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Study Identifies New Approach for Developing Simple-to-Use, ‘Shelf-Available’ COVID Treatment Options

AHA Publisher — Mon, 18 Jul 2022 07:00:26 +0000

Uniformed Services University of the Health Sciences (USU) via Newswise – An array of new, simple “shelf-available” SARS-CoV-2 treatment options could soon be available in the fight against COVID thanks to a new study, “Engineered ACE2-Fc counters murine lethal SARS-CoV-2 infection through direct neutralization and Fc-effector activities,” published July 13 in Science Advances. The researchers, led by Dr. Marzena Pazgier, Professor of Medicine at USU, Infectious Disease Division of Department of Medicine, in collaboration with researchers from the National Institutes of Health (NIH),Yale University, Centre de Recherche du CHUM (CRCHUM) at Université de Montréal and Dartmouth College, used a strategy to design new therapeutics to treat SARS-CoV-2 by adopting the protein that the virus naturally uses as an entry portal to infect human cells. The protein is called the ACE2 receptor and it is found on the surface of airway cells and other tissues. By making this protein in a soluble form (not bound to a cell) and by modifying it by attaching part of an antibody, researchers created a drug named ACE2-Fc. Because of the attached antibody portion, ACE2-Fc neutralizes the virus, and binds to cells of the immune system, signaling them to effectively eliminate the virus and infected cells. In addition, by structure-based design, the researchers identified and introduced three ACE2 mutations that significantly enhanced the activity of ACE2-Fc against most of currently known variants of SARS-CoV-2, including the Delta and Omicron variants. The researchers believe that by using this strategy it is possible to develop inexpensive, simple-to-use, shelf-available treatment options to combat the virus, shorten recovery times and reduce the severity of any subsequent complications, while also cutting down on the need for repeated vaccinations. Additionally, these new potential treatment options could also be suitable for patients with or without cardiovascular complications. With more than six million deaths worldwide as a result of the pandemic, there has been a significant impact on the general population and military members, dependents, veterans, and operations. Studies have also shown that about 10 percent of adults are also experiencing long-haul symptoms in the weeks after a COVID infection that can include cognitive issues, shortness of breath, activity-limiting fatigue, cough, and headaches. In this latest study, researchers sought to develop new treatment options that could prevent and treat new infections, therefore preventing long-haul symptoms, which could, ultimately, also help bypass the need for repeated vaccinations. “Our overall goal is to save lives by developing a simple-to-use COVID-19 treatment that could be used to prevent and treat current and future outbreaks. One huge advantage of utilizing ACE2 to counter coronaviruses is that SARS-CoV-2 and all its known mutants including Delta and the recent Omicron can be targeted and inactivated by ACE2-Fc therapeutic as they need to use ACE2 to bind and enter human cells. This means that no matter which variant of the virus infects or how much it has changed, this drug will always be able to bind to and kill it.” said Dr. Pazgier, the study’s lead and corresponding author. To read the original article click here.

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Tricking the Body to Treat Breast Cancer

