Category Archives: Immunology

CEL-SCI Initiates Development of Immunotherapy to Treat COVID-19 Coronavirus Infection – BioSpace

Predictions of success using the LEAPS peptides against COVID-19 coronavirus are based on previous studies conducted in collaboration with the National Institutes for Allergies and Infectious Diseases (NIAID) with another respiratory virus, pandemic influenza (H1N1). In those studies, LEAPS peptides elicited protection of mice from morbidity and mortality after the introduction of infection by activating appropriate T cell responses rather than an inflammatory response.

Although individuals of all ages are susceptible to COVID-19 coronavirus infection, the elderly and individuals with compromised lung function or immunosuppression are at highest risk for severe morbidity and mortality. It is believed that, in most cases, onset of symptoms takes between 2 and 14 days post infection, a period of time that may allow intervention for those at highest risk and with a known exposure.

Daniel Zimmerman, Ph.D. Senior VP of Research, Cellular Immunology at CEL-SCI Corporation, said, We believe that a LEAPS COVID 19 coronavirus peptide will reduce or arrest the progression of the virus infection and prevent tissue damage from inflammation resulting from lung infection by the virus. In short, we believe that we can stimulate the correct immune responses to the virus without producing unwanted inflammatory responses associated with lung tissue damage. That should be particularly important in the older population who is at highest risk of dying from this virus.

CEL-SCI CEO Geert Kersten added, CEL-SCI is currently in discussion with multiple health care partners to expeditiously move this critically important work forward. We look forward to combining the LEAPS technology, experience and expertise of CEL-SCI with the expertise of various partners to promote the rapid development of a LEAPS/COVID-19 product to help particularly those patients who are at very high risk from COVID-19 infection.

COVID-19 is a member of the coronavirus family which jumped to humans from an animal reservoir. Unlike human coronaviruses, which include the second most common cause of the common cold, COVID-19, like its cousins SARS and MERS coronaviruses, can replicate at the higher temperatures within the human lungs and, as a result, can cause highly morbid/mortal disease. It is thought that the morbidity and mortality in the at-risk population is due to lung damage resulting from inflammatory immune responses to the virus.

CEL-SCIs studies will utilize the LEAPS peptide approach which is unique in its proven ability in animals to elicit both a cell mediated antiviral response and an anti-inflammatory immunomodulating response by activating CD8 T lymphocytes. Previous studies showed that LEAPS immunogens can prevent lethal infection by herpes simplex virus (HSV) and influenza A, and stop the inflammatory disease progression of rheumatoid arthritis in animal models. LEAPS peptides against HSV demonstrated that the T cell response was sufficient to prevent viral disease, and if there was residual virus production, anti-viral antibody was generated to further control the spread of the virus.

The proposed LEAPS peptides are directed towards antigens within the NP protein of COVID-19 that elicit cytolytic T cell responses. Unlike glycoprotein spike antigens which are important for antibody based vaccines, these antigens are less variable between viral strains and less likely to change in response to antibodies elicited by prior infection or other vaccines. Cytolytic T cell responses attack the virus infected cellular factories within the infected host in order to eliminate the source of virus and help subdue the infection.

About LEAPS

The Ligand Antigen Epitope Presentation System (LEAPS) platform technology has demonstrated in several animal models the ability to design antigen-specific immunotherapeutic peptides that preferentially direct the immune response to a cellular (e.g., T-cell), humoral (antibody) or mixed response and are also capable of enhancing important T-regulatory (Treg) responses. Therefore, the LEAPS technology provides the opportunity to develop immunotherapeutic products for diseases for which disease associated antigenic peptide(s) sequences have already been identified, such as: a number of infectious diseases, some cancers, autoimmune diseases (e.g., RA), allergic asthma and allergy, select CNS diseases (e.g., Alzheimer's) and the COVID-19 virus.

The Company's LEAPS technology is currently also being developed as a therapeutic vaccine for rheumatoid arthritis and is supported by $1.5 million grant for IND enabling studies from the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

About CEL-SCI Corporation

CEL-SCI believes that boosting a patient's immune system while it is still intact should provide the greatest possible impact on survival. Therefore, in the Phase 3 study CEL-SCI treated patients who are newly diagnosed with advanced primary squamous cell carcinoma of the head and neck with Multikine* first, BEFORE they received surgery, radiation and/or chemotherapy. This approach is unique. Most other cancer immunotherapies are administered only after conventional therapies have been tried and/or failed. Multikine (Leukocyte Interleukin, Injection), has received Orphan Drug designation from the FDA for neoadjuvant therapy in patients with squamous cell carcinoma (cancer) of the head and neck.

CEL-SCI's Phase 3 study is the largest Phase 3 study in the world for the treatment of head and neck cancer. Per the study's protocol, newly diagnosed patients with advanced primary squamous cell carcinoma are treated with the Multikine treatment regimen for 3 weeks prior to the Standard of Care (SOC) which involves surgery, chemotherapy and/or radiation. Multikine is designed to help the immune system "see" the tumor at a time when the immune system is still relatively intact and thereby thought to better able to mount an attack on the tumor. The aim of treatment with Multikine is to boost the body's immune system prior to SOC. The Phase 3 study is fully enrolled with 928 patients and the last patient was treated in September 2016. To prove an overall survival benefit, the study requires CEL-SCI to wait until 298 events have occurred among the two main comparator groups.

The Company has operations in Vienna, Virginia, and in/near Baltimore, Maryland.

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. When used in this press release, the words "intends," "believes," "anticipated," "plans" and "expects," and similar expressions, are intended to identify forward-looking statements. Such statements are subject to risks and uncertainties that could cause actual results to differ materially from those projected. Such statements include, but are not limited to, statements about the terms, expected proceeds, use of proceeds and closing of the offering. Factors that could cause or contribute to such differences include, an inability to duplicate the clinical results demonstrated in clinical studies, timely development of any potential products that can be shown to be safe and effective, receiving necessary regulatory approvals, difficulties in manufacturing any of the Company's potential products, inability to raise the necessary capital and the risk factors set forth from time to time in CEL-SCI's filings with the Securities and Exchange Commission, including but not limited to its report on Form 10-K/A for the year ended September 30, 2019. The Company undertakes no obligation to publicly release the result of any revision to these forward-looking statements which may be made to reflect the events or circumstances after the date hereof or to reflect the occurrence of unanticipated events.

