Fate Therapeutics’ and Celyad’s CAR therapies in oncology offer potential – pharmaceutical-technology.com

October 19, 2020 medical

by Manasi Vaidya in New York.

Fate TherapeuticsandCelyadsnatural killer (NK) cell biology-focused cell therapies could overcome cell persistence challenges and consequent efficacy concerns with redosing strategies, experts said.

One of Fate Therapeutics lead products, FT596, is an allogeneic, multitargeted, chimeric antigen receptor (CAR) NK cell product. Celyads autologous CYAD-01 and CYAD-02 and allogeneic CYAD-101 are CAR T cell products using NK cell specificity to target T-cells. One analyst considered the potential to redose allogeneic products as a key item to consider while assessing clinical potential. While clinical data establishing the additive efficacy advantages of giving multiple doses is still preliminary, redosing allogeneic products could increase their expansion and persistence, experts said. Autologous therapies carry source constraints, so the ability to manufacture and administer allogeneic therapies is an advantage, they said.

While past NK cell therapy data has been mixed, experts saw potential in CAR NKs like FT596 or CAR T-cell products engineered to express NKG2D like CYAD-101, given the advancements in cell production.

Phase I FT596 results in B-cell lymphomas/ CLL are expected at either the American Society of Hematology (ASH) meeting in December or an investor meeting in early 2021, as per a second analyst report. Phase I data for CYAD-01 and CYAD-02 in relapsed/refractory (r/r) acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS) are expected by YE20, as per the companys August corporate presentation. Celyads allogeneic CYAD-101 is being tested in a Phase I alloSHRINK trial (NCT03692429) in metastatic colorectal cancer (CRC), which has a primary completion date of November 2020.

FT596s sales are expected to reach $136m in 2026, according to a GlobalData Consensus forecast. Celyad did not respond to a request for comment.

Increasing the persistence of cell therapies once they are infused into a patient has been a challenge, especially with NK cell-based therapies, experts said. The issue of persistence and consequent efficacy is significant because the potential efficacy with Celyad and Fate Therapeutics platforms remains largely unknown, they added.

Because the immune system can recognise foreign cells, cell products would not last for more than a few weeks, said Dr Marco Davila, medical oncologist, in the Department of Blood and Marrow Transplantation, Moffitt Cancer Center, Tampa, Florida. With CAR T-cell therapies, the expansion and persistence of CAR cells are said to correlate with the durability of response, said Dr David Sallman, assistant member, Department of Malignant Hematology, Moffitt Cancer Center.

Strategies involving multiple doses of cell therapies could maximise the total dose, improve duration, and increase efficacy magnitude with both autologous and allogeneic cell therapies, said Dr Tara Lin, associate professor of medicine, University of Kansas Medical Center, Kansas City. Multiple infusions of therapy could also potentially lead to complete remission, said Sallman. In Fate Therapeutics Phase I FT500 (NCT03841110) study, patients had been given up to six doses of the therapy, which was not found to be toxic, according to Fate Therapeutics CEO Scott Wolchko. Redosing has the potential to offer multiple infusions as maintenance therapy, said Dr Jeffrey Miller, professor of Medicine, Division of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis.

The persistence of allogeneic therapies is not well understood, and it is unknown how long cells need to persist to be effective or whether persisting cells confer durability of response, said Wolchko. Giving multiple doses is one way to overcome the lack of persistence if it is an important factor for efficacy, he said. In a 4Q19 call, the FDA said it was allowing the dose to be repeated on a patient-by-patient basis, Wolchko said. In the alloSHRINK study, CYAD-101 is administered three times with a two-week interval between each administration in metastatic CRC, as per ClinicalTrials.gov.

However, even if the engineered cells do not persist in the body, the response rate and ability to eradicate the disease should not be limited, said Davila. With a limited lifespan, allogeneic cell therapies would dissipate as the patients immune system recovers, said Dan Kaufman. With the incorporation of interleukin (IL)-12 or IL-15 into the cell product, the cell therapy could persist without exogenous cytokines, said Kaufman. The FT596 construct contains an IL-15 fusion protein.

Experts cited the data from a Phase I / II (NCT03056339) investigator-led effort at MD Anderson Cancer Center using cord blood-derived anti-CD19 CAR NK cells as an example of an effective CAR NK therapy. The study by Rezvani and colleagues showed a persistence challenge did not seem to hamper the response, because once a critical threshold for cell expansion is crossed, the activity can be mediated, Davila said. Eleven r/r patients with CD19-positive cancers, such as non-Hodgkins lymphoma or CLL, were treated with a single infusion; eight had a response, including seven with a complete remission (Rezvani et al. [2020] N Engl J Med, 382, pp. 545553). Even if the cells do not persist, they expand to sufficient levels to eradicate the disease before they are lost, Davila added.