AHA Publisher — Fri, 18 Mar 2022 07:00:43 +0000

Sanford Burnham Prebys via Newswise – With the help of two new grants from the National Institutes of Health totaling more than $4.4 million, Sanford Burnham Prebys professor Charles Spruck, Ph.D., and his team are refining a cutting-edge breast cancer treatment. The new approach, known as viral mimicry, tricks the body into thinking that it has a viral infection, stimulating immune responses that can help the body fight cancer and improve the effects of other treatments. “Modern cancer treatment relies on using multiple treatment strategies to minimize the risk of resistance, so the beauty here is that while we’ve found that our approach has anti-tumor properties when used alone, it also has the potential to work synergistically with other treatments,” says Spruck. “Fortunately, it is cancer-specific, so unlike chemotherapy, this treatment won’t harm healthy cells, thus also limiting adverse side effects.” ER+ Breast Cancer Is Treatable, But Frequently Recurs Breast cancer is the most common cancer globally, and about 70% of all breast cancer cases are ER+, meaning that cancer cells use the hormone estrogen to grow. In the United States, there are about 3 million people living with ER+ breast cancer. Because ER+ tumors rely on hormones to grow, they can be inhibited with anti-hormone therapies, which are much less toxic than standard chemotherapy. Early-stage ER+ breast cancer is usually responsive to treatment, but a significant proportion of patients go on to have a relapse when the cancer returns, often traveling to other areas of the body. These relapses tend to be much more treatment resistant and often occur many years after the initial cancer is gone. “For survivors, there’s always the risk of a relapse that could resist treatment and eventually kill them,” says Spruck. “That’s a terrifying prospect to live with, especially if you’re otherwise healthy and cancer-free. That’s why we need to develop better, less toxic treatments.” Useful Viruses Are in Our Genome The new approach takes advantage of a bizarre evolutionary feature of our genome called endogenous retroviruses (ERVs). These are small, repeated sections in our genome that were left behind by viruses infecting our ancient ancestors. Unlike regular viruses, ERVs do not make us sick. Instead, they help control gene expression by moving around and inserting themselves into different locations in our genome. ERVs don’t make us sick because they are usually silent, meaning that the proteins they encode are not expressed in the body. However, researchers have found that it’s possible to reactivate these fragments in cancer cells and fool the body into mounting an immune response. “The body thinks there’s an infection, which kicks the immune system into high gear,” says Spruck. “This makes cancer cells more receptive to immunotherapy and can slow tumor growth, but without the harsh side effects of chemotherapy.” Bringing Viral Mimicry to the Clinic With the new grants, the team will more fully explore how viral mimicry can be used to fight ER+ breast cancer. The team is also working on converting its approach, which has only been studied in a lab setting, into a drug that can be administered in the clinic. “We’re still a few years out from using this in the clinic, but we’ve seen that it works in the lab, and once it does make it into the clinic, it’s going to be safer and less toxic than current treatment options,” adds Spruck. The researchers are also confident that the method will be applicable to other cancers beyond ER+ breast cancer. “We discovered the pathway in breast cancer, but the fact remains that with a few exceptions, the majority of tumors are cold for most cancers,” says Spruck. “We’re not just improving breast cancer treatment, we’re opening a door to a new way of approaching cancer.” To read the original article click here.

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Pre-Infection Low Vitamin D Associated with Severe Covid

AHA Publisher — Mon, 21 Jun 2021 07:00:12 +0000

Naama Barak via Israel21c – Over a year and a half into the Covid crisis, most of us have already heard about the link between vitamin D deficiency and the coronavirus. But while previous research mostly measured vitamin D levels once patients were already sick, a new Israeli study shows that even pre-infection vitamin D deficiency is associated with increased Covid-19 severity and mortality. The study, conducted by researchers from Bar-Ilan University and its affiliate Galilee Medical Center, searched for vitamin D levels in the records of people with positive PCR tests for Covid who were admitted to the hospital between April 2020 and February 2021. It was recently published on MedRxiv and is now being submitted to a peer-reviewed journal. Of 1,176 patients admitted, 253 had vitamin D levels recorded 14 to 730 days prior to the positive test. Compared with mildly or moderately ill patients, those with severe or critical Covid were more likely to have severe pre-infection vitamin D deficiency, with levels less than 20 ng/mL. “This study can highlight the risks of vitamin D deficiency in terms of Covid-19,” said Dr. Amiel Dror, who led the study. “Vitamin D is often associated with bone health. We’ve shown that it may also play an important role in other disease processes, such as infection.” “It is still unclear why certain individuals suffer severe consequences of Covid-19 infection while others don’t,” added co-author Prof. Michael Edelstein. “Our finding adds a new dimension to solving this lingering puzzle.” This does not necessarily mean that giving vitamin D to Covid patients will decrease the risk of severe disease, the researchers note. However, it does underscore the need to understand how to mitigate the effect of vitamin D deficiency. To read the original article click here. For more articles from Israel21c click here.

