Category Archives: Immunology

Immunology

Spanish immunity expert on coronavirus: Those who have tested positive for antibodies are protected – EL PAS in English

Six months after the coronavirus began to spread across the world, there is still little understanding of how the human body responds to the infection. Knowing whether or not a person is immune to Covid-19 after recovering from the disease, and for how long, and why there are some people who do not contract the virus even though they are exposed to it and have no immunity, are some of the main questions immunologists are trying to answer.

Resolving these questions would reveal whether or not it would make sense to create immunity passports for the coronavirus, and shed light on what part of the population is at greatest risk to the SARS-CoV-2 virus.

Manel Juan, the head of the immunology department of the CBD-Clnic Hospital in Barcelona, is one of the researchers trying to solve these issues. This expert is currently coordinating a project between several medical centers in Europe to find out what happens in the immunological system of coronavirus patients when they have an excessive response to the virus (which is one of the ways that Covid-19 kills), and to create more accurate diagnostic tests. In some cases, current tests for Covid-19 fail to detect antibodies even though a person has recovered from the disease, or may even have developed immunity through exposure to other kinds of coronavirus that produce nothing more than cold-like symptoms.

Question. Do the current antibody tests allow us to know if we are immune to a new contagion?

Answer. The determining factor to know whether or not there is immunity are T-cells, which are the ones that offer protection. But the type of test needed to detect them is very complex, takes too long and is not practical. Thats why a test is done with a subrogated marker, which are the antibodies. If you are positive for IgG antibodies [the most common antibody in fighting bacterial and viral infections], we know that there has been a response by T-cells. Its all connected.

Q. If a person tests positive for Covid-19 antibodies, can they be considered protected? Or does it depend on their antibody levels?

A. Antibody levels are an approximation. It is a mistake to think of them as an absolute figure in a diagnosis. You can have low levels and this may be enough to know that the immune system is working. Saying that if you have more antibodies you will have more immunity, or longer-lasting immunity, is incorrect. Antibodies are not the only element that is immunizing and protecting us in the future. You can have a lot of antibodies yet immunity can last for a shorter period of time, and you can have practically none and it can last a long time. [...] Antibodies are not a real marker of immunity.

We know that patients who have had SARS, which is the most similar to Covid-19, have maintained antibodies for at least one or two years

Q. Does it make sense to create an immunity passport that offers a guarantee that a person is immune?

A. The passport makes sense from the point of view of knowing whether or not a person is immune, but the consequences of using this passport are complex. In the workplace, the existence of this passport could involve discrimination based on the presence or not of antibodies. Whats more, a person with a negative antibody test could also be protected. This is more of a political and social debate, even one for the unions.

Q. Is it possible for a person who tests positive for antibodies to contract the virus again or transmit it?

A. There have been millions of cases in the world and a clear reinfection due to a new entry of the virus once there were antibodies has not been detected. In cases where there was doubt as to whether this had happened, it was demonstrated that it was a reactivation of the same virus, which at that time, the immune system had not been able to eliminate sufficiently for it to not be detected by a PCR lab test. At any rate, among the millions of cases, there may be one who despite having the virus is not able to maintain protective immunity and avoid reinfection.

Q. Its also been suggested that a person with an asymptomatic infection will have a lower immunological response and could be reinfected, although with a less severe case. Is this something you rule out?

A. It has not been ruled out, but I believe that during the pandemic we have often forgotten the positive data that exists, or we have opted for the most negative possibility if there was still no data. This is not very scientific, although many scientists have argued this way. Researchers need data to affirm that this virus will last a long time or that a specific infection is protective or not. Until this is demonstrated, it is not possible to know. But science is also based on comparisons of similar situations. What we know now is that in patients who have had SARS, which is the most similar thing [to Covid-19] that we know of, even those who have not experienced symptoms, have maintained antibodies for at least one or two years.

A clear reinfection due to a new entry of the virus once there were antibodies has not been detected

Q. Your message is more positive than what is normally heard about the coronavirus.

A. I think that those who have transmitted the most negative version have based their views more on making sure that no one can later tell them but you said that than on actual science. Science is centered on the analysis of data, which is very often similar, because you never have 100% of biological figures. But we have enough information on viral infections, even on very similar viruses like SARS, which makes me think the way I do. We have to say that we will never know whether protection lasts one year until a year has passed, but all the data, for now, suggests that this is the case. [Spanish scientist and politician] Eduard Punset used to say that until proven otherwise, he would not die. In the end, he died. Looking around us everyone dies, so the most scientific thing to say is that everyone will die one day. This is similar. In biology, for now, what we know is that those who have antibodies are protected.

Q. If someone tested positive for antibodies two months ago, but negative today, would you say that person has lost their immunity?

A. You have to consider that they are immune, you cant worry about that. If they have generated IgG antibodies it is because there is a response from T-cells. It is the same thing that happens with vaccines. Vaccines work, although if you look later at the antibodies, you may not have them, but you are still protected, sometimes for five or 10 years. You dont keep measuring whether your antibody count has dropped. It doesnt work that way.

English version by Melissa Kitson.