* Multikine (Leukocyte Interleukin, Injection) is the trademark that CEL-SCI has registered for this investigational therapy, and this proprietary name is subject to FDA review in connection with the Company's future anticipated regulatory submission for approval. Multikine has not been licensed or approved for sale, barter or exchange by the FDA or any other regulatory agency. Similarly, its safety or efficacy has not been established for any use. Moreover, no definitive conclusions can be drawn from the early-phase, clinical-trials data involving the investigational therapy Multikine. Further research is required, and early-phase clinical trial results must be confirmed in the Phase 3 clinical trial of this investigational therapy that is in progress.

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AbbVie Partnering with Global Authorities to Determine Efficacy of HIV Drug in Treating COVID-19 | Small Molecules | News Channels -…

DetailsCategory: Small MoleculesPublished on Monday, 09 March 2020 14:35Hits: 281

- Unconfirmed media reports from China claim Kaletra/Aluvia (lopinavir/ritonavir) is effective in COVID-19 treatment. - AbbVie does not have access to Chinese clinical information and therefore cannot confirm its accuracy - AbbVie donated Aluvia to the Chinese government for experimental use against COVID-19 - AbbVie is working with global health authorities to determine the efficacy and safety of lopinavir/ritonavir against COVID-19 - AbbVie does not anticipate disruption to the medicine supply for HIV patients as a result of the investigation of the effectiveness against COVID-19

NORTH CHICAGO, IL, USA I March 9, 2020 I AbbVie (NYSE:ABBV) today confirmed the company's activities in the fight to address the COVID-19 public health crisis, including supporting the experimental use of the HIV medicine, Kaletra/Aluvia (lopinavir/ritonavir) to determine its efficacy in the treatment of COVID-19.

The company is collaborating with select health authorities and institutions globally to determine antiviral activity as well as efficacy and safety of lopinavir/ritonavir against COVID-19. AbbVie is supporting clinical studies and basic research with lopinavir/ritonavir, working closely with European health authorities and the U.S. Food and Drug Administration, Centers for Disease Control and Prevention, National Institutes of Health and Biomedical Advanced Research and Development Authority to coordinate on these efforts. Along with industry partners, the company has joined the Innovative Medicines Initiative to support research and discovery of targeted medicines against COVID-19.

"We are committed to helping in any way we can to address the COVID-19 public health crisis, which is why we responded quickly to the Chinese authorities' request for Aluvia in late January," said Richard A. Gonzalez, chairman and chief executive officer, AbbVie. "We are working with global health authorities to ensure we meet the need of COVID-19 patients, conduct the appropriate clinical trials to evaluate its efficacy and ensure uninterrupted supply of the drug Kaletra/Aluvia for HIV patients around the world."

No expected impact on drug supplyAbbVie has supplied Kaletra/Aluvia as an experimental option for the treatment of COVID-19 to multiple countries that have immediate patient needs due to the outbreak. The company plans to continue to respond to all appropriate requests for product while supporting all efforts to determine the safety and efficacy of this therapy in this patient population.

While helping respond to the COVID-19 crisis is a high priority, the company is committed to protecting the supply of Kaletra/Aluvia for HIV patients. AbbVie is actively assessing the increased demand for Kaletra/Aluvia and has taken steps to increase supply for COVID-19 patients without impacting treatment supply for HIV patients.

AbbVie continues to closely monitor manufacturing and supply chain resources around the world and does not anticipate any disruption to its medicine supply as a result of COVID-19.

About AbbVieAbbVie is a global, research and development-based biopharmaceutical company committed to developing innovative advanced therapies for some of the world's most complex and critical conditions. The company's mission is to use its expertise, dedicated people and unique approach to innovation to markedly improve treatments across four primary therapeutic areas: immunology, oncology, virology and neuroscience. In more than 75 countries, AbbVie employees are working every day to advance health solutions for people around the world. For more information about AbbVie, please visit us at http://www.abbvie.com. Follow@abbvie on Twitter,Facebook, LinkedIn or Instagram.

SOURCE: AbbVie

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How to boost your immune system to avoid colds and coronavirus – The Guardian

Its been a long, wet winter. Everybody has got colds, and now we are braced for a coronavirus epidemic. Boosting our immune system has rarely felt more urgent, but, beyond eating more tangerines and hoping for the best, what else can we do?

Sheena Cruickshank, a professor of immunology at the University of Manchester, has a shocking cold when we speak at a safe distance, over the phone. To know how to take care of your immune system, she says, first you need to understand the weapons in your armoury a cheeringly impressive collection, it turns out.

When you come into contact with a germ youve never met before, she says, youve got various barriers to try to stop it getting into your body. As well as skin, we have mucus snot is a really important barrier and a microbiome, the collective noun for the estimated 100tn microbes that live throughout our bodies, internally and externally. Some of these helpful bugs make antimicrobial chemicals and compete with pathogens for food and space.

Beneath these writhing swamps of mucus and microbes, our bodies are lined with epithelial cells which, says Cruickshank, are really hard to get through. They make antimicrobial products including, most relevant to coronavirus, antiviral compounds that are quite hostile.

If a pathogen breaches these defences, it has to deal with our white blood cells, or immune cells. One type, called macrophages, inhabit all our body tissue and, says Cruickshank, have all these weapons ready to go, but theyre not terribly precise. They report to the cleverer, adaptive white blood cells known as lymphocytes. They are the ones that remember germs, so if you meet that germ again, says Cruickshank, theyll just deal with it probably without you even knowing. Thats when youve got immunity and is the basis of vaccination. Its trying to bypass all the early stuff and create the memory, so you dont have to be sick.

