of this disease?

According to Sgourakis, the approach can be used to compare the T-cell repertoires of different cohorts of patients. It is known that as people age their T-cell repertoire declines, resulting in a weaker immune response to pathogens, which may explain why older people are more vulnerable to COVID-19. Sgourakis said: We can use this technology to screen patients and see what the gaps are in their T-cell repertoires and maybe use this as a diagnostic for which patients will need more intensive treatment.

This research was in close collaboration with researchers at the New York Genome Center and the University of Pennsylvanias Childrens Hospital and Perelman School of Medicine, all US.

Related topicsAnalytical techniques, Assays, Cell-based assays, Disease research, Drug Development, Immunology, Protein, Proteomics, Research & Development, Screening, t-cells

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High-throughput production of tetramer assay probes used for COVID-19 - Drug Target Review

Vivoryon Therapeutics Starts Development Program for Meprin Protease Inhibitors with Intended Therapeutic Use in Fibrosis, Cancer and Alzheimer’s…

HALLE (SAALE) / MUNICH and LEIPZIG, Germany, 16 April 2020 Vivoryon Therapeutics AG (Euronext Amsterdam: VVY, ISIN DE0007921835) announced today that the Company has entered into a research collaboration with the Fraunhofer Institute for Cell Therapy and Immunology (IZI) and acquired related patents from the Institute for a meprin protease inhibitor and assay platform. Under the guidance of PD Dr. Stephan Schilling, the Department of Drug Design and Target Validation will work together with Vivoryon to advance first-in-class small molecule meprin inhibitors. This collaboration will combine Vivoryons expertise in translating basic research into marketable small molecule therapeutics with the departments focus on discovery and development of new therapeutics that target putative pathologic post-translational modifications.

The metal-dependent proteases, meprin alpha and meprin beta, are emerging targets in kidney protection, fibrotic diseases, cancer and Alzheimers disease. Increased meprin expression and their mislocalization has been associated with tissue damage and collagen deposition in fibrosis, which can result in the loss of organ function. Meprin-targeted protease inhibitors thus have the potential to not only target symptoms, but also treat a range of indications including acute and chronic kidney disease and multiple organ fibrosis.

Dr. Michael Schaeffer, CBO at Vivoryon Therapeutics AG noted:The IP estate we have acquired from Fraunhofer IZI expands our current drug development portfolio and places us in a leading position to explore the full potential of meprin protease inhibitors. As a company, our goal is to consistently seek out opportunities that can further strengthen our pipeline with the ultimate vision of delivering novel therapies to patients in need. By working with Dr. Schilling and his team we are set to advance meprin inhibitors very quickly towards clinical testing in indications like fibrotic diseases or cancer.

PD Dr. Stephan Schilling, Head of Protein and Drug Biochemistry Unit at Fraunhofer Institute for

Cell Therapy and Immunology added:As the roles and functionality of meprin alpha and beta continue to become more distinguished through research, it is clear these metalloproteases represent interesting novel targets that could be developed into therapeutics for a variety of indications. As such, I am delighted that with this collaboration the groundbreaking research of our institute will eventually be translated into clinical programs by an experienced drug development company.

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For more information, please contact:

Vivoryon Therapeutics AG

Dr. Ulrich Dauer, CEO

Email:contact@vivoryon.com

Fraunhofer Institute for Cell Therapy and Immunology

Jens Augustin, Head of Press and Public Affairs

E-Mail:presse@izi.fraunhofer.de

Trophic Communications

Gretchen Schweitzer / Joanne Tudorica

Tel: +49 172 861 8540 / +49 176 2103 7191

Email:Trophic@vivoryon.com

About Vivoryon Therapeutics AG

With 20+ years of unmatched understanding in identifying post-translational modifying enzymes that play critical roles in disease initiation and progression, Vivoryons scientific expertise has facilitated the creation of a discovery and development engine for small molecule therapeutics. This platform has demonstrated success by developing a novel therapeutic in type 2 diabetes. In its current programs Vivoryon Therapeutics is advancing its lead product, PQ912, in Alzheimers disease and its entire portfolio of QPCT and QPCTL inhibitors in oncology and other indications.