In the Phase I THINK(NCT03018405) CYAD-01 data, decreased bone marrow blasts were observed in eight patients, including five objective responses and one stable disease for three or more months, as per the company presentation. Responding patients did have blast clearances, but some of the remissions were short-lived and the cells did not persist in the system, said Sallman. However, the short hairpin (sh) ribonucleic acid (RNA) technology employed CYAD-02, which could increase persistence and expansion, said Sallman (Fontaine et al., [2019]Blood, 134[Suppl 1], p. 3931). ShRNA technology allows T cell engineering without the need for gene editing to inhibit alloreactivity and increase persistence, according to Celyad.

Ongoing research on improving preconditioning regimens by combining additional drugs could also help with the persistence of allogeneic products, said Davila. It is not known whether every dose needs a conditioning regimen, but since conditioning regimens can suppress a patients immune system for several months, it may not be necessary before every therapy infusion, he added.

Patients will not have to receive a preconditioning regimen before every cell infusion, said Wolchko, adding redosing FT500 was found to be safe. Celyads protocol does not specify the preconditioning strategy for redosing. No predictive biomarkers are available to explain why some patients respond well and others do not, said Sallman, adding it is critical to identify potential responders. Nonetheless, there is no way to predict clinical efficacy based only on preclinical data, so data is still needed, said Miller.

The economic advantage to developing off-the-shelf therapies has driven interest in NK-cell based platforms, said Miller and Davila. If quick treatment is needed, then an allogeneic NK cell therapy would be better than an autologous therapy, which may take up to six weeks to manufacture, said Sallman. While the results with autologous CAR T-cell therapies have been significant, their scale-up and costs are challenging, said Kaufman. Related Report

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The ability to use induced pluripotent stem cell (iPSCs) or cord blood cells as a source would help scale up the cell manufacture and allow effective results, said Kaufman. iPSCs provide advancement in expansion protocols, which can provide multiple doses, Miller added. Fate Therapeutics has an iPSC-derived NK cell franchise. Also, since T cell therapies require donor apheresis to collect cells in a process lasting four to five hours, it is not feasible to keep going back to the same donor, said Miller.

Moreover, newer platforms are expected to improve on past NK cell therapy trials, specifically those showing mixed efficacy. Past studies had feasibility limitations in getting the required number of cells, said Miller. Those small studies were conducted at a time when cell isolation and production systems were not as advanced as they are now, said Davila.

Manasi Vaidya is a Senior Reporter for Clinical Trials Arena parent company GlobalDatas investigative journalism team. A version of this article originally appeared on the Insights module of GlobalDatas Pharmaceutical Intelligence Center. To access more articles like this, visit GlobalData.

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Fate Therapeutics' and Celyad's CAR therapies in oncology offer potential - pharmaceutical-technology.com

Cell Biology

Remnants of Ancient Parasites Could Be Shaping Our Response to the COVID-19 Coronavirus – SciTechDaily

October 19, 2020 medical

Packard Fellowship recipient Ed Chuong, assistant professor of molecular, cellular and developmental biology, works in his lab with undergraduate student Isabella Horton. Credit: Glenn Asakawa/CU Boulder

Why are some people more resilient to viruses than others?

The answer has eluded scientists for centuries and, in the age of COVID-19, has come to represent one of the holy grails of biomedical research.

Ed Chuong, an assistant professor of molecular, cellular and developmental biology at CU Boulder, proposes an intriguing answer: Exposure to ancient parasites by our ancestors forever altered our genome, shaping the varied responses of our immune systems today.

If you look closely at our genome, viruses have been shaping not only our lives but also our biology and evolution for hundreds of millions of years, said Chuong, who today was awarded the prestigious $875,000 Packard Fellowship to explore the idea. Its possible that ancient viral sequences from past pandemics are now lending a hand in helping us fight modern ones.

Say the word genome and most people think of the roughly 20,000 genes that encode the proteins necessary for life. But in reality, notes Chuong, we may be more virus than human. Previous research shows that at least half the human genome is made up bits of DNA left behind by viruses and other virus-like parasites, known as transposons, which slipped into cells of our primate ancestors over the past 50 million years.

In the human genome we can see traces of these invasions everywhere, like a fossil record of infections, said Chuong.

Ed Chuong in the lab with his research team. Credit: Glenn Asakawa/CU Boulder

Among those invaders were so-called endogenous retroviruses. As viruses do, they behaved selfishly at first, coaxing their host cells to make more copies so they could rip through the body and infect others. Over time, they lost their ability to sicken and spread, but infiltrated germ cells like sperm or eggs baking their genetic recipe into generations to come.

Scientists long assumed those remnants were useless junk DNA.

But in recent years, Chuong and others have discovered that, in some cases, they were coopted by mammalian hosts for evolutionary gain, influencing everything from cognition to reproduction to immune response.

In one landmark study, which sparked Chuongs interest in the field, scientists discovered a protein called Syncytin, derived from an endogenous retrovirus, which made the development of human placental tissue possible. Chuongs follow-up research, published in the journal Nature Genetics, found that endogenous retroviruses also serve as on-off switches for gene networks that influence placental development.