Our immune systems may have blind spots. This might mean that our immune response doesnt recognise certain bugs, she says, or the bugs have sneaky evasion strategies. Personally, my immune system is not necessarily very good at seeing colds. But a healthy lifestyle will ensure your defences are as good as they get.

Seeing as our bodies contain more cells belonging to microbes, such as bacteria and yeasts, than human ones, lets start with the microbiome. We live in a symbiotic relationship with our gut bacteria, says Prof Arne Akbar, the president of the British Society for Immunology and a professor at University College, London. Having the right ones around, that we evolved with, is best for our health. Anything we do that alters that can be detrimental.

Not only do our microbes form protective barriers, they also programme our immune systems. Animals bred with no microbiome have less well developed immune responses. Older people, and those with diseases that are characterised by inflammation, such as allergies, asthma, rheumatoid arthritis and diabetes, tend to have less varied gut microbiomes.

To feed your gut flora, Cruickshank recommends eating a more varied diet with lots of high-fibre foods. Being vegetarian isnt a prerequisite for microbiome health, but the more plant foods you consume, the better. The microbiome really likes fibre, pulses and fermented foods, she adds.

Kefir yoghurt and pickles such as sauerkraut and kimchi are among the fermented delicacies now fashionable thanks to our increasing knowledge of the microbiome. But the evidence for taking probiotic supplements, she says, is mixed. Its not a dead cert that they will survive the journey through your digestive tract, or that they will hang around long enough if they do. Its more effective to change your diet, says Cruickshank.

The skin microbiome is important, too, but we know less about it. High doses of ultraviolet light (usually from the sun) can affect it negatively, weakening any protective functions (as well as triggering immune suppression in the skin itself). Overwashing with strong soaps and using antibacterial products is not friendly to our skin microbiomes. Combinations of perfumes and moisturisers might well also have an effect, says Cruickshank.

To be immunologically fit, you need to be physically fit. White blood cells can be quite sedentary, says Akbar. Exercise mobilises them by increasing your blood flow, so they can do their surveillance jobs and seek and destroy in other parts of the body. The NHS says adults should be physically active in some way every day, and do at least 150 minutes a week of moderate aerobic activity (hiking, gardening, cycling) or 75 minutes of vigorous activity (running, swimming fast, an aerobics class).

The advice for older people, who are more vulnerable to infection, is to do whatever exercise is possible. Anythings better than nothing, says Akbar. But a lifetimes exercise could significantly slow your immune system declining with age. In 2018, a study by University of Birmingham and Kings College London found that 125 non-smoking amateur cyclists aged 55 to 79 still had the immune systems of young people.

The other side of the coin, says Akbar, is elite athletes who become very susceptible to infections because you can exercise to a point where it has a negative impact on your immune system. This problem is unlikely to affect most of us unless, says Cruickshank, youre a couch potato and suddenly try and run a marathon, this could introduce stress hormones and be quite bad for your immune system.

One of the many happy side-effects of exercise is that it reduces stress, which is next on our list of immune-boosting priorities. Stress hormones such as cortisol can compromise immune function, a common example of which, says Akbar, is when chickenpox strikes twice. If you have had it, the virus never completely goes away. During periods of stress, he says, it can reactivate again and we get shingles.

Forget boozing through the coronavirus crisis, because heavy drinking also depletes our immune cells. Some studies have suggested that the first-line-of-defence macrophages are not as effective in people who have had a lot of alcohol, says Cruickshank. And theres been suggestions that high alcohol consumption can lead to a reduction of the lymphocytes as well. So if the bug gets into you, youre not going to be as good at containing and fighting it off.

Cruickshank says that vitamin D has become a hot topic in immunology. It is used by our macrophages, and is something that people in Britain can get quite low on in the winter. Necking extra vitamin C, however, is probably a waste of time for well-fed westerners. Its not that vitamin C isnt crucial to immune function (and other things, such as bone structure). All the vitamins are important, says Cruickshank, but vitamin C is water soluble, its not one that your body stores. Eating your five a day of fruits and vegetables is the best way to maintain necessary levels.

Exercising and eating well will have the likely knock-on effect of helping you sleep better, which is a bonus because a tired body is more susceptible to bugs. One study last year found that lack of sleep impaired the disease-fighting ability of a type of lymphocyte called T cells, and research is demonstrating the importance of our natural biorhythms overall.

Janet Lord, a professor at the University of Birmingham, recently showed that vaccinating people in the morning is more effective than doing so in the afternoon. Your natural biorhythms are, to some extent, dictated by sleep, says Akbar. If youve got a regular sleep pattern, you have natural body rhythms and everythings fine. If they go out of kilter, then youve got problems.

The seriousness of an infection largely depends on the dose you are hit with, which could in turn depend on how contagious the carrier is when they cough near you. Were constantly exposed to germs, and we only get sick from a handful of those, says Cruickshank.

If youre reasonably young and healthy, says Akbar, the mild benefits you may achieve from being extra good probably wont fend off a severe dose of coronavirus or flu. The likely scenario if you catch the infection is, he says, youll be sick for a while and you will recover.

From a public-health perspective, when nasty viruses such as coronavirus are doing the rounds, Akbars priority is not boosting already healthy peoples immune systems, but protecting the vulnerable people. Older people dont respond that well to the flu jab, though its better for them to have it than not. Its a general problem of immune decline with ageing.

When we get older, he says, the barrier function in the gut doesnt work that well, so you have something called leaky gut syndrome, where bugs creep into our bodies causing mild infections. This causes inflammation around the body, as does the natural accumulation of old zombie cells, called senescent cells, and inflammation compromises the immune response.

Akbar is working on developing drug treatments to reduce inflammation in older people but they are a way off yet. Age 65 is when, medically, one is considered older, but thats arbitrary, says Akbar. Some old people might get problems much earlier. And there are older people who are totally healthy.