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Pre-Existing Coronavirus Antibodies Could Help Protect Children Against New Pandemic Strain

AHA Publisher — Mon, 09 Nov 2020 08:00:22 +0000

The Francis Crick Institute via EurekAlert – Researchers at the Francis Crick Institute and University College London have found that some antibodies, created by the immune system during infection with common cold coronaviruses, can also target SARS-CoV-2 and may confer a degree of protection against the new viral strain. In response to infection with a virus, the immune system creates antibodies to help fight it. These antibodies remain in the blood for a period after infection, and in the case of re-infection, they are able to tackle the virus again. In their paper, published in Science today (Friday 6 November), the scientists found that some people, notably children, have antibodies reactive to SARS-CoV-2 in their blood, despite not ever having being infected with the virus. These antibodies are likely the result of exposure to other coronaviruses, which cause a common cold and which have structural similarities with SARS-CoV-2. The researchers made this discovery while developing highly sensitive antibody tests for COVID-19. To see how well their assay tests were performing, they compared the blood of patients with COVID-19 to patients who had not had the disease. Surprisingly, they found that some people who had not been exposed to SARS-CoV-2 had antibodies in their blood which would recognise the virus. To confirm their findings, they analysed over 300 blood samples collected before the pandemic, between 2011 and 2018. Nearly all samples had antibodies that reacted with common cold coronaviruses, which was expected given how everyone has been exposed to these viruses at some point in their lives. However, a small fraction of adult donors, about 1 in 20, also had antibodies that cross-reacted with SARS-CoV-2, and this was not dependent on recent infection with a common cold coronavirus.* Notably, such cross-reactive antibodies were found much more frequently in blood samples taken from children aged 6 to 16. Kevin Ng, lead author and post-graduate student in the Retroviral Immunology Laboratory at the Crick says: “Our results show that children are much more likely to have these cross-reactive antibodies than adults. More research is needed to understand why this is, but it could be down to children being more regularly exposed to other coronaviruses. “These higher levels we observed in children could also help explain why they are less likely to become severely ill with COVID-19. There is no evidence yet, however, that these antibodies prevent SARS-CoV-2 infection or spread.” In the lab, the researchers tested the antibodies they found in blood from uninfected people to confirm they are able to neutralise SARS-CoV-2. They found the cross-reactive antibodies target the S2 subunit of the spike protein on the surface of the virus. George Kassiotis, senior author and group leader of the Retroviral Immunology Laboratory at the Crick says: “The spike of this coronavirus is made of two parts or subunits, performing different jobs. The S1 subunit allows the virus to latch onto cells and is relatively diverse among coronaviruses, whereas the S2 subunit lets the virus into cells and is more similar among these viruses. Our work shows that the S2 subunit is sufficiently similar between common cold coronaviruses and SARS-CoV-2 for some antibodies to work against both. “It was previously thought that only antibodies to the S1 could block infection, but there is now good evidence that some antibodies to S2 can be just as effective. This is exciting as understanding the basis for this activity could lead to vaccines that work against a range of coronaviruses, including the common cold strains, as well as SARS-CoV-2 and any future pandemic strains. “But it is important to stress that there are still many unknowns which require further research. For example, exactly how is immunity to one coronavirus modified by exposure to another? Or why does this activity decline with age? It is not the case that people who have recently had a cold should think they are immune to COVID-19.” A large study is now underway, in partnership with researchers at Imperial College London and University College London, to uncover the role that different antibodies and other immune defences play in protection against COVID-19 and how severely ill people become. To read the original article click here.