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Spanish immunity expert on coronavirus: Those who have tested positive for antibodies are protected - EL PAS in English

Immunology

Reven Announces the Appointment of Eminent Physician-Scientist Fatih M. Uckun, M.D., Ph.D., Internationally Recognized for His Seminal Contributions…

GOLDEN, Colo.--(BUSINESS WIRE)--Reven Holdings, Inc. (Reven), a privately held clinical stage biotechnology and pharmaceutical company dedicated to the discovery and development of novel treatment platforms for cancer, viral illnessesincluding COVID-19and inflammatory disorders, today announced the appointment of Dr. Fatih M. Uckun as its Chief Medical Officer and Chief Scientific Officer.

In his new position at Reven, Dr. Uckun will provide executive oversight for Revens global Research & Development and clinical programs. In addition, Dr. Uckun will contribute medical-scientific leadership and direction for Revens basic and translational research activities, R&D and clinical development programs in cancer, transplantation immunology, sepsis, metabolic disorders, inflammatory disorders, and the acute respiratory distress syndrome (ARDS) in patients with sepsis, including COVID-19 patients with viral sepsis.

Dr. Uckun stated, It is an exceptionally exciting time to join Reven to support a global registration strategy for its unique RJX platform. The components of RJX exhibited very promising activity in clinical studies involving ARDS patients and non-clinical studies in animal models of ARDS. The published data from these clinical, and recent non-clinical, studies confirming its unique mechanism of action, provide the medical-scientific rationale for Revens clinical development strategy for RJX. The clinical study in COVID-19 patients is a logical next step. I very much look forward to working with the talented and experienced leadership team of Reven and our collaborators. The goal is to diligently advance the RJX clinical trial program with the vision of developing RJX-based new treatments for COVID-19 patients, as well as patients with difficult-to-treat forms of cancer and inflammatory disorders who are in urgent need for therapeutic innovations.

As we move forward with our planned clinical trial of Rejuveinix (RJX) for treatment of COVID-19, Dr. Uckuns decades of drug development experience will be critical in successful execution and the establishment of effective collaborations with other stakeholders, said Peter Lange, Chief Executive Officer of Reven. Dr. Uckun embodies Revens core values: dedication to patients, passion for science, and excellence in execution. I am delighted to have the opportunity to welcome Dr. Uckun as part of Revens leadership team.

About Dr. Uckun

Dr. Uckun is an elected Member of the American Society for Clinical Investigation (ASCI), an honor society for physician-scientists, and an active member of several professional organizations. He received numerous awards for his work on monoclonal antibodies, recombinant cytokines and fusion proteins, radiation sensitizers, kinase inhibitors and targeted therapeutics for difficult-to-treat cancers, including the Stohlman Memorial Award of the Leukemia Society of America, the highest honor given to a Leukemia Society Scholar. He has served as a member of several editorial boards and National Institutes of Health grant review/special emphasis panels.

Dr. Uckun earned his doctoral degrees at the University of Heidelberg, Germany, where he also served as an active member of the autologous bone marrow transplant and peripheral stem cell transplant clinical research teams of the Tumor Center. Dr. Uckun completed his residency training in pediatrics, clinical fellowship training in Hematology/Oncology/Blood and Bone Marrow Stem Cell Transplantation, as well as postdoctoral research training in immunology and microbiology at the University of Minnesota. Dr. Uckun has more than thirty years of professional experience in developmental therapeutics with a special emphasis on targeted therapeutics/precision medicines and biopharmaceuticals. He has published more than 500 peer-reviewed papers, authored numerous review articles and book chapters, and is an inventor on numerous patents.

For eleven years, Dr. Uckun worked as a Professor of Bone Marrow Transplantation, Therapeutic Radiology-Radiation Oncology, Pharmacology, and Pediatrics as well as Director of the Biotherapy Institute at the University of Minnesota, where he became the first recipient of the Endowed Hughes Chair in Biotherapy. At the Keck School of Medicine of the University of Southern California, he was a Professor and Head of Translational Research in Leukemia and Lymphoma of the CCBD and a Principal Investigator of the Stem Cell-Regenerative Medicine Initiative for six years. From 2012 to 2015, Dr. Uckun served as chair of the Biotargeting Working Group and a Member of the Coordination and Governance Committee of the National Cancer Institute Alliance for Nanotechnology in Cancer.

Dr. Uckun has held executive positions in multiple biotechnology companies and has extensive regulatory experience. Prior to joining Reven, Dr. Uckun served as Vice President of Scientific Solutions at Worldwide Clinical Trials, Chief Medical Officer of Oncotelic and Mateon Therapeutics, Head of Immuno-Oncology at Ares Pharmaceuticals, and as Executive Medical Director and Strategy Lead in Global Oncology and Hematology at Syneos Health. Previously, he was Vice President of Research and Clinical Development at Nantkwest, and Chief Scientific Officer of both Jupiter Research Institute and Paradigm Pharmaceuticals. Dr. Uckun is a former Vice Chair of the New Agents Committee as well as a Member of the Leukemia Steering Committee of the Childrens Cancer Study Group, an NCI-funded cooperative clinical trials consortium that coordinated pediatric and adolescent/young adult leukemia trials at 120 institutions in the U.S., Canada, Australia and Europe.

Dr. Uckun has deep knowledge and experience in the treatment of infectious diseases and their complications. In particular, he has extensive experience in viral, fungal, and bacterial infections of immunocompromised hosts, septic shock, ARDS, systemic capillary leak syndrome and cytokine release syndrome (CRS). He served as the Principal Investigator of a virus neutralizer project funded by the Defense Advanced Research Projects Agency (DARPA) as part of its unconventional countermeasures program. Dr. Uckun directed several federally funded virology/innate immunity projects and published numerous peer-reviewed papers on RNA viruses and anti-viral agents.