In terms of coronavirus, says Cruickshank, its mostly spread by droplet transmission, as far as we can tell, so the biggest thing is hygiene. So wash your hands, and sneeze and cough into tissues, she suggests, between sniffles. No one can completely avoid getting sick, not even top immunologists.

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How to boost your immune system to avoid colds and coronavirus - The Guardian

Hinojosa: Working Together to Beat Cancer – Rio Grande Guardian

Cancer is the second most common cause of death in Texas adults, and the same is true inthe Rio Grande Valley.

According to the Texas Cancer Registry Annual Report 2019, anestimated 124,383 new cases of cancer will be diagnosed in Texas and an estimated45,524 Texans will die from cancer.

In 2017, Hidalgo County had2,411 cancer cases of which 814 resulted in death.

Last year, Dr. John Krouse, dean of the University of Texas Rio Grande Valley School ofMedicine, stated that cervical cancer in women occurs more frequently in the Valley andwhen it occurs the mortality rate is much higher in the Valley. That is just unacceptable.That is something we need to address, and we need to fix.I completely agreeand we have been taking the necessary steps to tackle these challenges.

The first step in this process was passing a bill in 2013 that created the University of TexasRio Grande Valley (UTRGV) and the accompanying School of Medicine (SOM).Thistransformational institution has brought millions of dollars in state and federalfunding to our region, increased our health care infrastructure and personnel, and hasallowed us to begin addressing many of our health care needs.

It has also opened the doors to public-private partnerships that benefit us all, such as theopening of the UTRGV Biomedical Research Building. This opening was made possible due to thecollaboration between the SOM, the City of McAllen, and DHR Health (DHR). This building,located in McAllen, is home to the South Texas Center of Excellence in CancerResearch and a new cancer immunology team that will focus on womens cancerstarting with cervical cancer and transitioning to breast cancer. I appreciate the City ofMcAllens financial contribution and commitment to fund this research program.Thiscooperative effort will lead to new treatment opportunities for patients with cancer.

To continue making progress to address the challenge with Breast and Cervical Cancer, I secured $2.7 million in State funds to support the Cervical Dysplasia and Cancer Immunology Center.We have been working to transfer the Center from the University of Texas Medical Branch to UTRGV School of Medicine. This will improve cooperation and coordination of diagnoses, treatment and research to fight Breast and Cervical Cancer.

Another program that could help improve cancer diagnosis and prognosis for those in theValley is a biorepository for cancer research. DHR is currently working to obtain a Cancer Prevention and Research Institute of Texas (CPRIT) grant that will allow them to expand the current BorderBioRepository at DHR to establish a cancer biorepository.

These efforts will be of great benefit to the women in the Valley and South Texas, but there is still more to bedone. Cancer has no boundaries and can impact anyone regardless of age, gender, or race.For this reason, we are working with community leaders in both the public and privatesector on establishing a world-class cancer treatment clinic that will provide care toValley patients here at home. We are pursuing partnerships with the best entities in thefield, to make this vision a reality.

In the past six months, we have met with CPRIT leadership to advocate not only for additional funding to help prevent cancer, but also for financial support to recruit oncologists and expand our cancer treatment infrastructure in South Texas. CPRIT is a key funding source for cancer research and treatment provided to our universities, medical schools, and other entities committed to fighting cancer. For this reason, I advocated for and supported the appointment of Dr. Ambrosio Hernandez to the CPRIT Board. He is a physician with extensive experience in public health, is a dedicated public servant, and understands the needs of our communities.

We have also pushed for additional partnerships with the best entities in the field, such as M.D. Anderson. UTRGV is currently in the process of developing an oncology program that will assist in actively recruiting clinical oncologists to increase our clinical workforce in this field and provide guidance and expertise in developing best practices and treatments for patient care.

We must give our South Texas patients all the help they can get from modern medicine in the fight against cancer here at home. We will keep working to secure the partnerships and investments necessary so that in the future our patients in South Texas will have access to top notch facilities and world-class doctors. By working together, we can ensure that Valley residents have all of these resourcesavailable to them during their battle. Working together, we can beat cancer.

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Coronavirus Market Correction: Where to Invest $1,000 Right Now – Motley Fool

What should I do?

That's the question that's on the mind of many investors right now. Fears about the global coronavirus outbreak have caused a market correction. A natural instinct is to flee -- run as fast as you can away from the stock market. But I suspect most investors know that this natural instinct isn't the best choice. The smarter approach is to take advantage of the buying opportunity that the market correction presents.

And that leads to another question: What stocks should I buy? There are actually plenty of good answers to that question because there are plenty of great stocks.

My view is that there are three kinds of stocks that you should consider buying during the market downturn. First, look at stocks that have held up well despite the overall market downturn -- the exceptions to the rule. Second, check out stocks that are dirt cheap because of the correction. And third, invest in stocks that are simply great businesses to own no matter what happens with the overall market.

If you have some available cash, I think that investing $1,000 in each of the following three stocks that represent each of those categories is a great place to start.

Image source: Getty Images.

Few stocks have been able to defy the gravity of the overall stock market decline in recent days. But Gilead Sciences (NASDAQ:GILD) is one of them. It helped a lot that a World Health Organization (WHO) official stated recently that Gilead's experimental drug remdesivir appears to have the most potential in being effective at treating COVID-19, the disease caused by the novel coronavirus.

While Gilead's promising antiviral drug remdesivir is the reason why the stock has risen by a double-digit percentage this year, it's not the main reason I like the biotech stock. There are actually four other things that I like even more about Gilead than its coronavirus program. The first three relate to the company's current drugs and pipeline candidates.

Gilead continues to be a juggernaut in HIV. Biktarvy appears destined to become the most successful HIV drug in history. Thanks to the company's 2017 acquisition of Kite Pharma, Gilead is a leader in cancer cell therapy -- an area that I think will gain momentum in the future. The biotech is also poised to enter the immunology market if filgotinib wins FDA approval later this year in treating rheumatoid arthritis. Some analysts project that filgotinib could generate peak annual sales of close to $6 billion if approved for multiple indications.