http://www.vivoryon.com

About Fraunhofer-Gesellschaft

The Fraunhofer-Gesellschaft, headquartered in Germany, is the worlds leading applied research organization. With its focus on developing key technologies that are vital for the future and enabling the commercial exploitation of this work by business and industry, Fraunhofer plays a central role in the innovation process. As a pioneer and catalyst for groundbreaking developments and scientific excellence, Fraunhofer helps shape society now and in the future. Founded in 1949, the FraunhoferGesellschaft currently operates 74 institutes and research institutions throughout Germany. The majority of the organizations 28,000 employees are qualified scientists and engineers, who work

with an annual research budget of 2.8 billion euros. Of this sum, 2.3 billion euros is generated through

contract research.

http://www.izi.fraunhofer.de

Forward Looking Statements

Information set forth in this press release contains forward-looking statements, which involve a number of risks and uncertainties. The forward-looking statements contained herein represent the judgment of Vivoryon Therapeutics AG as of the date of this press release. Such forward-looking statements are neither promises nor guarantees but are subject to a variety of risks and uncertainties, many of which are beyond our control, and which could cause actual results to differ materially from those contemplated in these forward-looking statements. We expressly disclaim any obligation or undertaking to release publicly any updates or revisions to any such statements to reflect any change in our expectations or any change in events, conditions or circumstances on which any such statement is based.

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Vivoryon Therapeutics Starts Development Program for Meprin Protease Inhibitors with Intended Therapeutic Use in Fibrosis, Cancer and Alzheimer's...

Could genetics explain why some COVID-19 patients fare worse than others? – Live Science

Certain genetic differences might separate people who fall severely ill with COVID-19 from those who contract the infection but hardly develop a cough, a new preliminary study suggests.

The research is still in its early days, though, experts say.

The immune system can react to viruses thanks, in part, to specific genes that help cells spot unfamiliar bugs when they enter the body. The genes, known as human leukocyte antigen (HLA) genes, contain instructions to build proteins that bind to bits of a pathogen; those proteins serve as warning flags to alert immune cells. The immune cells, once trained to recognize these bits, jumpstart the process of building antibodies to target and destroy the invasive germ.

Within each individual, HLA genes code for three different classes of proteins; in other words, HLAs come in a variety of flavors, and depending on which HLAs you have, your body may be better or worse equipped to fight off certain germs including SARS-CoV-2, the virus that causes COVID-19.

In a new study, published April 17 in the Journal of Virology, researchers used computer models to predict which combination of HLAs might be best at binding SARS-CoV-2, and which might be worst.

If certain HLAs can bind well to a large proportion of the virus's proteins, "we expect there to be a more protective immune response," authors Abhinav Nellore and Dr. Reid Thompson, who lead a computational biology research group at the Oregon Health and Science University, told Live Science in an email. A better bind means that the viral proteins are more likely to be presented to immune cells and prompt the production of specific antibodies, the authors said.

"If the interaction is not stable, you will not have a proper [immune] response," said Dr. Shokrollah Elahi, an associate professor in the Department of Dentistry and adjunct associate professor in the Department of Medical Microbiology and Immunology at the University of Alberta, who was not involved in the study.

Related: 10 deadly diseases that hopped across species

But a stable bond, alone, does not guarantee the best immune response, Elahi added. If an HLA binds a viral protein that happens to be critical for the germ to replicate and survive, the subsequent antibody activity will likely target the virus more effectively than that prompted by a less important protein, Elahi said.

"This is an issue we did not address in our analysis," the authors noted. Instead, the team focused on predicting how well different HLA types could bind to bits of SARS-CoV-2. Their analysis identified six HLA types with a high capacity to bind different SARS-CoV-2 protein sequences, and three with a low capacity to do so. Specifically, a HLA type known as HLA-B*46:01 had the lowest predicted capacity to bind to bits of SARS-CoV-2.