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Covid-19 Pneumonia Drug Candidate Being Prepared Rapidly

AHA Publisher — Fri, 30 Oct 2020 07:00:47 +0000

Abigail Klein Leichman via Israel21c – RedHill Biopharma of Tel Aviv is collaborating with two pharmaceutical manufacturers in Europe and Canada to ramp up manufacturing of its drug candidate opaganib (Yeliva) or severe Covid-19 pneumonia. The orally administered drug, which has anti-inflammatory and antiviral capabilities, could then meet potential demand for emergency use as the pandemic continues worldwide. Under a compassionate use program, Covid-19 patients treated with opaganib in an Israeli hospital were discharged without requiring intubation and mechanical ventilation, whereas one-third of the matched case-control group required intubation and mechanical ventilation. “Opaganib demonstrated potent antiviral activity against SARS-CoV-2, the virus that causes Covid-19, completely inhibiting viral replication in an in vitro model of human lung bronchial tissue,” RedHill reports. Opaganib is currently in global randomized, double-blind, parallel-arm, placebo-controlled Phase 2/3 and US Phase 2 studies in hospitalized patients with severe Covid-19 pneumonia requiring supplemental oxygen. The US Phase 2 study is approaching completion of enrollment in eight sites, with initial results expected before the end of this year. The Phase 2/3 study is enrolling up to 270 patients across 15 study sites in six countries by year’s end. RedHill is in discussions with US government agencies regarding rapid advancement of opaganib manufacturing toward potential emergency use applications. Opaganib also has the potential to target multiple oncology, viral, inflammatory and gastrointestinal indications. It has FDA orphan drug status for the treatment of cholangiocarcinoma and is being evaluated in a Phase 2a study in advanced cholangiocarcinoma and in a Phase 2 study in prostate cancer. For the ongoing studies with opaganib, click here

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Why Is Obesity So Common in COVID-19 Patients?

AHA Publisher — Sun, 26 Jul 2020 07:00:39 +0000

Pennington Biomedical Research Center via Newswise – A hormone that connects the body’s metabolism and immune response system may explain why COVID-19 is so dangerous for people with obesity. “The problem for people with obesity is that their leptin levels are always high, and that can affect the response to a COVID-19 infection,” said Candida Rebello, PhD, RD, lead author of a new paper that traces the link between obesity and the virus. The hormone leptin regulates appetite and metabolism. Leptin also regulates the cells that fight infection. Leptin is produced by fat cells, and to a lesser extent by tissues in the lungs. The more fat a person has, the more leptin circulates in their body. Elevated leptin levels hamper the body’s ability to fight off infections, in the lungs and elsewhere, Dr. Rebello said. High leptin levels promote a low-grade systemic inflammatory state. “If you have obesity, there are a number of underlying health issues that make it more difficult for you to fight off a COVID-19 infection,” said John Kirwan, PhD, Pennington Biomedical Executive Director and a co-author of the review. “Your entire body, including your lungs, may be inflamed. Your immune response is likely compromised, and your lung capacity reduced. “Add in a virus that further weakens the body’s ability to fight infection, that can limit the body’s ability to control lung inflammation, and you have the recipe for disaster.” COVID-19 vaccine developers should take the immunocompromised state resulting from obesity into consideration, in much the same way they would advancing age. The researchers say the role of leptin in COVID-19’s development bears investigation along with the viral proteins that alter the immune systems of people with obesity. One potential avenue of treatment may be a drug that prevents inflammatory responses to the virus. Another potential avenue of investigation includes examining how proinflammatory fat tissue in people with obesity might contribute to activating fewer infection-fighting cells and why those cells die more quickly. To read the original article click here.

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Florida Medical School Dean: COVID-19 Affects Some Blood Types More Than Others

AHA Publisher — Thu, 16 Jul 2020 07:00:49 +0000

Lorie Johnson via CBN News – The state of Florida has seen the most dramatic rise in coronavirus cases. Recently, CBN News spoke to a doctor there who says the death rate remains low. He also explained why the virus affects some people more harshly than others. Doctors say when a person becomes infected with COVID-19 their blood type can make a big difference in how sick they get. “This is kind of a curious thing, but if you have A+ blood type you probably have about a thirty percent greater chance of ending up in the hospital than if your blood type is O,” Dr. Charles Lockwood, dean of the University of South Florida Morsani College of Medicine in Tampa told CBN News. Young people tend to avoid hospitalization, too, and that’s largely who’s testing positive, causing the death rate to plummet. “From at one point, about five percent to about 1 point. As of today, 1.5 percent in the state and in Tampa, in Hillsborough County, it’s actually below one percent. It’s .09 percent. So that’s one of the lowest case fatality rates on the planet, quite literally,” Lockwood noted. School children carry the lowest risk of both acquiring the infection and becoming very ill. “For the most part I think schools should reopen,” Lockwood explained. “There are some areas of the state where I might not be quite as enthusiastic, but for the most part I think we are going to be OK.” Florida hospitals reportedly made it past the peak. “We know that emergency room visits for COVID-like illnesses and influenza-like illnesses are dropping, and that’s the first sign that things may be improving,” Lockwood said. Doctors now rely on treatments they didn’t have before, such as Remdesivir and the affordable Dexamethasone, both scientifically proven to work and readily available. To read the original article click here. For more articles from CBN News click here.