That leaves the fourth reason I like Gilead: Its dividend. Most biotechs don't pay dividends, but Gilead is yet again an exception to the rule. Its dividend yield currently stands at close to 3.6%. Gilead has increased its dividend payout by 58% since initiating its dividend program in 2015. With more dividend increases probably on the way and growth drivers in HIV, oncology, and immunology (plus potentially with its coronavirus drug), Gilead should provide market-beating returns over the long run.

TD Ameritrade Holding (NASDAQ:AMTD) has fallen hard during the market downturn. Shares of the online brokerage are down nearly 30%, a significantly worse performance than its peers. TD Ameritrade stock now trades at less than 14 times expected earnings.

Granted, it's not just worries about the coronavirus outbreak that have caused TD Ameritrade's stock to drop. The antitrust division of the Department of Justice is investigating the pending acquisition of TD Ameritrade by Charles Schwab (NYSE:SCHW). There's a possibility that the deal could be blocked.

But those fears could be overblown. Schwab and TD Ameritrade say they're cooperating fully with the DOJ and expect the transaction to close in the second half of this year.

What if the DOJ prevents the acquisition? I still think the future for TD Ameritrade looks bright. Investors continue to flock to online brokerages. The greatest generational transfer of wealth is on the way. Research firm Cerulli Associates estimates that over the next 25 years $68 trillion will shift from older parents to their children. A lot of that money will be invested in stocks, creating a major opportunity for TD Ameritrade whether it remains an independent entity or not.

Last -- and certainly not least -- Brookfield Infrastructure Partners (NYSE:BIP) is just a great business to own. I'd make that claim even if the stock hasn't performed pretty well this year (which it has).

If you can think of a type of infrastructure asset, Brookfield Infrastructure probably owns it. Cell towers, data centers, electricity transmission systems, natural gas pipelines, ports, railroads, toll roads, and more are all in the company's portfolio.

I personally bought shares of Brookfield Infrastructure earlier this year, mainly because I think the company's business model is rock-solid. Brookfield doesn't have to worry about a viral epidemic impacting its financial strength. Close to 95% of its adjusted EBITDA comes from regulated or contracted revenue that won't change with twists and turns in the overall economy.

Brookfield Infrastructure also pays a dividend that yields more than 4%. The company has boosted its dividend payout by 52% over the last five years. With Brookfield's strategy of selling lower-performing assets to reinvest in more promising assets, I look for solid earnings growth plus more dividend increases in the future.

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New ‘Immuno-Engineering to Improve Immunotherapy’ Center formed to advance cancer therapy – The Medical News

Harvard University's Wyss Institute of Biologically Inspired Engineering and its collaborating institutions, the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS), Dana-Farber Cancer Institute (Dana-Farber), and Harvard's Department of Stem Cell and Regenerative Biology, announce the formation of a new NIH-funded Immuno-Engineering to Improve Immunotherapy (i3) Center. The cross-institutional and cross-disciplinary i3 Center includes world-leading researchers in the cancer immunology and bioengineering fields and will create biomaterials-based approaches to enable anti-cancer immuno-therapy in settings where it currently is limited, such as in myeloid malignancies and solid tumors.

The Harvard i3 Center is part of NIH's Cancer MoonshotSM initiative that was formed to accelerate cancer research to make more therapies available to more patients, while also improving the ability to prevent cancer and detect it at an early stage.

We aim to develop new technologies that induce robust anti-cancer T cell immunity, and we also hope that the i3 Center's highly cross-disciplinary and cross-fertilizing mechanisms will provide a center of gravity for many future efforts in the immuno-therapy space across and beyond our collaborating institutions."

David Mooney, Ph.D., Wyss Institute Founding Core Faculty member, one of the two principal investigators (PIs) of the i3 Center

Mooney also is the Robert P. Pinkas Family Professor of Bioengineering at SEAS and leads the Wyss Institute's broader Immuno-Materials Initiative. His team has developed a number of strategies that use immune-modulating biomaterials to trigger and enhance T cell-mediated immune responses against tumors. Most notably, together with clinical collaborators, they succeeded in creating the first implantable vaccine ever to eliminate melanoma tumors in mice, which the Wyss Institute and Dana-Farber are investigating in an ongoing Phase I clinical trial at the Dana-Farber.

F. Steven Hodi, Jr., M.D., Director of Melanoma Center and The Center for Immuno-Oncology at Dana-Farber, and Professor of Medicine at Harvard Medical School (HMS), is leading the clinical cancer vaccine trial, and is the i3 Center's other PI. Hodi has been at the forefront of developing cancer immunotherapies using "immune checkpoint inhibitors," a class of drugs able to re-activate tumor-destroying T cells that are muted in the tumor microenvironment. "The funding for this center provides a unique opportunity to unite key investigators for translating fundamental advancements in immunology and biomedical engineering into highly synergistic approaches to improve the treatments for cancer patients," said Hodi.

Using both in vivo and ex vivo biomaterials-based approaches, the i3 Center aims to boost tumor-specific activities of cytotoxic T cells, by boosting different stages of the normal process by which T cells develop, and acquire anti-cancer activity. T cells' normal development starts in the bone marrow where hematopoietic stem cells generate T cell progenitor cells. These migrate to the thymus to differentiate into nave T cells, which then travel further to lymph nodes. There, they encounter cancer-derived antigens presented to them by specialized antigen-presenting cells (APCs) that can activate T cells to recognize and eliminate cancer cells.

In relation to "adoptive T cell" therapies in which T cells are given to patients to fight their cancers, one team at the i3 Center will be led by Dana-Farber researchers Catherine J. Wu, M.D., and Jerome Ritz, M.D., who along with Mooney, will develop and test biomaterials that can better mimic normal APCs in activating and directing the function of patient-derived T cells outside the human body, prior to their transplantation. Wu is Chief of the Division of Stem Cell Transplantation and Cellular Therapies, and Ritz is Executive Director of the Connell and O'Reilly Families Cell Manipulation Core Facility at Dana-Farber.