The development of the placenta enabled live birth in mammals and was a major step in the evolution of our species and these ancient viruses played a key role, he said.

Chuong has since shifted his attention to the immune system, showing in 2016 that ancient viruses helped shape the interferon response the cellular alarm system that sounds within hours of infection.

We found fragments of old viruses that normally lay silent but turn on during infection, and when they do, they turn on nearby immune genes, he said.

Notably, when those viral fossils are removed and the cell is then infected, the immune response is muted.

Our study was one of the first demonstrations of an ancient virus being co-opted for host defense and now necessary to fight modern viruses, he said.

Chuong, who arrived at the BioFrontiers Institute in 2018, was working under stay-at-home orders early in the pandemic when he began to think more about why different people respond to infection, including SARS-CoV-2, differently.

He wondered: Could these ancient retroviruses provide another hidden layer of explanation?

Chuong wrote a grant proposal centered around that question. On Thursday, the David and Lucile Packard Foundation named him among 20 early-career scientists across the nation to receive their award.

In a year when we are confronted by the devastating impacts of a global pandemic, racial injustice and climate change, these 20 scientists and engineers offer us a ray of hope for the future, said Frances Arnold, chair of the Packard Fellowships Advisory Panel.

Chuong suspects that ancient parasites could be influencing human immunity today in one of two ways: Either different populations were exposed to different viruses in their evolutionary history, leaving them with different cellular machinery with which to fight off new threats; or they share the same bits of ancient DNA but much newer influences (in utero or in the environment) have silenced or awakened that immune machinery in ways that make some resilient and others vulnerable.

To learn more, he and his team will amass population-wide datasets of immune cells from humans and other mammals and apply high-powered computing techniques to sequence their genome, looking not only at genes present but also at transposons.

He has pioneered a mind-blowing new way of thinking about how genomics works, said Lee Niswander, chair of the Department of Molecular, Cellular and Developmental Biology. For him to be able to follow his nose and see where the science takes him is really exciting.

While the science is young, Chuong hopes that it ultimately could lead to new diagnostic tests or even new treatments.

Learning how and why immune responses vary within a population could transform our ability to predict individual responses to infection and autoimmune diseases, Chuong said. To get this kind of recognition that these ideas are worth pursuing is incredible.

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Remnants of Ancient Parasites Could Be Shaping Our Response to the COVID-19 Coronavirus - SciTechDaily

Cell Biology

Researchers report the discovery of innate immune signaling pathway in fibroblasts – News-Medical.net

October 19, 2020 medical

Reviewed by Emily Henderson, B.Sc.Oct 16 2020

Vanderbilt University researchers have reported the counterintuitive discovery that certain chemotherapeutic agents used to treat tumors can have the opposite effect of tissue overgrowth in normal, intact mammary glands, epidermis and hair follicles. The researchers also are the first to report the discovery of an innate immune signaling pathway in fibroblasts--the spindle-shaped cells responsible for wound healing and collagen production--that causes cells to proliferate. Such signaling pathways previously were attributed only to immune cells.

The article describing the research, "DNA Damage Promotes Epithelial Hyperplasia and Fate Mis-specification via Fibroblast Inflammasome Activation," was published in the journal Developmental Cell on Oct. 13.

The findings of this work, led by postdoctoral fellow Lindsey Seldin and Professor and Chair of the Department of Cell and Developmental Biology Ian Macara, have broad implications for diseases associated with the immune system like psoriasis, as well as cancer and stem cell research.

Understanding the functionality of stem cells and the way that their behavior is regulated has been a longstanding research interest for Seldin. "Normal stem cells have an amazing ability to continuously divide to maintain tissue function without forming tumors," she explained. "We wanted to understand what happens to these cells in their native environment when subjected to damage, and if the response was connected to a specific tissue."

By testing perturbations to the epidermis, mammary gland and hair follicles vis--vis mechanical damage or DNA damage through chemotherapeutic agents, the researchers saw a paradoxical response: Stem cells, which otherwise would divide slowly, instead divided rapidly, promoting tissue overgrowth.

When the tissues were subjected to DNA damage, their stem cells overly proliferated, giving rise to different cells than they normally would.

This was a very perplexing result. We were determined to figure out if this was a direct response by the stem cells themselves or by inductive signals within their environment."

Lindsey Seldin, the paper's lead author

The key clue was that stem cells isolated from the body did not behave the same way as in intact tissue--an indication that the response must be provoked from signals being sent to the stem cells from other surrounding cell types.

The investigators turned their attention to fibroblasts, the predominant component of the tissue microenvironment. When fibroblasts in the epidermis were removed, the stem cell responsiveness to DNA damage was diminished, indicating that they played an important role. RNA sequencing revealed that fibroblasts can signal by way of inflammasomes--complexes within cells that help tissues respond to stress by clearing damaged cells or pathogens, which also in this case caused stem cells to divide. "This is an astounding discovery," said Macara. "Inflammasome signaling has previously been attributed only to immune cells, but now it seems that fibroblasts can assume an immune-like nature."