About Rejuveinix (RJX)

RJX is an intravenous (IV) formulation of known physiologically compatible compounds that is being developed for more effective supportive therapy of patients with sepsis, including COVID-19 patients with viral sepsis and acute respiratory distress syndrome (ARDS). The RJX formulation is a solution of buffered acid products, electrolyte components, and vitamins, including ascorbic acid, cyanocobalamin, thiamine hydrochloride, riboflavin 5 phosphate, niacinamide, pyridoxine hydrochloride, and calcium d-pantothenate, and magnesium sulfate heptahydrate, a mineral with a negative oxidation-reduction potential. The components of RJX exhibited promising activity in clinical studies involving ARDS patients and/or non-clinical studies in animal models of ARDS. The published data from these clinical and non-clinical studies provided the medical-scientific rationale for Revens clinical development strategy for RJX and a clinical study in COVID-19 patients. The clinical tolerability of RJX was confirmed in a recently completed double blind, placebo-controlled Phase 1 dose-escalation study in healthy volunteers (ClinicalTrials.gov Identifier: NCT03680105).

About Reven Holdings, Inc.

Reven Holdings, Inc., a Delaware corporation, through its Golden, Colorado-based operating company Reven, LLC, is a biopharmaceutical company. Revens vision is to make a difference in the world by making its products accessible to everyone suffering the effects of vascular and metabolic related diseases. Reven is committed to being the premier, research-intensive biopharmaceutical company that advances the health and well-being of people around the world. Its primary product, Rejuveinix (RJX), targets patients suffering from COVID-19, sepsis, vascular and metabolic related diseases as well as specific patient populations suffering PAD and other cardiovascular related medical conditions.

Revens Cautionary Note on Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, included in this communication regarding strategy, future operations, future financial position, prospects, plans and objectives of management are forward-looking statements. Words such as may, on-track, expect, anticipate hope, vision, optimism, design, exciting, promising, will, conviction, estimate, intend, believe and similar expressions are intended to identify forward-looking statements. Forward-looking statements contained in this press release include, but are not limited to, statements about future plans, the progress, timing, clinical development, scope and success of future clinical trials, the reporting of clinical data for the companys product candidates and the potential use of the companys product candidates to treat various disease indications. Each of these forward-looking statements involves risks and uncertainties, and actual results may differ materially from these forward-looking statements. Many factors may cause differences between current expectations and actual results, including unexpected safety or efficacy data observed during preclinical or clinical studies, clinical trial site activation or enrollment rates that are lower than expected, changes in expected or existing market competition, changes in the regulatory environment, failure of collaborators to support or advance collaborations or product candidates, and unexpected litigation or other disputes. These risks are not exhaustive; the company faces known and unknown risks, including the risk factors described in the companys periodic SEC filings. Forward-looking statements are based on expectations and assumptions as of the date of this press release. Except as required by law, the company does not assume any obligation to update forward-looking statements contained herein to reflect any change in expectations, whether as a result of new information regarding future events, or otherwise.

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Reven Announces the Appointment of Eminent Physician-Scientist Fatih M. Uckun, M.D., Ph.D., Internationally Recognized for His Seminal Contributions...

Immunology

We developed tools to study cancer in Tasmanian devils. They could help fight disease in humans – The Conversation AU

Emerging infectious diseases, including COVID-19, usually come from non-human animals. However our understanding of most animals immune systems is sadly lacking as theres a shortfall in research tools for species other than humans and mice.

Our research published today in Science Advances details cutting edge immunology tools we developed to understand cancer in Tasmanian devils. Importantly, these tools can be rapidly modified for use on any animal species.

Our work will help future wildlife conservation efforts, as well as preparedness against potential new diseases in humans.

Tasmanian devil populations have undergone a steep decline in recent decades, due to a lethal cancer called devil facial tumour disease (DFTD) first detected in 1996.

A decade after it was discovered, genetic analysis revealed DFT cells are transmitted between devils, usually when they bite each other during mating. A second type of transmissible devil facial tumour (DFT2) was detected in 2014, suggesting devils are prone to developing contagious cancers.

In 2016, researchers reported some wild devils had natural immune responses against DFT1 cancers. A year later an experimental vaccine for the original devil facial tumour (DFT1) was tested in devils artificially inoculated with cancer cells.

While the vaccine didnt protect them, in some cases subsequent treatments were able to induce tumour regression.

But despite the promising results, and other good news from the field, DFT1 continues to suppress devil populations across most of Tasmania. And DFT2 poses an additional threat.

Read more: Deadly disease can 'hide' from a Tasmanian devil's immune system

In humans, there has been incredible progress in treatments targeting protein that regulate our immune system. These treatments work by stimulating the immune system to kill cancer cells.

Our teams analyses of devil DNA showed these immune genes are also present in devils, meaning we may be able to develop similar treatments to stimulate the devil immune system.

But studying the DNA blueprint for devils takes us only so far. To build a strong house, you need to understand the blueprint and have the right tools. Proteins are the building blocks of life. So to build effective treatments and vaccines for devils we have to study the proteins in their immune system.

Until recently, there were few research tools available for this. And this problem was all too familiar to researchers studying immunology and disease in species other than humans, mice or rats.

You could build a house with just a saw, hammer and nails but a better and faster build requires a larger, more versatile toolbox.