"We need to make efforts to enhance the ability of the immune system to recognize tumor cells. One direction my laboratory is taking makes use of innovative biomaterials to help us to efficiently expand polyclonal tumor-specific functionally-effective T cells ex vivo in a way that can be readily translated to the clinical setting. In our studies, we are currently focusing on melanoma and acute myeloid leukemia," said Wu, whose research interests include understanding the basis of effective human anti-tumor responses, including the identification and targeting of the tumor-specific antigens.

A second project explores the use of DNA origami, biocompatible nanostructures composed of DNA, to create cancer vaccines. DNA origami could provide significant advantages in presenting tumor-specific antigens and immune-enhancing adjuvants to APCs because the concentrations, ratios, and geometries of all components can be modulated with nano-scale precision to determine configurations that are more effective than other vaccination strategies. The project will be run by Wyss Institute Core Faculty member William Shih, Ph.D., Derin Keskin, Ph.D., lead immunologist at Dana-Farber's Translational Immunogenomics Lab, and Mooney.

In a third project, David Scadden, M.D., the Gerald and Darlene Jordan Professor of Medicine at Harvard University, and Professor at Harvard's Department of Stem Cell and Regenerative Biology, and Mooney, based on their previous work, will engineer biomaterials that recreate key features of the normal hematopoietic stem cell niche in the bone marrow. Such implantable biomaterials could help rapidly amplify T cell progenitor cells, and enhance T cell-mediated anti-cancer immunity.

The i3 Center's investigators anticipate that it will stimulate additional cross-disciplinary concepts and research, due to the culture of continuous interactions, sharing of findings, data and samples between all investigators, as well strong biostatistical expertise provided by Donna Neuberg, Sc.D., a senior biostatistician broadly involved with exploring immune-modulating cancer interventions at the Dana-Farber.

"This new i3 Center for cancer immunotherapy innovation really embodies how the Wyss Institute with its unparalleled capabilities in bioengineering and serving as a site for multidisciplinary collaboration, and can liaise with clinicians and researchers at our collaborating institutions to confront major medical problems and bring about transformative change," said Wyss Founding Director Donald Ingber, M.D., Ph.D. He is also the Judah Folkman Professor of Vascular Biology at HMS and the Vascular Biology Program at Boston Children's Hospital, and Professor of Bioengineering at SEAS.

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New 'Immuno-Engineering to Improve Immunotherapy' Center formed to advance cancer therapy - The Medical News

NIH-funded i3 Center formed to advance cancer immunotherapy – Harvard Gazette

Steven Hodi Jr., the i3 Centers other PI, and director of Melanoma Center and the Center for Immuno-Oncology at Dana-Farber, and professor of medicine at Harvard Medical School (HMS), is leading the clinical cancer vaccine trial. He has been at the forefront of developing cancer immunotherapies using immune checkpoint inhibitors, a class of drugs able to re-activate tumor-destroying T cells that are muted in the tumor microenvironment. The funding for this center provides a unique opportunity to unite key investigators for translating fundamental advancements in immunology and biomedical engineering into highly synergistic approaches to improve the treatments for cancer patients, said Hod

Using both in vivo and ex vivo biomaterials-based approaches, the i3 Center aims to boost tumor-specific activities of cytotoxic T cells, by boosting different stages of the normal process by which T cells develop, and acquire anti-cancer activity. T cells normal development starts in the bone marrow where hematopoietic stem cells generate T cell progenitor cells. These migrate to the thymus to differentiate into nave T cells, which then travel further to lymph nodes. There, they encounter cancer-derived antigens presented to them by specialized antigen-presenting cells (APCs) that can activate T cells to recognize and eliminate cancer cells.

In relation to adoptive T cell therapies in which T cells are given to patients to fight their cancers, one team at the i3 Center will be led by Dana-Farber researchers Catherine J. Wu and Jerome Ritz, who along with Mooney, will develop and test biomaterials that can better mimic normal APCs in activating and directing the function of patient-derived T cells outside the human body, prior to their transplantation. Wu is chief of the Division of Stem Cell Transplantation and Cellular Therapies, and Ritz is executive director of the Connell and OReilly Families Cell Manipulation Core Facility at Dana-Farber.

We need to make efforts to enhance the ability of theimmune systemto recognizetumor cells. One directionmylaboratoryis taking makes use of innovative biomaterialsto help us to efficiently expandpolyclonaltumor-specificfunctionally-effectiveT cellsex vivoin a way that can be readily translated to theclinical setting. In our studies, we are currently focusing on melanoma and acute myeloid leukemia, said Wu, whose research interests include understanding the basis of effective human anti-tumor responses, including the identification and targeting of the tumor-specific antigens.

A second project explores the use of DNA origami, biocompatible nanostructures composed of DNA, to create cancer vaccines. DNA origami could provide significant advantages in presenting tumor-specific antigens and immune-enhancing adjuvants to APCs because the concentrations, ratios, and geometries of all components can be modulated with nano-scale precision to determine configurations that are more effective than other vaccination strategies. The project will be run by Wyss Institute Core Faculty member William Shih, Derin Keskin, lead immunologist at Dana-Farbers Translational Immunogenomics Lab, and Mooney.

In a third project, David Scadden, professor at Harvards Department of Stem Cell and Regenerative Biology, will collaborate with Mooney to build on their previous work. They will engineer biomaterials that recreate key features of the normal hematopoietic stem cell niche in the bone marrow. Such implantable biomaterials could help rapidly amplify T cell progenitor cells, and enhance T cell-mediated anti-cancer immunity. Scadden also is the Gerald and Darlene Jordan Professor of Medicine at Harvard University, and co-director of the Harvard Stem Cell Institute.