The same HLA type cropped up in a 2003 study published in the journal BMC Medical Genetics, which assessed patients infected with SARS-CoV, a closely related coronavirus that caused an outbreak of severe acute respiratory syndrome in the early 2000s. The study found that, in a group of patients of Asian descent, the presence of HLA-B*46:01 was associated with severe cases of the infection. In their paper, the research group noted that more clinical data would be needed to confirm the connection and the same goes for the new study of SARS-CoV-2, Nellore and Thompson said.

"The most substantial limitation of our study is that this was conducted entirely on a computer and did not involve clinical data from COVID-19 patients," the authors said. "Unless and until the findings we present here are clinically validated, they should not be employed for any clinical purposes," they added.

"In the body, we have so many things interacting," Elahi said. HLAs represent just one piece of a large, intricate puzzle that comprises the human immune system, he said. To better understand the variety of immune responses to COVID-19, Elahi and his research group aim to assess markers of immune system activity in infected patients and also catalog the ratio of immune cell types present in their bodies. While taking age, sex and other demographic factors into account, these so-called immunological profiles could help pinpoint when and why the illness takes a turn in some patients.

The clinical data could be assessed in parallel with genetic data gathered from the same patients, Elahi added. Similarly, Nellore and Thompson said that "COVID-19 testing should be paired with HLA typing, wherever [and] whenever possible," to help determine how different HLA types relate to symptom severity, if at all. Partnerships with genetic testing companies, biobanks and organ transplant registries could also offer opportunities to study HLA types in larger populations of people, they said.

"We cannot in good conscience predict at this point who will be more or less susceptible to the virus because we have not analyzed any clinical outcomes data with respect to HLA type to know that any of our predictions are valid," the authors said. If future studies support the notion that some HLA genes protect people from the virus, while others place patients at greater risk, those in the latter group could be first in line for vaccination, they added.

"In addition to prioritizing vaccinating the elderly or those with preexisting conditions, one could prioritize vaccinating people with HLA genotypes that suggest the SARS-CoV-2 virus is more likely to give them worse symptoms."

The authors went on to analyze how well HLAs can bind SARS-CoV-2 as compared with other coronaviruses, such as those that cause the common cold and infect humans often. They identified several viral bits shared between SARS-CoV-2 and at least one of these common viruses, suggesting exposure to one germ could somewhat protect the body against the other.

"If someone was previously exposed to a more common coronavirus and had the right HLA types ... then it is theoretically possible that they could also generate an earlier immune response against the novel SARS-CoV-2," the authors said. On the other hand, exposure to a similar virus could leave the body ill-equipped to fight off the new one, if, for instance, "the body is using an old set of tools that aren't ideally suited to address the new problem," the authors said.

Originally published on Live Science.

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Could genetics explain why some COVID-19 patients fare worse than others? - Live Science

Outlook 2020: ‘Passionate about helping to train the next generation of physicians, scientists,’ Judith James says – Oklahoman.com

Name: Dr. Judith James, 52.

Career highlights: Oklahoma Medical Research Foundation vice president of Clinical Affairs; member and program chair, Arthritis & Clinical Immunology Research Program; Lou C. Kerr Endowed Chair in Biomedical Research; associate vice provost for Clinical and Translational Science; George Lynn Cross Professor of Research, professor of medicine, professor of pathology, adjunct professor of microbiology and immunology, Oklahoma University Health Sciences Center.

Community impact: As a leader in the Oklahoma Shared Clinical Translational Resources, James helps oversee partnerships between 29 entities within the state whose mission is to improve health and health outcomes. Along with universities, the program includes tribal health services.

James also works with the Cherokee Nation and the Chickasaw Nation at outreach clinics to improve tribal members with rheumatic diseases.

Life philosophy and advice to young women: "I am incredibly passionate about helping to train the next generation of physician and physician scientists," James said. "When I started in medical school, less than 30% of my class was female. And now we're close to 50%. And so I hope that I will encourage, inspire, motivate and facilitate their ability to think about how they can help improve the health and research training, for everyone. But especially for women."