Seldin intends to replicate this work in the mammary gland to determine whether fibroblasts initiate the same innate immune response as in the epidermis, and more broadly how fibroblasts contribute to the development of cancer and other diseases associated with the immune system.

Source:

Journal reference:

Seldin, L & Macara, I (2020) DNA Damage Promotes Epithelial Hyperplasia and Fate Mis-specification via Fibroblast Inflammasome Activation. Developmental Cell. doi.org/10.1016/j.devcel.2020.09.021.

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Researchers report the discovery of innate immune signaling pathway in fibroblasts - News-Medical.net

Immunology

Review Article, Authored by ZyVersa Therapeutics’ Esteemed Scientific Advisors, Demonstrates the Role of Inflammasomes in the Exacerbated Immune…

October 19, 2020 medical

Authored by esteemed experts in immunology and leaders at the forefront of inflammasome research at University of Miami Miller School of Medicine

Highlights inflammasomes as promising drug targets for treatment of COVID-19 and its associated complications

Overviews current and pipeline drugs with potential to treat COVID-19 and its complications, including information about IC 100, ZyVersa Therapeutics' novel inflammasome inhibitor targeting the adaptor ASC component

WESTON, Fla., Oct. 12, 2020 /PRNewswire/ --ZyVersa Therapeutics, Inc. (ZyVersa), a clinical stage specialty biopharmaceutical company developing first-in-class drugs for treatment of inflammatory and renal diseases, is pleased to announce that Frontiers in Immunology has just published a review article titled, The Inflammasome in Times of COVID-19. This article addresses how inflammasome signaling pathways contribute to the hyperactive immune response leading to poor outcomes in patients with COVID-19 infection. It summarizes data on the mechanism of inflammasome activation by COVID-19 infection and the role of inflammasomes in development of common COVID complications, acute respiratory distress syndrome, ventilator-induced lung injury, and disseminated intravascular coagulation. It also addresses potential mechanisms by which inflammasomes may contribute to the damaging effects of inflammation in the cardiac, renal, digestive, and nervous systems of COVID-19 patients. Finally, it addresses inflammasomes as potential drug targets. To review the publication, Click Here.

"Tissue damage associated with inflammasome-precipitated over-activation of the inflammatory response in patients infected with COVID-19 tends to be more detrimental than damage induced by the viral load of SARS-CoV-2," says Dr. Juan Pablo de Rivero Vaccari, Research Assistant Professor, Department of Neurological Surgery, University of Miami Miller School of Medicine, and an author of the manuscript. "Thus, modulation of the inflammatory response is critical to improving patient outcomes."

Story continues

"As an ASC inhibitor, IC 100 targets all common inflammasomes, and its mechanism of action is independent of triggers and types of inflammasomes," stated Stephen C. Glover, Co-founder, Chief Executive Officer, and President of ZyVersa Therapeutics. "Based on this, and the promising data in animal models of diverse chronic and acute diseases, including acute respiratory distress syndrome, we are excited about the potential of IC 100 as an effective therapeutic option for a broad range of inflammatory conditions."

About COVID-19

Coronaviruses are a large family of viruses that can cause illness. There are several known coronaviruses that cause respiratory infections, ranging from the common cold to more severe diseases such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and COVID-19. COVID-19 was identified in Wuhan, China in December 2019. COVID-19 is caused by the virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new virus in humans causing respiratory illness which can be spread from person-to-person through respiratory droplets.

The estimated incubation period is between 2 and 14 days with a median of 5 days. COVID-19 is associated with inflammasome activation, which triggers what is often called a "cytokine storm," with massive activation of pro-inflammatory cytokines including IL-1, IL-6, TNF, and IL-8.

A wide range of COVID-19 symptoms have been reported, with most patients experiencing mild symptoms, such asfever, cough, chest pain, nausea, and body pain. Around 5% of patients develop severe symptoms including respiratory failure, septic shock, and/or multiple organ dysfunction or failure. These patients have a high mortality rate. Current care for patients with COVID-19 is primarily supportive to help relieve symptoms and manage respiratory and other organ failure. There are no specific approved treatments at this time, but many are under investigation.

About IC 100

IC 100 is a novel humanized IgG4 monoclonal antibody that inhibits the inflammasome adaptor protein ASC. IC 100 attenuates both initiation and perpetuation of the inflammatory response. It does so by binding to a specific region of the ASC component of multiple types of inflammasomes, including NLRP1, NLRP2, NLRP3, NLRC4, AIM2, Pyrin. Intracellularly, IC 100 binds to ASC, inhibiting inflammasome formation, thereby blocking activation of IL-1 early in the inflammatory cascade. IC 100 also binds to ASC in ASC Specks, both intracellularly and extracellularly, further blocking activation of IL-1 and the perpetuation of the inflammatory response that is pathogenic in inflammatory diseases. Because active cytokines amplify adaptive immunity through various mechanisms, IC 100, by attenuating cytokine activation, attenuates the adaptive immune response as well.