The i3 Centers investigators anticipate that it will stimulate additional cross-disciplinary concepts and research, due to the culture of continuous interactions, sharing of findings, data and samples between all investigators, as well strong biostatistical expertise provided by Donna Neuberg, a senior biostatistician broadly involved with exploring immune-modulating cancer interventions at the Dana-Farber.

This new i3 Center for cancer immunotherapy innovation really embodies how the Wyss Institute with its unparalleled capabilities in bioengineering and serving as a site for multidisciplinary collaboration, and can liaise with clinicians and researchers at our collaborating institutions to confront major medical problems and bring about transformative change, said Wyss Founding Director Donald Ingber. He is also theJudah Folkman Professor of Vascular Biologyat HMS and the Vascular Biology Program at Boston Childrens Hospital, and Professor of Bioengineering at SEAS.

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NIH-funded i3 Center formed to advance cancer immunotherapy - Harvard Gazette

Fighting infection with curiosity – Pursuit

As a child I wanted to be an artist, not a scientist. But my mum, who was an artist, wanted me to do a sensible degree she was concerned that its tough to have a stable job as an artist.

So when I went to university in the UK, where I did a degree in biology.

The irony, of course, is that you never have an entirely stable job in science either. During the first couple of years of my degree I didnt take it very seriously, and science as a career wasnt on the cards for me at all.

Then in the third year of my degree, everything changed when I contracted glandular fever. Studying immunology coincided with having an infection that made me feel terrible.

Im a fixer, so I started to research what was wrong with me and what could be done about it.

Until that point, science had largely just been learning from textbooks and recalling information. By doing self-directed research, I started to realise how completely fascinating viruses and the immune system are.

I absolutely fell in love with immunology and went on to do my PhD on the immune response to Epstein-Barr virus the virus that causes glandular fever.

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It was while studying for my PhD that I became obsessed with research. My mentor was world expert Professor Alan Rickinson at the University of Birmingham. He had actually worked with Tony Epstein and Yvonne Barr, who had first discovered the virus.

I began researching the role of T cells, a type of white blood cell that combats viral infection which Ive now been researching ever since.

Alan gave me free rein and I found research was totally creative and exciting. I dont draw artistically much these days, but sketch out my scientific ideas all the time.

When I dream about a problem or an ongoing issue in the lab, I wake up and think, was it that molecule we should look at? and Id draw out the molecular pathways of how something might theoretically work.

By researching T cells I realised how amazing they are they can fight HIV, malaria and cancer. I began looking around for post-doctoral opportunities in T cell research. I went to a Keystone conference in the US where Professor Frank Carbone from the University of Melbourne presented his then unpublished work on tissue-resident memory T-cells (Trms).

Up until this point, T cell research had largely focused on T cells that circulate in the blood, but Trms are specialised to operate in tissues of the body such as the skin, where they can more effectively control localised virus infections.

Listening to him I was just blown away and decided right then and there to ask him for a post-doc position in Melbourne. I was nervous just going up to him cold because I can be pretty shy, but sometimes you just need to do it. And he said sure.

It was the best and worst time of my life. It was the best time because the work was so exciting. But it was a high pressure situation working in a highly competitive field, plus the pressure to publish and win grants.

And it is soul-destroying when no matter how hard you push or how many hours you work sometimes your experiments just dont work or go anywhere and you cant see the wood for the trees.

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That is why it can be tough for young researchers working on single projects. In that respect, being head of a lab is somewhat easier because you can put projects that arent working aside for a while, and work on something else before coming back to them.

I have had projects that have been dead for years that Ive been able to reinvigorate in the wake of new discoveries or new technology.

My turning point came when for the first time I was able to demonstrate that embedded Trms could stop a skin infection. We were vaccinating mice by embedding Trm in the skin and then subsequently infecting that skin site with herpes simplex virus.

This is a virus that causes an ulcer-like lesion on the skin, so you can really see when youve stopped the infection. Thats when I realised that this stuff really works!

The endgame now is to work out how to engineer and boost the numbers of Trms where you want them so they can better fight infections. Just a few years ago this was a bit of a pipe-dream, but so many people are working in this area of research now that Trm-based therapies are very possible.

There are already phase I clinical trials under way for embedding Trms in the liver to treat malaria, as well as for embedding them in the mucosa to fight simian immunodeficiency virus (SIV), which is the primate version of HIV.

Our team are now also working with pharmaceutical companies to design drugs that target molecules to boost Trms.

What I worry most about in the Australia research sector is funding for discovery research. There is a real push now towards funding translational research that is focused on applying discoveries.

But if that comes at the expense of funding basic research, it will discourage researchers from doing blue-sky research and making discoveries the danger is that then the discovery pipeline will run out and there will be fewer ideas left to translate.

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Like many fields, medical research can be a bit of a boys club. It can be intimidating to be the only woman in the room. Its getting better all the time, but Ive had some horrifically condescending things said to me. You have to develop a thick skin.

Just from observation, I dont think women put themselves forward as much as men, and this means women can be overlooked more often. You have to be prepared to stand up for yourself and sometimes have the difficult conversations.

It isnt easy and it certainly goes against my nature, but every time Ive had a tough conversation Im always happy that I did.

I never planned to be a Laboratory Head. I really enjoyed my time as a post-doctoral researcher focused on the fun stuff that is making breakthroughs and solving puzzles. But then you get grants and fellowships, and suddenly you can employ people and start to build a team.

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I find that a huge responsibility, mentoring young scientists and keeping different projects on track. But as a team, and together with collaborators, the work we can do now is incredibly broad.

I know it sounds cheesy but the research is so fun and so collaborative. Its what has always surprised me.

As told to Andrew Trounson

Banner: A computer illustration of a T cell interacting with another part of the immune system, a dendritic cell. Picture: Getty Images

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Fighting infection with curiosity - Pursuit

Coronavirus is not killing 3.4% of patients. How the rate got inflated and why it will get lower – Houma Courier

In February, Chinese researchers said 2.3% of people infected in that country had died from the coronavirus. This week, world health officials put the worldwide figure at 3.4%, a figure that President Donald Trump labeled Wednesday night as false.