In our new research, weve added more than a dozen tools to the toolbox for understanding tumours in Tasmanian devils. These are Fluorescent Adaptable Simple Theranostic proteins or simply, FAST proteins.

The term theranostic merges therapeutic and diagnostic. FAST proteins can be used as a therapeutic drug to treat a disease, or as a diagnostic tool to determine its cause and better understand it.

A key feature of FAST proteins is they can be tagged with a fluorescent protein marker, and can be released from the cells that we engineered in the lab to make them.

This way, we can collect and observe how the proteins attach and interact with other proteins without needing to add a tag later in the process.

To understand this, imagine trying to use a tiny key in a tiny lock in the dark. It would be difficult, but much easier if both were tagged with a coloured light. In the context of the immune system, its easier to understand what we need to turn on or off if we can see where the proteins are.

By mapping how proteins within the devils immune system interact, we can find better ways to stimulate the immune system.

The FAST system is also adaptable, meaning new targets can be cut-and-pasted into the system as theyre identified, like changing the bits on a drill. Therefore, its useful for studying the immune systems of other animals too, including humans.

Also, the system is simple enough that most people with basic cell culture and molecular biology experience could use it.

Read more: A virus is attacking koalas' genes. But their DNA is fighting back

Cancer cells in humans and animals can travel via the bloodstream to spread, or metastasise, throughout the body. Identifying single tumour cells in blood can shed light on how cancer invades devils organs and kills them.

Using FAST tools, we discovered CD200 a protein that inhibits anti-cancer responses in humans is highly expressed in devils. With FAST tools, we were able to mix DFT2 cancer cells into devil blood and pick them out, despite there being about one cancer cell for every 1,000 blood cells.

CD200 is a powerful off switch for the immune system, so identifying this off switch allows us it can help us produce a vaccine that disables the switch.

By rapidly sifting out the best ways to stimulate the devils immune system, FAST tools are accelerating our research into developing a preventative vaccine to protect devils from DFT.

COVID-19 has once again brought emerging infectious diseases onto the global stage. The ability to rapidly develop immunology tools for new species means we can jump into action when a new virus jumps into humans.

Additionally, species are going extinct at an alarming rate, and wildlife disease is increasingly threatening conservation efforts.

Understanding how the immune systems of other animals fight diseases could provide a blueprint for developing vaccines and therapeutics to help them.

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We developed tools to study cancer in Tasmanian devils. They could help fight disease in humans - The Conversation AU

Immunology

SARS-CoV-2 Immunity Likely To Be Higher Than Antibody Testing Has Shown – Technology Networks

A recent preprint study published in bioRxiv, suggests that many people who contract SARS-CoV-2 but have mild or no clinical signs still develop so-called T-cell-mediated immunity to the virus, even in the absence of a positive antibody test. The researchers conclude that this is likely to mean that public immunity is probably higher than antibody testing has so far suggested.The multi-centered team based at the Karolinska Institutet and Karolinska University Hospital performed immunological analyses on over 200 people, including unexposed individuals as well as exposed family members and individuals with acute or convalescent COVID-19. From this they mapped the functional and phenotypic landscape of SARS-CoV-2-specific T-cell responses.

T cells are an important subset of our immune cells, pivotal in the immune systems ability to recognize and destroy virus-infected cells in our bodies and mount an immune response on re-exposure to a previously encountered infection. Cytotoxic T cells are essential in destroying virus-infected cells, whilst a phenotypically distinct group of T cells, sometimes called memory T cells, are important in the development of long-term immunity.

In a University press release, Marcus Buggert, Assistant Professor at the Center for Infectious Medicine, Karolinska Institutet, and one of the papers main authors commented, Advanced analyses have now enabled us to map in detail the T-cell response during and after a COVID-19 infection. Our results indicate that roughly twice as many people have developed T-cell immunity compared with those who we can detect antibodies in.

The team showed that even in the absence of a detectable antibody response, a robust memory T cell response could be measured in many individuals, akin to the response seen following vaccination against other viral infections.

Professor Danny Altmann, British Society for Immunology spokesperson and Professor of Immunology at Imperial College London, said, Among the many studies of cellular (T cell) immunity to SARS-CoV-2 that have appeared in the past few months, this is one of the most robust, impressive and thorough in the approaches used. It adds to the growing body of evidence that many people who were antibody-negative actually have a specific immune response as measured in T-cell assays, confirming that antibody testing alone under-estimates immunity.

Whilst this could be good news for public health, T-cell testing is less straight-forward than antibody detection, and so may be less accessible for mass testing endeavors.

Altmann continued, The big unknown for the moment is which parameters of immunity offer the most faithful indicator of true, protective immunity from future infection. So far, there is a sense from some studies that functional, virus-neutralizing antibody is one such correlate of protection. We urgently need experimental studies to help confirm whether T-cell immunity alone can give protection. This sentiment was echoed by Buggert. Larger and more longitudinal studies must now be done on both T cells and antibodies to understand how long-lasting the immunity is and how these different components of COVID-19 immunity are related.

This article is based on research findings that are yet to be peer-reviewed. Results are therefore regarded as preliminary and should be interpreted as such. Find out about the role of the peer review process in research here. For further information, please contact the cited source.