For more information about inflammasomes, Click Here to review our White Paper.

About ZyVersa Therapeutics, Inc.

ZyVersa is a clinical stage specialty biopharmaceutical company leveraging advanced, proprietary technologies to develop first-in-class drugs. Our focus is on patients with inflammatory or renal diseases who have significant unmet medical needs. Our lead anti-inflammatory candidate is IC 100, a novel monoclonal antibody that inhibits the inflammasome adaptor protein ASC. IC 100 has potential to treat a broad range of inflammatory diseases. Our lead renal candidate is Phase 2a-ready VAR 200, a cholesterol efflux mediator for treatment of a rare renal disease, focal segmental glomerulosclerosis(FSGS). For more information, please visit ZyVersa.com.

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SOURCE ZyVersa Therapeutics, Inc.

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Review Article, Authored by ZyVersa Therapeutics' Esteemed Scientific Advisors, Demonstrates the Role of Inflammasomes in the Exacerbated Immune...

Immunology

Trump says he may now be ‘immune’ to the coronavirus. Here’s what we know about COVID-19 and immunity. – Poynter

October 19, 2020 medical

Since his return from Walter Reed National Military Medical Center, President Donald Trump has repeated that he may now be immune to the coronavirus.In a videoreleased shortly after he arrived back at the White House, he said, Now Im better, and maybe Im immune, I dont know.

In a55-minute interviewon Fox Business, he made several claims about his health and COVID-19 immunity, saying, When you catch it you get better, and then youre immune, and jokingly referred to himself as a perfect physical specimen.

But medical experts say there are still a lot of unknowns about COVID-19 immunity.

Do all recovered COVID-19 patients become immune, regardless of the severity? For how long? Will the virus behave like the flu, requiring a vaccine each year? How do we achieve herd immunity?

We spoke with immunology and infectious disease experts about what they have learned and still dont know about COVID-19 and immunity.

Heres what we found out.

A person achieves immunity to a disease when the bodys immune system has fought off the virus once and is now strengthened to resist further attack. The immune system has a kind of memory for previous pathogens, allowing the body to have a quicker, stronger response the next time it encounters a past invader.

This can happen naturally or via vaccine.

Medical experts say its hard to know for certain the strength and length of immunity for recovering COVID-19 patients, because its a new virus and not enough studies have been done. However, there are indicators that suggest there is some natural protection against the disease post-recovery.

The biggest clue is that recovered patients rarely get reinfected with COVID-19, experts said, especially when considering the huge number of people who have been infected with the virus around the world.

The very high-level picture is pretty stable, said Dr. Sarah Fortune, chair of the Immunology and Infectious Diseases department at Harvard T.H. Chan School of Public Health.

Both the clinical data and the animal studies suggest that there is meaningful protection against disease, Fortune said. Its not as if youre seeing rampant recurrent infections with recurrent severe symptoms. Its not as if there are no cases, but by and large youre seeing substantial protection against disease.

Experts also said previous studies that looked at common cold coronaviruses showed that people develop immunity for extended periods of time (at least a year), though it varied slightly from case to case.

There may be some differences in the level of immunity for those who had a serious infection, versus those who only experienced mild symptoms, researchers say. Generally, patients who dealt with a severe infection are likely going to have a higher antibody count.

But that doesnt mean that your mild infection isnt providing you enough immunity to protect you against the disease, Fortune said. Even if its lower, it appears to be completely proficient in protecting you against the disease. And, in most of the people who are infected, they develop a mild case and we arent seeing many reinfections.

Theres no standard time frame for immunity after someone recovers from COVID-19. Different public health groups have different estimates, with the most conservative being aboutfour months

Researchers say its likely that people are immune for longer, but note that with a rapidly spreading disease that has no cure, people should keep their guard up rather than return to life as normal and put themselves and others at risk.

One common misconception immunologists raised is the public perception of immunity in general, with many people thinking youre either immune or youre not. Thats not how it works.

Protection is not like a light switch, its like a dimmer switch, Fortune said. You will be more protected in the beginning, and over time that protection might wane, but its not going to just go away.

For example, as a persons immunity wanes, they may eventually get infected from the virus again, but not actually get sick. Or even further out, they may get infected and then have mild symptoms but nothing severe.

The takeaway: The loss of immunity is gradual, not drastic.

Registered Nurse Kath Olmstead gives volunteer trial participant Melissa Harting a blinded study experimental vaccine for COVID-19 developed by the National Institutes of Health and Moderna Inc. at the United Health Services facility, Monday, July 27, 2020. (AP Photo/Hans Pennink

The flu is a respiratory virus like the coronavirus, but its also quite different. The flu rapidly shifts and mutates, making it more resistant to long-term immunity. Thats why there is a new vaccine each year.

If the virus that causes COVID-19 continues to behave like other coronaviruses, people will likely have more stable immunity from a limited vaccination schedule.

Theres no evidence, so far, that people will need to be vaccinated each year because of the virus mutating, said Dr. Stanley Perlman, a professor of microbiology and immunology at the University of Iowa. That may be because of their immunity waning, but not because the virus is changing.