Dale Denwalt, Staff writer

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Outlook 2020: 'Passionate about helping to train the next generation of physicians, scientists,' Judith James says - Oklahoman.com

New research gives further evidence that autoimmunity plays a role in Parkinsons disease – Newswise

Newswise LA JOLLAA new study co-led by scientists at the La Jolla Institute for Immunology (LJI) adds increasing evidence that Parkinsons disease is partly an autoimmune disease. In fact, the researchers report that signs of autoimmunity can appear in Parkinsons disease patients years before their official diagnosis.

The research could make it possible to someday detect Parkinsons disease before the onset of debilitating motor symptomsand potentially intervene with therapies to slow the disease progression.

The study, published in the April 20, 2020, issue of Nature Communications, was co-led by LJI professor Alessandro Sette, Dr. Biol. Sci, and Professor David Sulzer, Ph.D., of the Columbia University Medical Center.

Scientists have long known that clumps of a damaged protein called alpha-synuclein build up in the dopamine-producing brain cells of patients with Parkinsons disease. These clumps eventually lead to cell death, causing motor symptoms and cognitive decline.

Once these cells are gone, theyre gone. So if you are able to diagnose the disease as early as possible, it could make a huge difference, says LJI research assistant professor Cecilia Lindestam Arlehamn, Ph.D., who served as first author of the new study.

A 2017 study led by Sette and Sulzer was the first to show that alpha-synuclein can act as a beacon for certain T cells, causing them to mistakenly attack brain cells and potentially contribute to the progression of Parkinsons. This was the first direct evidence that autoimmunity could play a role in Parkinsons disease.

The new findings shed light on the timeline of T cell reactivity and disease progression. The researchers looked at blood samples from a large group of Parkinsons disease patients and compared their T cells to a healthy, age-matched control group. They found that the T cells that react to alpha-synuclein are most abundant when patients are first diagnosed with the disease. These T cells tend to disappear as the disease progresses, and few patients still have them ten years after diagnosis.

The researchers also did an in-depth analysis of one Parkinsons disease patient who happened to have blood samples preserved going back long before his diagnosis. This case study showed that the patient had a strong T cell response to alpha-synuclein ten years before he was diagnosed with Parkinsons disease. Again, these T cells faded away in the years following diagnosis.

This tells us that detection of T cell responses could help in the diagnosis of people at risk or in early stages of disease development, when many of the symptoms have not been detected yet, says Sette. Importantly, we could dream of a scenario where early interference with T cell responses could prevent the disease from manifesting itself or progressing.

Sulzer added, One of the most important findings is that the flavor of the T cells changes during the course of the disease, starting with more aggressive cells, moving to less aggressive cells that may inhibit the immune response, and after about 10 years, disappearing altogether. It is almost as if immune responses in Parkinsons disease are like those that occur during seasonal flu, except that the changes take place over ten years instead of a week.

In fact, already therapies exist to treat inflammation from autoreactive T cells, and these TNF therapies are associated with lower incidence of Parkinsons disease. Going forward, the researchers are especially interested in using a tool called a T cell-based assay to monitor patients already at risk for Parkinsons to see if they could benefit from TNF therapies. These patients include people with REM sleep disorders and certain genetic mutations.

The researchers hope to study more Parkinsons patients and follow them over longer time periods to better understand how T cell reactivity changes as the disease progresses.

The study, titled -Synuclein-specific T cell reactivity is associated with preclinical and early Parkinsons disease, was supported by the National Institutes of Healths (NIH) National Institute of Neurological Disorders and Stroke (R01NS095435, P50NS108675), the NIH National Institute on Aging (P50AG08702), the Parkinsons Foundation, the Michael J. Fox Foundation, JPB Foundation, William F. Richter Foundations, and the UCSD-LJI Program in Immunology.

Additional study authors included Rekha Dhanwani, John Pham, Rebecca Kuan, April Frazier, Juliana Rezende Dutra, Elizabeth Phillips, Simon Mallal, Mario Roederer, Karen S. Marder, Amy W. Amara, David G. Standaert, Jennifer G. Goldman, Irene Litvan, and Bjoern Peters.