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SARS-CoV-2 Immunity Likely To Be Higher Than Antibody Testing Has Shown - Technology Networks

Immunology

Nobelists: scientists ‘circled the wagons’ over coronavirus threat – Times Higher Education (THE)

Scientists have circled the wagons during the coronavirus pandemic, Nobel laureates have argued, and been afraid to have a truly open debate about whether the virus is as deadly as feared and if lockdowns are justified.

Michael Levitt, a winner of the chemistry prize in 2013 and, since February, an outspoken contrarian voice on the pandemic, said he had received only abuse from fellow scientists for questioning predictions of catastrophic death tolls.

Using statistical analysis across different countries with varying degrees of lockdown, Professor Levitt has repeatedly and publicly argued that the virus slows far earlier than would be expected if everyone was susceptible, possibly indicating some kind of prior immunity.

Just 15 per cent of the population needs to be infected to reach herd immunity, he believes.

The data had very clear things to say, he told the Lindau Nobel Laureate Meeting, an annual gathering of prizewinning academics and young researchers, itself moved online due to coronavirus.

But when sharing his results, nobody said to me, let me check your numbers. They all just said, stop talking like that, he said.

At the beginning of the crisis, scientists failed to collectively ask basic questions like does this thing grow exponentially, said Professor Levitt, Robert W. and Vivian K. Cahill professor in cancer research at Stanford University.

Physicists and theoretical chemists who understand trajectories were often better qualified to analyse the pandemic than epidemiologists, who see their job not as getting things correct, but preventing an epidemic, leading them to overstate the threat, he argued in a debate on the role of science in a crisis.

We should never have listened to the epidemiologists, Professor Levitt said. They have caused hundreds of billions of dollars worth of suffering and damage, mainly on the younger generation, he said. Its going to make 9/11 look like a baby story.

Instead of one or two voices dominating the debate, scientific institutions like the Royal Society should have formed a committee back in February to convene a range of experts, Professor Levitt argued.

Instead, we let economics and politics dictate the science, he said. For me, the worst opposition I got was from very, very prominent scientists, who were so scared that the non-scientists would break quarantine and infect them.

Many experts have pushed back against Professor Levitts arguments. As yet, there is no proof of widespread immunity to Covid-19, and the spread has slowed in many countries following lockdowns.

Still, Professor Levitt was not the only laureate to worry that scientists had hidden uncertainty during the pandemic. Saul Perlmutter, a physics prizewinner in 2011, said when scientists felt under attack because the democratic system fails to heed them, there was a tendency to circle the wagons and hide all the conversations that need to happen.

Scientists get scared about whether politicians will respond to them and so take a frozen moment of science and stick to that line until somebody hears it in the political world, said Professor Perlmutter, Franklin W. and Karen Weber Dabby of physics at the University of California, Berkeley.

But Peter Doherty, an immunology expert who won the medicine prize in 1996, defended other aspects of the scientific response to coronavirus, arguing that in the hunt for treatments and a vaccine, researchers had worked with extraordinary speed, and with extraordinary cooperation.

I think science comes out of it very well in fact, and I think thats the general perception, said Professor Doherty, laureate professor of microbiology and immunology at the University of Melbourne.

david.matthews@timeshighereducation.com

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Nobelists: scientists 'circled the wagons' over coronavirus threat - Times Higher Education (THE)

Immunology

In what does Cuba’s genetic study of patients recovered from COVID-19 consist of? – OnCubaNews

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The appearance at the end of 2019 of a new coronavirus and its rapid spread throughout the world until it became a pandemic, has put the scientific community to work with an intensity rarely observed.

Although currently the main international research is focused on the search for the vaccine, the mass immunization as the only way to stop such a contagious virus, another question arises from a characteristic of the virus, or rather how each person responds to the contagion: Why do some die from COVID-19 and others dont get to feel the slightest symptom?

The answer may lie in genetics; thats why Cuba launched a research that takes this factor into account in the response of those who suffered from the disease and those who have already been discharged.

According to the director of the National Center for Medical Genetics, Beatriz Marcheco, the project includes clinical-epidemiological, laboratory, basically hematological, immunological, and DNA studies.

The research began its clinical stage in early June, in the provinces of Pinar del Ro, Cienfuegos and Las Tunas, as well as the municipality of La Lisa, in Havana.

The study seeks to find out the blood group and factor of each individual and to study the subpopulations of lymphocytes that participate in the immune response, using flow cytometry and Elisa assays, explained the specialist in an interview with Granma daily.

Cuba studying genetic factors of patients recovered from COVID-19

After taking the blood sample, these are taken to the laboratories of the National Center for Medical Genetics to submit them to the tests related to the study, in which the Immunoassay Center also participatesthe Immunoglobulin g test is done there to identify if the person has specific antibodies against the SARS-CoV-2 virusand the Center for Molecular Immunology.

The results could help scientists to characterize all the factors related to the incidence of the disease, its lethality and clinical and therapeutic approach in each case.

If, for example, an individual is identified as being more vulnerable to symptoms or severity, strategies to prevent such severity could be applied with early therapeutic interventions, Marcheco added.

By identifying the genetic factors related to clinical severity, we will be taking a significant step at the same time in the objective of developing personalized treatments that respond to individual genetic characteristics, strengthening the implementation of population-based prevention strategies, she explained.

The studies we are conducting also allow us to appreciate how each person is recovering individually from a disease that strongly damages the immune system. Therefore, the research project contains actions that are part of the strategy of our health system in the post-COVID-19 stage of each patient, she said.