Fortune agreed. Theres no evidence that Sars-Cov-2 (the virus that causes COVID-19) is going to, or has undergone, a really dramatic re-shuffling that makes it escape either a natural immunity or even a vaccine-induced immunity, she said. Thats not to say that its not possible there wont be a new one in the future, but just that the virus doesnt share the same characteristics of the seasonal, whole-scale remaking of itself that the flu does.

Positive test results dont guarantee immunity. The presence of antibodies only means that the person has been exposed to the virus in the past.

How sensitive, or how good, the antibody test is, and the amount of antibodies a person has, weighs heavily on whether or not they would be considered immune from the virus.

The same thing is true with a PCR diagnostic COVID-19 test.

Some people have very positive PCR tests and thats more of a worry than someone with fluctuating PCR tests negative one day, positive the next because they have less of a viral load, Perlman said. Its the same thing with antibodies. You can test positive for antibodies but have so little that it doesnt really protect you, or you can have a high number of antibodies, which means youre better protected. The amount matters.

Herd immunity is the idea that when enough people in a population are immune, either by having the infection or receiving a vaccine, the virus will have trouble spreading. Thats because an infected person is less likely to encounter a non-immune person to pass it on to, making them a dead-end in the chain of transmission.

When that happens enough times on a large scale, it drives its rate down and eventually gets the disease under control, but it doesnt necessarily eradicate it.

The U.S. is still considered far from adequate COVID-19 herd immunity, and experts say there would have to be many more cases and deaths before we get there if a vaccine doesnt arrive first. Fewer than 1 in 10 Americans show signs of past infection as of late July, according to a Sept. 25studypublished in The Lancet journal.

So, experts agree that the ideal way to achieve herd immunity is with a vaccine. While some immunity within a population is better than none, with a virus that spreads through the air, the higher the number of people who are immune, the better.

Different numbers have been tossed around by scientists on just how much of the population needs to be immune in order for herd immunity to work well. The mathematical model for Sars-Cov-2 which is derived based on the virus transmission characteristics and on how the population behaves puts it around 60-70 people out of every 100.

For the most highly contagious diseases, like measles, scientists say about 94% of the population needs to be immunized to achieve that level of protection.

That doesnt mean that it goes away when we reach herd immunity, it just means that youre not propagating the epidemic, Fortune said. People should have that in mind with herd immunity, and with the future, its not like one day, we achieved herd immunity and its gone.

This article was originallypublished by PolitiFact, which is owned by the Poynter Institute, and is republished here with permission. See the sources for this articlehereand more of their fact-checkshere.

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Trump says he may now be 'immune' to the coronavirus. Here's what we know about COVID-19 and immunity. - Poynter

Immunology

Revealing Key Immunology Insights with Spatial Analysis – Technology Networks

October 17, 2020 medical

The immune system is a complex, dynamic and heterogeneous entity, making it particularly challenging to explore. To gain a more comprehensive understanding of immunity, scientists must be able to characterize specialized cell types, the functional states of individual cells and information on spatiotemporal resolution within healthy and diseased tissues.Download this listicle to learn more about:

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Revealing Key Immunology Insights with Spatial Analysis - Technology Networks

Immunology

UCB Snags Eli Lilly UK Research Site, Plans to Invest 1 Billion Over Five Years for R&D – BioSpace

October 17, 2020 medical

UCB is investing more than 1 billion (roughly 1.29 billion USD) over five years to expand its research and development (R&D) capabilities in the U.K., which will include a transition to a newly acquired 47-acre R&D campus from Eli Lilly located in Windlesham, Surrey.

The global neurology- and immunology-focused biopharma announced Friday it has signed an agreement to acquire the new campus from Eli Lilly to support the companys cutting-edge research and development, early manufacturing and commercialization of medicines for patients with severe neurological and immunological diseases.

Formerly, the facility was Eli Lillys second-largest research site worldwide. Exactly one year ago, Eli Lilly announced it was closing the doors to its neuroscience-focused Erl Wood research center in Surry. The Indianapolis, IN.-based pharmaceutical company said it planned to do so by the end of 2020, effectively impacting 270 staff members and resulting in possibly 80 redundancies. Approximately a third of the non-laboratory workers at the Eli Lilly site was moved to another nearby location. This news followed some months after the company also announced it was cutting 250 jobs at its 1,400-employee factory in Eastern France for the purposes of modernization.

The new U.K. site will be home to one of the companys three global R&D hubs, in addition to those located in Belgium and the U.S. Following completion of the acquisition, which is expected for November 2020, UCB will perform a complete state-of-the-art refurbishment of the campus before staff at its current U.K. headquarters in Slough, Berkshire, move in.

While UCBs five-year plan to invest 1 billion in the U.K. effort will include the new facility, both UCB and Eli Lilly have yet to disclose the financial details on the acquisition. According to UCB, the five-year, 1 billion investment will also support the addition of 650 high-value jobs in scientific research, translational medicine, clinical development, early manufacturing and commercial roles in the region.