DOI: 10.1038/s41467-020-15626-w

About La Jolla Institute for Immunology

The La Jolla Institute for Immunology is dedicated to understanding the intricacies and power of the immune system so that we may apply that knowledge to promote human health and prevent a wide range of diseases. Since its founding in 1988 as an independent, nonprofit research organization, the Institute has made numerous advances leading toward its goal: life without disease.

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New research gives further evidence that autoimmunity plays a role in Parkinsons disease - Newswise

William Frankland obituary – The Guardian

When Bill Frankland began practising in the 1940s, allergy medicine was barely a discipline. The allergist Adam Fox said: To say Bill Frankland was the grandfather of allergy medicine doesnt do it justice. He wasnt the grandfather in the sense of being the oldest but in the sense of being the originator of the speciality. He did the original trials and founded the British society. He was still practising in his 90s and 100s, and remained the doctor people wanted to see.

On his release from a Japanese prisoner of war camp in 1945, Frankland, who has died aged 108, returned to St Marys hospital, Paddington, in London, where he had trained. He had suffered with hay fever since he was nine, and when he saw an advertisement for a part-time assistant in the allergy department, he applied. In February 1946 he became full-time and for the next 70 years was gripped by allergy medicine, which he said was like a fascinating detective story.

Frankland worked at the allergy clinic at St Marys hospital for more than 30 years, and was its director from 1958 until he retired in 1977. A few years later it was renamed the Frankland Allergy Clinic. It was the busiest in the country, and it is estimated that Frankland oversaw the desensitisation treatment of around 30,000 hay fever patients. At the same time, he also ran the hospitals pollen farm near Woking, Surrey, until it closed in 1970.

In 1948 the British Association of Allergists was formed with 30 members and Frankland as its secretary. It grew rapidly as it widened its scope to include immunology, becoming the British Society for Allergy and Clinical Immunology (BSACI) in 1973. Frankland was its president from 1963 to 1966 and remained at its heart all his life.

When he began his career in the late 1940s antihistamines had recently come on stream to treat allergies. Frankland was involved in several trials, demonstrating that two antihistamines reduced hay fever symptoms but were not effective for asthma.

Allergen desensitisation for hay fever had been used since 1911, but had not been properly evaluated. Frankland had read about double-blind placebo-controlled trials and wanted to apply them to his discipline. Patients at that time were injected with a grass-pollen extract called Pollaccine to desensitise them.

Frankland was concerned that it contained material that gave unwanted side-effects and wanted to determine exactly which part of the pollen extract was effective. In 1953 he recruited 200 hay fever patients and showed that a purified pollen protein worked just as well as Pollaccine. His paper, published in 1954, was a milestone: the first double-blind randomised clinical trial in immunotherapy; 65 years later, Frankland was gratified to see it celebrated on the 2018 cover of the journal Allergy.

In the 40s and 50s it was difficult for hay fever patients to control their symptoms without information on what type of pollen and how much of it was in the air. Frankland knew that atmospheric levels of pollen were being measured in Cardiff and wanted to do the same in London. In 1953 he installed a Hirst spore trap on the roof of the nurses home at St Marys and recruited a biologist (whose name he was amused to recount was Miss Hay) to provide daily pollen counts and analyse the prevalence of different pollens. Initially the information went out once a week to members of the British Association of Allergists, but, to disseminate it further, in 1963 Frankland persuaded the Times and the Daily Telegraph to print a daily pollen count. (It is now part of the weather forecast and coordinated by the Met Office.)

As well as his other duties at St Marys, in the 40s Frankland spent two years as Sir Alexander Flemings clinical assistant. He took care of Flemings patients, reporting on their progress every morning at 10am even though Fleming preferred to discuss other subjects.

Frankland said: He just wasnt interested in clinical medicine once he looked down a microscope, he continued looking down a microscope

In 1948 the publisher Butterworths asked for a new chapter on sensitivities in Flemings bestseller Penicillin: Its Practical Application, and Fleming tasked Frankland with writing it. Fleming himself did not accept that people could be allergic to penicillin, saying adverse reactions must be the result of drug impurities. When he read Franklands draft, he crossed out the last sentence: With the increasing use of penicillin, it is to be expected that allergic reactions will become more common, substituting: With the increasing use of penicillin, reactions due to impurities will become less common. Frankland disagreed, but did not feel he should argue with the Nobel prize winner.