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Viruses Can Steal Our Genetic Code to Create New Human-Virus Genes

AHA Publisher — Wed, 24 Jun 2020 07:00:58 +0000

Mount Sinai Health System via Newswise – Like a scene out of “Invasion of the Body Snatchers,” a virus infects a host and converts it into a factory for making more copies of itself. Now researchers have shown that a large group of viruses, including the influenza viruses and other serious pathogens, steal genetic signals from their hosts to expand their own genomes. This finding is presented in a study published online today and in print June 25 in Cell. The cross-disciplinary collaborative study was led by researchers at the Global Health and Emerging Pathogens Institute at Icahn School of Medicine at Mount Sinai in New York, and at the MRC-University of Glasgow Centre for Virus Research in the UK. The cross-disciplinary team of virologists looked at a large group of viruses known as segmented negative-strand RNA viruses (sNSVs), which include widespread and serious pathogens of humans, domesticated animals and plants, including the influenza viruses and Lassa virus (the cause of Lassa fever). They showed that, by stealing genetic signals from their hosts, viruses can produce a wealth of previously undetected proteins. The researchers labeled them as UFO (Upstream Frankenstein Open reading frame) proteins, as they are encoded by stitching together the host and viral sequences. There was no knowledge of the existence of these kinds of proteins prior to this study. These UFO proteins can alter the course of viral infection and could be exploited for vaccine purposes. “The capacity of a pathogen to overcome host barriers and establish infection is based on the expression of pathogen-derived proteins,” said Ivan Marazzi, PhD, Associate Professor of Microbiology at Icahn School of Medicine and corresponding author on the study. “To understand how a pathogen antagonizes the host and establishes infection, we need to have a clear understanding of what proteins a pathogen encodes, how they function, and the manner in which they contribute to virulence.” Viruses cannot build their own proteins, so they need to feed suitable instructions to the machinery that builds proteins in their host’s cells. Viruses are known to do this through a process called “cap-snatching,” in which they cut the end from one of the cell’s own protein-encoding messages (a messenger RNA, or mRNA) and then extend that sequence with a copy of one of their own genes. This gives a hybrid message to be read. “For decades we thought that by the time the body encounters the signal to start translating that message into protein (a ‘start codon’) it is reading a message provided to it solely by the virus. Our work shows that the host sequence is not silent,” said Dr. Marazzi. The researchers show that, because they make hybrids of host mRNAs with their own genes, viruses (sNSVs) can produce messages with extra, host-derived start codons, a process they called “start snatching.” This makes it possible to translate previously unsuspected proteins from the hybrid host-virus sequences. They further show that these novel genes are expressed by influenza viruses and potentially a vast number of other viruses. The product of these hybrid genes can be visible to the immune system, and they can modulate virulence. Further studies are needed to understand this new class of proteins and what the implications are of their pervasive expression by many of the RNA viruses that cause epidemics and pandemics. Ed Hutchinson, PhD, corresponding author and a research fellow at MRC-University of Glasgow Centre for Virus Research, said, “Viruses take over their host at the molecular level, and this work identifies a new way in which some viruses can wring every last bit of potential out of the molecular machinery they are exploiting. While the work done here focusses on influenza viruses, it implies that a huge number of viral species can make previously unsuspected genes.” Researchers say the next part of their work is to understand the distinct roles the unsuspected genes play. “Now we know they exist, we can study them and use the knowledge to help disease eradication,” said Dr. Marazzi. “A large global effort is required to stop viral epidemics and pandemics, and these new insights may lead to identifying novel ways to stop infection.” This study was supported by funders including the National Institute of Allergy and Infectious Diseases and the UK Medical Research Council. To read the original article click here.