We have a strong track record of discovering medicines in the UK which go on to make a difference to the lives of patients worldwide, said UCB CEO, Jean-Christophe Tellier, in a statement. I am delighted to have signed an agreement to secure this new campus for our U.K. hub, from which our scientists will be able to continue to develop their extensive collaborations with some of the most innovative universities, bio-techs and medical research charities, bringing even greater benefit for patients.

Tellier added, This new UK site will not only support our ambitions for future drug discovery but will be well-placed to enable us to achieve our 2030 global sustainability goals and provides an environment which supports the physical and mental wellbeing of our people essential to helping us thrive.

This isnt the first acquisition under UCBs belt. Earlier this summer, UCB announced the news that it had acquired clinical-stage pharmaceutical company Engage Therapeutics for an upfront cash payment of $125 million. Additional potential milestone payments of up to $145 million were also part of the deal. Engage was in the process of developing alprazolam, a single-use therapeutic for the rapid treatment of active epileptic seizures. The acquisition gave UCB worldwide rights to the therapy, in addition to giving them the power to take over further clinical development, submission, launch and commercialization procedures.

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Immunology

COVID-19 Preventative Measures Associated With Reduced Asthma Hospitalizations – PR Web

October 17, 2020 medical

This would suggest that asthma control improved during the pandemic. It illustrates the importance of environmental factors when it comes to treating and managing patients with asthma. - Atsushi Miyawaki, MD, PhD

MILWAUKEE (PRWEB) October 13, 2020

According to new research published in The Journal of Allergy and Clinical Immunology: In Practice (JACI: In Practice), preventative measures used to slow the spread of COVID-19 in Japan have also lowered the rate of hospitalizations for asthma.

Researchers used the Diagnosis Procedure Combination inpatient database to conduct their research. The data on all hospitalizations per week across 272 hospitals nationwide from December 30, 2019, to May 31, 2020, was gathered and compared to the same periods in 2017, 2018, and 2019.

A total of 16,317 hospitalizations for asthma were observed in the study. Asthma hospitalizations in 2017-2019 and 2020 showed parallel trends until week eight. Researchers observed a decline in asthma hospitalizations from week nine onwards in 2020. Hospitalizations for COVID-19 were first observed during week seven of 2020. Further analysis found the average number of asthma hospitalizations significantly decreased during weeks nine to 22 in 2020 compared to 2017-2019 for both children and adults.

Asthma hospitalizations usually indicate that an individuals asthma is not currently under control, said Atsushi Miyawaki, MD, PhD, corresponding author for the study. This would suggest that asthma control improved during the pandemic. It illustrates the importance of environmental factors when it comes to treating and managing patients with asthma.

One possible explanation for the results is that increased hygiene by individuals to reduce their chances of contracting COVID-19 would also reduce their exposure to asthma triggers. Enhanced preventative measures by individuals concerned that COVID-19 may trigger asthma, such as frequent cleaning and reduced smoking, may also have helped to remove allergen triggers. Individuals may have also been more likely to use preventative asthma medications. Another explanation might be that community prevention measures may have helped suppress other respiratory infections, which can cause asthma exacerbations.

You can learn more about asthma and COVID-19 on the American Academy of Allergy, Asthma & Immunology website, aaaai.org.

The American Academy of Allergy, Asthma & Immunology (AAAAI) represents allergists, asthma specialists, clinical immunologists, allied health professionals and others with a special interest in the research and treatment of allergic and immunologic diseases. Established in 1943, the AAAAI has more than 7,100 members in the United States, Canada and 72 other countries. The AAAAIs Find an Allergist/Immunologist service is a trusted resource to help you find a specialist close to home.

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Immunology

Virtually Supported Home Peanut Introduction is Viable Option – MD Magazine

October 17, 2020 medical

With the impact of the coronavirus disease 2019 (COVID-19) lockdown measures continuing to be felt across the US, access to healthcare resources for the management of allergic disease are still limited.And although in-person services may be offered by clinics, concern or fear over exposure to the virus can certainly hinder patient use of such services.

And yet, certain allergic conditions, such as peanut allergies in high-risk infants, require expedited assessments and active management.

A report written by Douglas Mack, MD, Assistant Clinical Professor, Pediatrics, McMaster University, and colleagues detailed the first known use of a virtually supported home peanut introduction in infant patients at risk of developing peanut allergy. The program was conducted earlier this year in April.

Prior to initiation of the virtual program, infants were screened for eligibility in a private-practice allergist setting using the telehealth platform Doxy.me.

Patients were eligible if they had physician-diagnosed severe eczema, physician diagnosed egg allergy, SPT3 mm or 0.35 kU/L without prior ingestion, perceived high-risk by caregiver, or had caregiver anxiety to introduce a particular food.

Excluded from the study were patients with a history of systemic IgE-mediated reaction to the food in questions; had certain underlying conditions, such as uncontrolled asthma, cardiac conditions, respiratory conditions; or used a beta-blocker.