In his long career Frankland treated many patients including, in 1979, Saddam Hussein, whose symptoms were caused by cigarettes rather than asthma. He told him: If youre not eating, sleeping or praying, youre smoking. If you carry on, you wont be president in two years time. Saddam heeded the advice and later flew Frankland out to Baghdad for a celebratory lunch.

As well as asthma and hay fever, Frankland was interested in many different allergies, and, in the now no longer permissible tradition of self-experimentation, in 1955 allowed the South American insect Rhodnius prolixus to bite him weekly so he could observe the reaction. He got the insect from the London School of Hygiene and Tropical Medicine and kept it in the glove compartment of his car. After eight weeks, he had a severe anaphylactic reaction and was saved by two injections of adrenaline. Three hours later, he helped a nurse push her car. The strenuous exercise brought on anaphylaxis again, requiring a third shot of adrenaline. This experience led to his interest in the delay that is possible in allergic reactions.

Frankland was born near Bexhill-on-Sea, East Sussex. His father, Henry, was a vicar and his mother, Rose (nee West), a musician. He was an identical twin and nearly didnt survive because he was born prematurely and was tiny, weighing just over 3lb (1.4kg). The family moved to Cumberland (now Cumbria), in north-west England, and Frankland remembered getting postcards from his father who was away during the first world war.

When he was nine he caught tuberculosis, and was unimpressed with the doctor treating him, deciding he could do a better job and should study medicine. He went to St Bees school in the county and then to Queens College, Oxford, to study natural sciences. His studies were interrupted for six months when he returned home to care for his elder sister Ella, who had scarlet fever. She died in October 1933 and he returned to Oxford before moving to St Marys hospital, qualifying as a doctor in 1938.

Two days before the second world war was declared in September 1939, Frankland volunteered as a civilian medical practitioner in the army. He was shipped out to Singapore, where his life was saved a second time. Another doctor and I decided to spin a coin to determine our assignments, he said. I called heads and won. The man who lost went to [the] Alexandra hospital where he was brutally murdered by Japanese forces in 1942.

Frankland, however, was captured and became a Japanese PoW. In 1943 he was moved to Pulau Blakang Mati (now Sentosa Island), off Singapores southern coast, where his two days of tropical medicine training were scant preparation for the array of malnutrition, malaria, dengue and beri-beri he faced. He was nearly bayoneted to death during a punishment bashing from Japanese soldiers, and his life was saved yet again when the Americans dropped atomic bombs on Hiroshima and Nagasaki in 1945, ending the war and preventing mass shooting of PoWs.

Frankland returned home in October of that year. He had married Pauline Jackson, an optometrist, in 1941, and had treasured her letters. When he arrived in Liverpool, he was asked if he wanted to see a psychiatrist and replied: No. I want to see my wife.

Frankland decided not to talk about his experiences to Pauline or to his family. He said: When I got back, I thought Im alive and this is marvellous. Im going to forget everything Ive gone through. When he was nearly 100, he told a colleague he watched a TV programme about VE Day and had his first flashback. Thereafter he was amenable to talking about his experiences.

When Frankland left St Marys in 1977, he became an honorary consultant at Guys hospital in London, where he saw patients into his 90s. He also worked as an expert witness in court cases, and continued to write papers and attend conferences. Each year he presented the BSACI William Frankland award. He had a wide circle of friends and a great zest for life, remembered by one colleague as enjoying tea at the Ritz and riding a dodgem car aged 103.

Pauline died in 2002, and two years ago Frankland moved from his flat in Marylebone to accommodation in the Charterhouse, central London. When asked about his life, Frankland said: I have been very lucky.

He is survived by two sons and two daughters, 10 grandchildren and six great-grandchildren.