That may not be the best choice of words, but Trump has a point: Any calculation of a death rate is premature at this point, and the real figure is almost certainly lower. With the help of a special kind of blood test, better numbers are on the way.

The issue is not that health agencies cant count, but that in the heat of an epidemic, patients with mild or no symptoms do not seek treatment, arent immediately identified, and therefore arent counted as survivors in calculating fatalities. Plus, testing those who do seek treatment has been seriously delayed in some countries, including the United States.

So on Tuesday, when the World Health Organization divided the 3,112 deaths known at that point by the 90,870 confirmed patients, for a death rate of 3.4%, they really should have been dividing by a bigger denominator if only they knew what it was.

You get an unfairly high estimate of the severity and the case fatality risk, Marc Lipsitch, professor of epidemiology at the Harvard Chan School of Public Health, said at a press briefing.

The blood screening that will provide better estimates is called a serologic test, which allows researchers to identify people who were infected with a virus weeks after they recover, said Catharine Paules, an infectious diseases physician at Penn State Health Hershey Medical Center.

That is different from the kind of rapid testing that takes place during an epidemic, when samples from suspected patients (in this case, nasal swabs) are tested for the virus itself. Soon after a person recovers, the virus can no longer be detected.

Serologic testing, on the other hand, detects the presence of antibodies that patients immune systems have produced in response to the virus, Paules said. These antibodies are produced at detectable levels within a few weeks of the initial exposure.

Rather than looking for the actual virus, a serologic test is looking for an individuals immune response to the virus, she said.

With some viruses, such as measles, antibodies can be detected years after a person was infected. With respiratory viruses, antibody levels tend to decline more quickly, but should still be detectable for several months after an infection, she said.

Armed with a serologic test, epidemiologists can test the blood from a representative sample of community members, arriving at a robust estimate of how many people were infected in a broader population. Such screening already is underway in Singapore, using a test developed by researchers at Duke-NUS, a medical school in that country with ties to Duke University. Other countries are still in the process of developing such tests.

In all likelihood, epidemiologists say, the true death rate is well below 3.4%, and even lower than the 2.3% in the Chinese study.

Yet that is not entirely good news, if it means the virus has been circulating undetected in much higher numbers. If the virus were to kill, say, 1% of 300,000 infected patients, thats the same result as 3% of 100,000: 3,000 deaths.

Generally, testing a persons blood for antibodies is done in two phases, said Stanley Perlman, a University of Iowa professor of microbiology, immunology and pediatrics.

The first round commonly involves a technique called ELISA, which makes use of customized enzymes (the E in the acronym) to detect the antibodies in question, said Perlman, a member of the American Association of Immunologists.

The second round, called a neutralizing assay, involves directly putting a patients blood sample to the test, by seeing if it will neutralize the actual virus.

In the short term, physicians are focused on treating the sick. But before long, they will have a better idea of the true scope of the problem.

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Coronavirus is not killing 3.4% of patients. How the rate got inflated and why it will get lower - Houma Courier

Children are more likely to have other allergies if they have FPIES – Health Europa

The researchers from the Childrens Hospital of Philadelphia (CHOP) have found that children with a rare food allergy known as food protein-induced enterocolitis syndrome (FPIES), have a significantly higher chance of being diagnosed with other allergic conditions. These conditions include eczema, traditional food allergy and asthma. However, the researchers also found that FPIES did not directly cause those other allergies.

The condition causes repetitive vomiting, diarrhoea, and lethargy several hours after eating a trigger food, frequently cows milk, soy, and grains. The condition typically develops during infancy, although it can sometimes occur in older children and adults.

Melanie Ruffner, M.D., Ph.D., attending physician in the Division of Allergy and Immunology and the Center for Pediatric Eosinophilic Disorders at CHOP said: This work refines our view of the natural history of FPIES and expands our understanding of the relationship between this condition and other allergic diseases,

Its important for clinicians to keep in mind that patients with FPIES have a higher frequency of allergic manifestations and therefore provide appropriate screening and care as needed.

Previous research has collectively shown patients with FPIES have increased rates of eczema, other food allergies and asthma so-called atopic allergies researchers have not investigated the association between FPIES and other allergies to look for a potential causal link.

To begin the investigation Ruffner and her collaborators looked at a cohort of more than 150,000 paediatric patients, of which 214 had FPIES. The researchers followed the patients over a period of time to see if there were differences in the timing of when FPIES patients developed atopic allergies compared to other patients. The investigators then compared the rate of atopic allergies in FPIES patients to those without FPIES.

The results published in the Journal of Allergy and Clinical Immunology: In Practice, reveals that those with FPIES had substantially higher allergy rates than patients without the condition.

FPIES patients were diagnosed with traditional food allergy at about six times the rate of those without FPIES and with atopic dermatitis at about twice the rate. The research team found that there was a slightly smaller increase in the rate of asthma diagnoses, but those with FPIES were still diagnosed at a higher rate than those without the disease.

However, when the research team looked at the timing of the development of allergies, and whether a diagnosis of FPIES would lead to atopic allergies later in life, they did not find a causal link between the two.

Therefore, FPIES does not cause other allergic disorders but instead is associated with them unlike the progression of atopic disorders like eczema in infants to hay fever, food allergies and asthma in older children.

David Hill, M.D., Ph.D., corresponding author, attending physician in CHOPs Division of Allergy and Immunology explained that: Although there is an increased rate of atopic allergies in patients with FPIES, our analyses demonstrate that a prior diagnosis of FPIES does not increase the rate of atopic allergies later in life,

This pattern of association supports a yet-unknown cause, such as a shared predisposition to both types of allergy.

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Children are more likely to have other allergies if they have FPIES - Health Europa