During this first consultation, parents or guardians were informed about the risks and benefits of either prolonging peanut avoidance until the first in-person visit or participating in the virtually-support food introduction process.

If they chose to proceed with the program, then consent was obtained, and they were prescribed an epinephrine autoinjector and rupatadine.

In the next visit with the physicians, caregivers were then informed about the process, possible symptoms, and treatment.

Then they were instructed to prepare peanut putter by dissolving 2 teaspoons of it in 2-3 teaspoons of hot water, then letting it cool.

Caregivers then gradually introduced 2 g of peanut butter every 10-15 minutes over 45 minutes 1 hour.

If any symptoms occurred, the guardian used the telehealth program to contact the physicians for further assessment. If the physicians were unable to be reached, then caregivers were instructed to administer epinephrine and/or antihistamine or contact emergency medical services.

However, if no symptoms occurred, then the physicians would advise ingestion of the food of similar or increased amounts 2-3 per week.

Mack and colleagues referenced recent clinical guidelines that provide a framework for at-home management of anaphylaxis. They suggest that using these guidelines would be necessary in the event of such reactions during the virtually supported food introduction.

Nonetheless, they noted that no reactions were reported during the food introduction process, which they considered to be consistent with the current evidence that anaphylaxis is rare and non-threatening with first ingestion in infancy. Thus, they emphasized that mild reactions can generally be managed with antihistamine and/or observation.

Even before COVID-19, lack of allergist resources presented significant barriers to the introduction of peanut to at-risk patients where there was hesitance, they wrote.

During COVID-19, the need to provide alternative forms of care is heightened. Virtually supported introduction may represent a future option after COVID-19 to improve access for patients who live in remote areas, or otherwise have limited access to allergists, or for clinicians with overburdened clinics.

They acknowledged that the implementation of such a strategy requires formal evaluation of safety, cost-effectiveness, caregiver/physician acceptability, sustainability, and patient satisfaction.

The report, Virtually supported home peanut introduction during COVID-19 for at-risk infants, was published online in The Journal of Allergy and Clinical Immunology: In Practice.

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Virtually Supported Home Peanut Introduction is Viable Option - MD Magazine

Immunology

Allergy Partners Discusses Ways to Differentiate Between Cold, the Flu, or COVID-19 – Benzinga

October 17, 2020 medical

ASHEVILLE, N.C., Oct. 16, 2020 /PRNewswire-PRWeb/ -- Here is how you can tell the difference In the best of times, it can be hard to tell the difference between symptoms of a cold and the flu. With the COVID-19 pandemic, understanding what these symptoms are versus those of COVID-19 is even more important than ever.

Facts The virus causing COVID-19, called SARS-CoV-2, is part of a family of viruses called Coronaviruses. This is a large family of viruses that cause illnesses ranging from the common cold to more severe respiratory illnesses. Coronaviruses can develop in animals and, through mutation, come to infect humans. SARS-CoV-19 is a mutated coronavirus that emerged in China in late 2019. It can cause severe respiratory illnesses such as pneumonia and can be fatal. Yet, in some people the symptoms can be mild. You should seek immediate medical care for any of the following:

Because cold and flu symptoms can appear like some of the symptoms of COVID-19, it is very important to monitor your symptoms closely. The Centers for Disease Control (CDC) has an interactive symptom tracker you can use to determine if you should seek care for possible COVID-19 infection at: https://www.cdc.gov/coronavirus/2019-ncov/symptoms-testing/symptoms.

Most importantly, keep in contact with your Allergy Partners physician. Our offices remain open and we are offering Telemedicine services to make sure you and your family remain well during this challenging time. Our experienced allergists are anxious to discuss any questions or concerns you may have about COVID-19 and how we can best manage your health together.

WILLIAM A. MCCANN, M.D. Born and raised outside of Baltimore, Dr. McCann has called North Carolina home since completing medical school. After his pediatrics training at Duke, he practiced general pediatrics for three years in Hendersonville. During this time, he realized that his passion lies in the treatment of allergies and asthma. After a brief sojourn in Augusta, Georgia for allergy and immunology training, he returned to Western North Carolina and joined Allergy Partners.

RICHARD L. WASSERMAN, M.D., PHD. Dr. Wasserman received his medical degree from the Mt. Sinai School of Medicine/University of Texas Southwestern Medical School and completed his Pediatrics Residency at Children's Hospital of Philadelphia. Dr. Wasserman completed fellowship training in Bone Marrow transplantation/Immunology at the Children's Hospital of Philadelphia, Postdoctoral Cancer/Immunology at the University of Texas Southwestern Medical School, and Immunology/Rheumatology at The Rockefeller University.

Allergy Partners, PLLC is the nation's largest single specialty practice with multiple locations across the United States. Our allergists provide evaluation and treatment of following conditions:

SOURCE Allergy Partners

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Allergy Partners Discusses Ways to Differentiate Between Cold, the Flu, or COVID-19 - Benzinga