Alfred William Frankland, immunologist, born 19 March 1912; died 2 April 2020

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William Frankland obituary - The Guardian

TWC Discourse: Why Humanity Failed to Prevent COVID-19 Pandemic Despite Knowing About Its Possibility – The Weather Channel

Migrant workers from other states stand in a crowded, congested queue to collect food ration handed by the Worli police personnel in Mumbai, Maharashtra.

Short-sightedness while surveilling for potentially threatening infections, and failure to maintain transparency at the beginning of the COVID-19 outbreak, led to humanitys failure in preventing the viral disease from becoming a pandemic, according to two world-renowned, leading virologists.

The Weather Channel, in a live session, spoke to Dr Bellur S Prabhakar, Professor of Microbiology and Immunology, and Senior Associate Dean for Research, University of Illinois College of Medicine, Chicago; and Dr Polly Roy, Professor of Virology in London School of Hygiene and Tropical Medicine, UK about everything related to past and future of novel coronavirus.

When asked if anyone had seen such a large-scale pandemic coming, Dr Prabhakar explained: In the scientific community, it is extremely well known that virus pandemics are inescapable, and are likely to occur periodically.

Therefore, the world at large is trying its best to conduct active surveillance, which involves constantly looking out for potential infectious agents that can create global calamities like the one we are seeing right now.

Unfortunately, the governments are somewhat short-sighted, and they dont always invest sufficient time, energy, and financial resources to keep this active surveillance effective and uninterrupted. And when you fail to maintain active surveillance, infections can creep up on you, and suddenly get out of control. Thats what happened in the ongoing pandemic.

Dr Prabhakar has a broad experience in virology, immunology, and public health, and has been extensively working on autoimmune diseases for over 30 years.

Along with the lack of surveillance to detect the infection, the lack of transparency at the beginning of the COVID-19 outbreak, and the failure to distribute information on the virus widely and immediately also cost us dearly in the fight against this pandemic, adds Dr. Dr. Polly Roy.

Not getting the information very quickly cost us this time. Had we known from the beginning about the possibility of human-to-human transmission, then we would have taken apt precautions from the beginning, she said.

Recognising her contributions to virology research, Dr Roy has been conferred multiple awards and recognition, including the Indian Science Congress General President's Gold Medal, awarded by the Prime Minister of India and an Officer of the Order of the British Empire award, presented by the Queen. She is even involved with the development of vaccine for COVID-19, which can be a reality within next 12 to 18 months.

Both experts, however, remain optimistic about the future! If we learn from our past experiences, become more transparent about information, improve funding for research on infectious diseases, and make huge investments in public health systems worldwide, humanity will collectively become more equipped to successfully tackle such pandemics in the future, they conclude.

**

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TWC Discourse: Why Humanity Failed to Prevent COVID-19 Pandemic Despite Knowing About Its Possibility - The Weather Channel

Switzerland to Launch First COVID-19 Vaccine in August – Immunology Expert – UrduPoint News

GENEVA (UrduPoint News / Sputnik - 20th April, 2020) Swiss immunologists will be ready to start vaccinating people against COVID-19 domestically as early as August, Martin Bachmann, the head of the immunology chair at Bern University, said on Monday.

Bachmann is currently leading a group of experts from several Swiss universities for developing a so-called genetically synthesized vaccine based on virus-like particles. Such vaccines - in use for Hepatitis B, for example - work by breaking down the protein which the virus uses to attach to a cell.

"We plan to immunize first people in August and then to conduct a large vaccination in October," Bachmann said at a press conference with the Association of Foreign Correspondents at the UN Office in Geneva.

According to the expert, the novel coronavirus is genetically stable and, unlike influenza, is most likely to not require more than one vaccine in a relatively long period of time.

"Our strategy is to achieve the immunization of at least all of Switzerland's population within the next six months and then begin producing the vaccine for the global market. This is an ambitious goal, but I assure you we have good chances," Bachmann said.

The team of experts expects to distinguish the most effective working samples of the vaccines by the end of April for them to then be tested in the Zurich and Bern university hospitals.