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Reprogramming of Immune System Cures Child with Often-Fatal Fungal Infection

AHA Publisher — Wed, 17 Jun 2020 07:00:54 +0000

University of California, Los Angeles (UCLA), Health Sciences via Newswise – In the June 11 issue of the New England Journal of Medicine, a team of UCLA physicians and scientists describes the first case of immune modulation being used to cure a severe and often fatal fungal infection. The team “retuned” a 4-year-old’s immune system so that it could fight off disseminated coccidioidomycosis. The case, originally reported by UCLA in 2019, could pave the way for a new treatment for the infection, which affects hundreds of Americans each year, primarily in the Southwest, and kills approximately 40% of the people who contract it. The technique described in the study could also suggest a new paradigm for treating other severe fungal infections, bacterial infections such as tuberculosis, and severe viral infections such as influenza and COVID-19. “Immune modulation isn’t currently part of the strategy with any of these severe infections,” said Dr. Manish Butte, the report’s senior author, who holds the E. Richard Stiehm Endowed Chair in Pediatric Allergy, Immunology and Rheumatology at the David Geffen School of Medicine at UCLA. “Our case suggests that rather than hoping to get the upper hand with more and more antibiotics or antifungals, we can have some success by combining these established approaches with the new idea of programming the patient’s immune response to better fight the infection.” Each year, more than 100,000 people are infected with Coccidioides fungi, which reside in the soils of California, Arizona and West Texas. Most people who are infected are asymptomatic, and about 20,000 experience the minor respiratory illness commonly known as Valley fever. The vast majority of people with Valley fever respond well to antifungal medications, but approximately 1% of the infections progress to disseminated coccidioidomycosis, in which the infection spreads rapidly throughout the body, leading to bone and tissue damage, and in many cases death. “Historically, severe infections have been seen as ‘bad luck,’” Butte said. “Doctors haven’t looked at how we can harness the immune systems of these patients to fight the infection.” According to a 2019 study in the International Journal of Environmental Research and Public Health, California spends between $700 million and $900 million a year in direct and indirect costs related to the care of people infected by the cocci fungus, including more than $300 million to care for the approximately 200 people with disseminated coccidioidomycosis. The boy who was treated by Butte and his team had previously been treated with high doses of multiple antifungal medicines, but by the time he arrived at UCLA, he could barely walk or talk and required a feeding tube to eat. When UCLA physicians homed in on the patient’s immune system, they concluded that his T cells — the white blood cells that play a key role in the body’s immune response — were failing to properly recognize the invading fungus. The T cells were responding as though the infection was a parasitic infection rather than a fungal one. That prompted the team to supplement the boy’s antifungal medications with an immune stimulator called interferon-gamma. And Dr. Maria Garcia-Lloret, a pediatric allergist and immunologist, suggested adding yet another medication, dupilumab, which was developed as a medication for allergic diseases and had never before been used to treat infections. Dupilumab is a prescription drug that has not been approved by the FDA as a treatment for disseminated coccidioidomycosis. The combination of immune modulators restored the proper programming to the patient’s T cells — and the boy’s infection went away in a month. The UCLA research team cites that the immunomodulatory approach has the potential to enhance the ability of patients to clear other types of fungal, bacterial, and viral infections that are not responding to established therapies. In partnership with the Bakersfield, California-based Valley Fever Institute and the drugs’ manufacturers — Horizon Therapeutics, Regeneron Pharmaceuticals and Sanofi Genzyme — the UCLA researchers are planning to test the two drugs on other people with disseminated coccidioidomycosis. They also plan to study the approach for treating other types of severe infections. To read the original article click here.

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