The screening also includes the study of a first-degree relative (mother, father, son or daughter, brother or sister) who lives with the positive case and was exposed to the virus, but had no symptoms nor was positive for COVID-19.

The study of these subjects can be very useful in identifying protective factors against the virus and that is also important in terms of prevention, the scientist concluded.

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In what does Cuba's genetic study of patients recovered from COVID-19 consist of? - OnCubaNews

Immunology

Health Matters: Repeat of Covid-19 Update – Fact from Fiction – Red River Radio

Airs Thursday, July 2, 2020, at 6 p.m. REPEAT -Information about COVID-19 in the news and on social media can be confusing. Tune in for Health Matters, Thursday at 6 p.m. Dr. Randall Brewer will be joined by Dr. Andrew Yurochko, PhD, Professor of Microbiology and Immunology, and Dr. Jeremy Kamil, Associate Professor of Microbiology and Immunology, both with LSU Health Shreveport, to help us separate fact from fiction and also tell us if the virus is showing mutations. This is a repeat broadcast and no calls will be taken.

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Health Matters: Repeat of Covid-19 Update - Fact from Fiction - Red River Radio

Immunology

Dragons of immunology | Opinion – Chemistry World

Since everyone is being forced these days to think about immunology, lets consider it in terms of chemistry and drug discovery. You can get two very different perspectives based on where you stand. From one view, inflammation and immune response might look like a wonderfully productive area for small molecules. Aspirin, dexamethasone, ibuprofen, hydrocortisone there are classic drugs that work on and near these pathways and have been used successfully by uncounted millions of patients. In the modern era, the list of best-selling prescription drugs prominently features antibodies and fusion proteins aimed at immunologic targets such as TNF-alpha and CD20, as treatments for inflammatory diseases from rheumatoid arthritis to cancer.

But from another vantage point, the whole field is full of trap doors, dead ends, and irritable dragons. Dexamethasone and other such steroids have such powerful effects (and powerful side effects) that they have to be administered carefully and for short periods. Thats why compounds such as ibuprofen were hailed as being anti-inflammatories that (good news!) werent steroids. The list of potential side effects for those antibodies is also long and impressive. To pick a particularly dramatic example that many will recall, a 2006 attempt by TeGenero to create a super-agonist for the T-cell receptor CD28 led to catastrophic effects in the Phase 1 volunteers, many of whom barely survived the initial dose.

Thats what the immune system has to offer: tremendous power, but power that can be aimed in all sorts of directions. And because immunology itself is so wildly, insanely complicated, there are a bewildering number of potential targets to think about. Were looking at hundreds of millions of years of evolutionary tinkering; there are layers upon layers of tangled, interlocking signaling pathways and mechanisms. Theres the innate immune system always on but rather nonselective and the adaptive system that features a gigantic combinatorial chemical library of antibodies that we all carry around with us for our entire lives slower to get going, but capable of feats of recognition that we still have trouble matching in the laboratory. Those aeons of evolution have been a walk down the narrow path between too little activity, opening the door to fatal infections, and too much, leading to autoimmune syndromes and responses to an infection that are worse than the disease itself. Its little wonder that the systems are encrusted with regulatory loops, flywheels, and gear-shifting mechanisms.

As usual, most of what drug discovery has to offer is an assortment of grit, sand, and spanners to throw into this apparatus. We are far, far better at shutting particular enzymes and receptors down than we are in turning any particular signal up. When you do see a drug mechanism that enhances some sort of activity, odds are good that it works by inhibiting something else that was in turn suppressing the desired target. A great number of interesting ideas in the field dont seem to be amenable to small-molecule manipulation at all, which is where those antibodies come in. The requisite binding sites can be too large and the selectivity needed to target them may be too great for anything other than a good-sized protein to have a chance.

Thats meant that immunology has been a proving ground for new therapeutic ideas and new modes of action. Monoclonal antibodies and fusion proteins are just the beginning. Mechanisms targeting protein expression, intra- and extracellular localisation, degradation, and the intricate varieties of post-translational modification are all highly relevant to immune and inflammation pathways. Add in the number of genetic immunological problems that can occur in the population, which would be targets for gene therapy or RNA mechanisms, and you have the whole range of cutting-edge drug research being brought in.

Most of these are too early in the process to be of likely use against the Covid-19 pandemic, of course. But we are learning a great deal about immunology very quickly under these conditions, with the huge efforts going into characterising the pathogen; treating the overactive immune response to it; and developing antibodies and vaccines against it. Well come out of this, and well come out of it with more tools and more knowledge than when we went in all acquired at a faster pace than we ever would have achieved otherwise. Lets take the benefits where we can find them!

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Dragons of immunology | Opinion - Chemistry World

Immunology

What’s the answer to slowing the spread of COVID-19 for older adults? – Aspen Times

Theres a lot of stupid floating around out there.

Thats what South Carolina Gov. Henry McMaster said during a recent news conference in which he pleaded with the public to make better decisions to slow the spread of COVID-19.

Thats the best quote ever its how you explain the recent surge (in cases), said Dr. Michael Schmidt, PhD, a professor of microbiology and immunology at the Medical University of South Carolina.

Dr. Schmidt is the guest host of an upcoming webcast, How Colorado Can Work Smarter to Slow the Spread of COVID-19 in Older Adults, presented by Renew Senior Communities. Renew CEO Lee Tuchfarber is co-hosting.