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Switzerland to Launch First COVID-19 Vaccine in August - Immunology Expert - UrduPoint News

Immunology | medicine | Britannica

Immunology, the scientific study of the bodys resistance to invasion by other organisms (i.e., immunity). In a medical sense, immunology deals with the bodys system of defense against disease-causing microorganisms and with disorders in that systems functioning. The artificial induction of immunity against disease has been known in the West at least since Edward Jenner used cowpox injections to protect people from smallpox in 1796. But the scientific basis for immunology was not established until a century later, when it was recognized that: (1) proliferating microorganisms in the body cause many infectious diseases and (2) the body has certain chemical and cellular components that recognize and destroy foreign substances (antigens) within the body. This new understanding led to highly successful techniques of immunization that could mobilize and stimulate the bodys natural defenses against infectious disease.

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history of medicine: Immunology

Dramatic though they undoubtedly were, the advances in chemotherapy still left one important area vulnerable, that of the viruses. It was

It was only in the 20th century, however, that a comprehensive understanding was gained of the formation, mobilization, action, and interaction of antibodies and antigen-reactive lymphocytes, which are the two main active elements of the immune system. Modern immunology, besides using such basic techniques as vaccination, has become increasingly selective and sophisticated in its manipulation of the bodys immune system through drugs and other agents in efforts to achieve a desired therapeutic goal. Immunologic understanding is crucial to the treatment of allergies, which are themselves hypersensitive reactions by the bodys immune system to the presence of harmless antigens such as pollen grains. Immunosuppressive techniques use drugs to suppress the immune systems tendency to reject and attack antigenic bone grafts and organ transplants that have been medically introduced into the host tissue. Immunology also encompasses the increasingly important study of autoimmune diseases, in which the bodys immune system attacks some constituent of its own tissues as if it were a foreign body. The study of immune deficiencies has become an area of intensive research since the appearance of AIDS (acquired immune deficiency syndrome), a disease that destroys the bodys immune system and for which there is currently no cure.

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Immunology | medicine | Britannica

Temperatures and Pollen Counts Both Predicted to Rise This Week – Centralia Chronicle

It's on, allergy sufferers. Especially if you're sensitive to tree pollen.

Pollen counts are predicted to soar for the rest of this week as temperatures hit the mid-60s through most of the Puget Sound region on Wednesday and potentially 70 degrees on Thursday and Friday.

Pollen count is predicted to be "very high" Thursday through Sunday, according to the Northwest Asthma & Allergy Center.

Seattle-area allergy experts say that once your allergies are activated -- and apparently Western Washington is one of the best places to discover whether you're allergic to tree pollen -- you take a deep breath on a beautiful spring day like Wednesday and instantly your mast cells jump into action.

"The key feature of allergies and our immune system in general is also the reason they are persistent and frustrating," said Dr. Jakob von Moltke, an assistant professor of immunology at the UW School of Medicine. "You can go a whole winter without any issues, and then your immune system is triggered in seconds."

And allergists say the masks many people are wearing lately haven't really mitigated pollen allergy symptoms: sneezing, runny noses, postnasal drip, and itchy, puffy, watery eyes. (That said, you should wear one when you're out in public, to protect yourself and others from the novel coronavirus -- especially if you're sneezing, which launches your germs into the air.)

"If there is a difference (for allergy sufferers during the pandemic), it may be because people are not walking around outside a lot and are staying indoors, which is what we recommend," said Dr. Lahari Rampur, a UW Medicine allergy and immunology professor.

It can help to keep your windows closed, said Dr. Scott Itano, medical center chief at Kaiser Permanente Northgate Medical Center.

Most plants release their pollen in the middle of the night, so leaving windows open at night -- as many people do when the weather gets warm -- is one of the "worst things you can do," he said. "Then, you will be allergic inside and outside your house."

And if you are taking medicine to combat allergies, such as allergy pills and nasal steroid sprays, Itano recommends taking it at night before bed to help suppress the allergic reaction before it happens.

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Temperatures and Pollen Counts Both Predicted to Rise This Week - Centralia Chronicle