This is a plague for which the human race has a choice, Dr. Schmidt said. We already know how to stop this virus dead in its tracks.

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Much of the discussion will focus on how we can do our part as a society to slow the spread, but Dr. Schmidt will also discuss promising light at the end of the tunnel. From the potential that oral polio vaccines can safely and cheaply protect the U.S. population to excitement over bluetooth technology expanding the efficiency of contact tracing, Dr. Schmidt said various stop-gap measures could make a big difference until theres a COVID-19 vaccine.

The only thing more infectious than this virus is hope, he said.

Personal responsibility

The way we control the virus is really straightforward, Dr. Schmidt said its hygiene.

Wearing a mask to protect others, washing your hands and keeping a physical distance of at least six feet from other people are the most effective safety precautions.

If weve learned one thing, there are a lot of folks out there who are infected and dont know it, he said. The mere act of speech actually can spread the virus. So, if youre out carrying your business and talking, wear a mask.

Physical distancing is your only hope if youre not wearing a mask. The hope being that the virus dissipates in the air before smashing into your face.

Many medical folks are wearing face shields because the virus can come in from your tear ducts, Dr. Schmidt said.

As for hand hygiene, simple soap and water is all you need. The Centers for Disease Control and Prevention recommends washing hands for at least 20 seconds.

Strict safety protocols have proven to work at Renew Senior Livings two communities in Aurora and Glenwood Springs. Tuchfarber said all residents at both communities have remained COVID-free while a great number of the senior living facilities in Colorado have experienced outbreaks.

Renew put various safety measures in place for staff before they enter the building, and theyve even provided staff with meals to take home to their families to decrease their need to go to the grocery store. Much of this decision-making is data-driven, with various phases of safety measures implemented depending on the R-naught (Ro), which is the estimate of the number of people to whom each infected person spreads the virus.

Theres an inherent spreadability of the virus itself, but theres also an environmental factor, Tuchfarber said. So behavior can really affect the Ro.

What: How Colorado Can Work to Slow the Spread of COVID-19 for Older Adults, a webcast talk series presented by Renew Senior Communities.

When: Wednesday, July 1, 3 to 4 p.m.

Where: Register for free at renewsenior.com.

Featured co-host: Dr. Michael Schmidt, PhD, is a professor of microbiology and immunology at the Medical University of South Carolina. He is a well-published expert in the area of

infectious disease control and pandemics. He ran the American Society for Microbiology

and set its research priorities for vaccines and testing. He hosts a podcast called, This

Week in Microbiology. Dr. Schmidt is an advisor to MicrogenDx, the second largest next

generation testing lab in the U.S.

Testing

Testing serves a vital role in understanding and controlling the spread of COVID-19, Dr. Schmidt said. He points to data from Taiwan, a densely populated island that has managed to keep its number of confirmed cases of COVID-19 to date to less than 450 thanks to aggressive testing and contract tracing.

Going forward, given that we know there is significant asymptomatic and presymptomatic transmission of the virus, pre-emptive testing may be a way we help slow the spread of the virus in areas that have suddeningly seen a surge in an increase in new cases, he said. Simply, local areas may wish to routinely screen random members within their community looking for an up-turn in the number of cases. Such a program will be especially important to companies with public-facing employees, so that they can ensure that their employees and customers are as safe as possible.

Renew is working on a strategy for preemptive testing rather than waiting for a positive case and then reacting to it. Tuchfarber said Renew should be implementing that new protocol very soon.

Preemptive testing of all staff on a regular basis, unprompted by a positive test result, is presently a rarity in our industry, but is an important measure to assure safety. We are preparing to integrate this program in our COVID-19 safety regimen, Tuchfarber said. This is an extra measure of safety that we feel strongly about taking.

Facilitating a global response

In an effort to facilitate a global response, scientists are looking at three strategies: diagnostics, therapeutics and vaccines.

Diagnostics essentially look at how we can slow the spread faster and better, while therapeutics focus on the use of drugs.

If were going to restart the economy, we need two to three drugs so the virus doesnt adapt to the drugs like it did with HIV and hepatitis C in the 1980s, Dr. Schmidt said.

Vaccines are the area for which Dr. Schmidt is truly excited. There are more than 90 candidate vaccines currently being studied, with microbiologists, structural biologists, physiologists and others all pulling in the same direction.

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What's the answer to slowing the spread of COVID-19 for older adults? - Aspen Times

Immunology

Cause of Common Autoinflammatory Disease May Have Protected Ancestors From Plague – Technology Networks

Researchers have discovered that Mediterranean populations may be more susceptible to an autoinflammatory disease because of evolutionary pressure to survive the bubonic plague. The study, carried out by scientists at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, determined that specific genomic variants that cause a disease called familial Mediterranean fever (FMF) may also confer increased resilience to the plague.

The researchers suggest that because of this potential advantage, FMF-causing genomic variants have been positively selected for in Mediterranean populations over centuries. The findings were published in the journal Nature Immunology.

Over centuries, a biological arms race has been fought between humans and microbial pathogens. This evolutionary battle is between the human immune system and microorganisms trying to invade our bodies. Microbes affect the human genome in many ways. For example, they can influence some of the genomic variation that accumulates in human populations over time.

"In this era of a new pandemic, understanding the interplay between microbes and humans is ever critical," said Dr. Dan Kastner, NHGRI scientific director and a co-author on the paper. We can witness evolution playing out before our very eyes.

One such microbe is Yersinia pestis, the bacterial agent responsible for a series of well-documented bubonic plague(link is external) epidemics that led to over 50 million deaths.

FMF, like the plague, is an ancient disease. It is the most common periodic fever syndrome, and symptoms of FMF include recurrent fevers, arthritis, rashes and inflammation of the tissues that line the heart, lungs, and abdominal organs. FMF may also lead to renal failure and death without treatment. The disease appears across the Mediterranean region and mostly affects Turkish, Jewish, Armenian and Arab populations.

Genomic variants in the MEFV gene cause FMF. MEFV encodes a protein called pyrin. In healthy people, pyrin plays a role in the inflammatory response of the body. Pyrin is activated when there is an immune response (for example, in the event of an infection). Pyrin increases inflammation and the production of inflammation-related molecules.

In contrast, FMF patients produce abnormal pyrin because of genomic variants (mutations) in the MEFV gene. Mutated pyrin does not need an infection or other immune trigger to be activated; rather, it is able to directly predispose people to seemingly unprovoked episodes of fever and inflammation.

The MEFV mutations also have other usual properties. Researchers have discovered that people with only one copy of a MEFV genomic variant that causes FMF do not get the disease. Also, prior to effective treatment, those with two copies have high mortality rate by the age of 40, but usually live long enough to have children.

Despite the lower survival rate, almost 10% of Turks, Jews, Arabs and Armenians carry at least one copy of an FMF-causing genomic variant. If chance were the only factor, that percentage would be much lower.

The researchers proposed that this higher percentage was a consequence of positive natural selection, which is an evolutionary process that drives an increase in specific genomic variants and traits that are advantageous in some way.

"Just like sickle cell trait is positively selected for because it protects against malaria, we speculated that the mutant pyrin in FMF might be helping the Mediterranean population in some way," said Jae Jin Chae, Ph.D., senior author of the paper and a staff scientist in NHGRI's Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch. "The mutant pyrin may be protecting them from some fatal infection."

The team turned to Yersinia pestis, the infamous bubonic plague-causing bacterium, as a possible candidate for driving the evolutionary selection for FMF mutations in the Mediterranean population.

It turns out Yersinia pestis contains a particular molecule that represses the function of pyrin in healthy individuals. In doing so, the pathogen suppresses the body's inflammatory response to the infection. This way, the body cannot fight back.

"Inflammation is a process in which white blood cells protect the body from infection. From the host's point of view, inflammation helps us survive. From the bacteria's point of view, inflammation is something to be evaded by any means available," said Daniel Shriner, Ph.D., staff scientist in the Center for Research on Genomics and Global Health at NHGRI.

Researchers were struck by the fact that Yersinia pestis affects the very protein that is mutated in FMF. They considered the possibility that FMF-causing genomic variants may protect individuals from the bubonic plague caused by Yersinia pestis.

The idea that evolution would push for one disease in a group to fight another may seem counterintuitive. But it comes down to what is the least bad option.

The average mortality rate of people with bubonic plague over centuries has been as high as 66%, while, even with a carrier frequency of 10%, less than 1% of the population has FMF. Theoretically, the evolutionary odds are in the latter's favor.

But first, the team had to verify if two of the genomic variants that cause FMF had indeed undergone positive selection in Mediterranean populations.

For this, they performed genetic analysis on a large cohort of 2,313 Turkish individuals. They also examined genomes from 352 ancient archaeological samples, including 261 from before the Christian era. The researchers tested for the presence of two FMF-causing genomic variants in both groups of samples. They also used population genetics principles and mathematical modeling to predict how the frequency of FMF-causing genomic variants changed over generations.

"We found that both FMF-causing genomic variants arose more than 2,000 years ago, before the Justinian Plague and the Black Death. Both variants were associated with evidence of positive selection," said Elaine Remmers, Ph.D., associate investigator in NHGRI's Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch.

Researchers then studied how Yersinia pestis interacts with FMF-causing genomic variants. They took samples of particular white blood cells from FMF patients. In addition, they took samples from people who carry just one copy of the genomic variants (hence, do not get the disease).

The team found that Yersinia pestis does not reduce inflammation in white blood cells acquired from FMF patients and people with one copy of FMF-causing genomic variants. This finding is in stark contrast to the fact that Yersinia pestis reduces inflammation in cells without FMF-associated mutations.

The researchers thought that if Yersinia pestis does not reduce inflammation in people with FMF, then perhaps this could potentially increase patients' survival rate when infected by the pathogen.

To test this hypothesis, the researchers genetically engineered mice with FMF-causing genomic variants. They infected both healthy and genetically engineered mice with Yersinia pestis. Their results showed that infected mice with the FMF-causing genomic variant had significantly increased survival as compared to infected healthy mice.

These findings, in combination, indicate that over centuries, FMF-causing genomic variants positively selected in Turkish populations play a role in providing resistance to Yersinia pestis infection. Whether the same is true for other Mediterranean populations remains to be seen. The study offers a glimpse into the unexpected and long-lasting influence of microbes on human biology.

ReferencePark, Y.H., Remmers, E.F., Lee, W. et al. Ancient familial Mediterranean fever mutations in human pyrin and resistance to Yersinia pestis. Nat Immunol (2020). https://doi.org/10.1038/s41590-020-0705-6.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Cause of Common Autoinflammatory Disease May Have Protected Ancestors From Plague - Technology Networks