About the Author Reprints By Helen Branswell Nov. 9, 2015 Reprints @HelenBranswell Tags infectious diseasepublic healthSARS The new study was published in the journal Nature Medicine.The UNC scientists wanted to see if cousin viruses — coronaviruses that are carried by Chinese horseshoe bats — also posed a threat to people. They used one, SHC014, as a representative of the group.advertisement They inserted a key part of the virus, its spike protein, into a SARS virus and then ran experiments to see if the hybrid virus could infect human respiratory tract cells (in a dish) and mice that were vulnerable to the SARS virus.It did.“I think the existence of viruses that can jump directly is the important part, that was unanticipated,” lead author Vineet Menachery, who researches viral immunology, told STAT in an interview.“Based on what was known in the literature, we would have expected that viruses coming out of bats would have needed that one-in-million mutation.”Another coronavirus expert, Dr. Stanley Perlman at the University of Iowa, suggested the paper was a useful investigation. But he noted the hybrid virus was attenuated — weakened — and said the virus would probably need to adapt more in people before it could spread widely.SARS wasn’t a highly transmissible virus. Many patients didn’t infect anyone else during the 2003 outbreak. Once hospitals learned how to recognize the disease and put stringent infection control measures in place — isolating patients and requiring staff treating them to wear the right protective equipment — the outbreak was contained.The SHC014 virus is part of a cluster of related coronaviruses, explained senior author Ralph Baric, a professor of epidemiology at UNC. Some are quite similar to the SARS virus while others are more distant relatives, varying in terms of their genetic structures by between 5 percent and 60 percent. SHC014 was about 12 percent different from SARS.A coronavirus expert, Baric said if the viruses were too distantly related to SARS — more than 25 percent different — they would not be able to make a hybrid that would infect human cells. “Not all SARS-like coronaviruses have the inherent potential to replicate in mammalian cells and replicate in human cells.”And being able to do something in the artificial confines of a laboratory does not guarantee it will happen in nature. For a bat virus to start infecting people, the bat would have to come into contact with people in a way that would allow transmission. Even if a single person became infected, the virus would have to work efficiently in human cells, producing lots of copies of itself that could be coughed or sneezed out toward the airways of other people.“There are a lot of steps down this road,” Menachery said. “SHC014 has taken a step ahead. But there’s still a lot of other factors that are involved.”He and his co-authors noted they had to stop some of their work because of US government policies. The US has a moratorium on so-called gain-of-function research, which includes some research that enhances the ability of a pathogen such as a virus to infect people or spread among them.The authors expressed concern their findings might prompt further constraints on their work — something Dutch virologist Ron Fouchier hoped the team could avoid. Fouchier’s publication of a paper exploring what it would take to make H5N1 bird flu viruses more transmissible was one of the triggers for the gain-of-function research review.Figuring out the potential these viruses have to infect people is important, said Fouchier, who works at Erasmus Medical Center in Rotterdam, especially in light of ongoing outbreaks involving the coronavirus known as MERS, or Middle East respiratory syndrome. Scientific shorthand for coronavirus is CoV.“The MERS-CoV continues to cause problems, and we need to deal with that virus with whatever technology and lab work we have available, including gain-of-function research if needed,” Fouchier said in an email. Viruses that are related to SARS and that are found in some species of bats could become a source of future human outbreaks, according to a new study released Monday. And it appears that there are fewer barriers to that spillover than scientists initially thought.Researchers at the University of North Carolina at Chapel Hill said a virus in the same family as SARS — severe acute respiratory syndrome — appears to be able to infect human respiratory tract cells. The finding came as a surprise because the team thought the virus would have had to go through a process known as adaptation — meaning it would have had to acquire the ability to infect human cells by first learning how to infect the cells of another mammal.It’s believed that is how SARS went from being a bat virus to a major international outbreak that infected 8,400 people in 2003, killing at least 916 of them. In the case of SARS, the virus was probably passed from bats to palm civets and from palm civets to people.advertisement Helen Branswell Senior Writer, Infectious Disease Helen covers issues broadly related to infectious diseases, including outbreaks, preparedness, research, and vaccine development. A SARS-like virus found in bats could become a source of future human outbreaks, scientists say. Eric Gay/AP In the LabSARS-like virus in bats shows potential to infect humans, study finds
The Independent Panel on the Global Response to Ebola has made 10 recommendations for changes, based on lessons learned from the West African Ebola outbreak and aimed at protecting against future devastating health emergencies.Read more: International panel calls for an overhaul of WHOThe panel, convened by the Harvard Global Health Institute and the London School of Hygiene and Tropical Medicine, said the changes it is proposing fall into four themes: preventing major disease outbreaks; responding to major disease outbreaks; producing and sharing of data, knowledge and technology through research; and governing the global system for preventing and responding to outbreaks.These are paraphrased versions of their recommendations:advertisement Senior Writer, Infectious Disease Helen covers issues broadly related to infectious diseases, including outbreaks, preparedness, research, and vaccine development. A health worker with Doctors Without Borders carries a child suspected of having Ebola in October 2014 in Paynesville, Liberia. John Moore/Getty Images By Helen Branswell Nov. 22, 2015 Reprints The global community should come up with a strategy for strengthening health systems, including funding to help developing countries do so.The WHO should publicly commend countries that report disease outbreaks promptly and name and shame those that delay reporting. Financial incentives to compensate countries for losses linked to transparent disease reporting should be created.The WHO should set up a permanent outbreak response center with a guaranteed budget. It should report directly to the director general.The WHO should name a permanent emergency committee of experts to advise it on the threat posed by outbreaks. The committee should be able to convene itself and should consider adopting a graded system of warnings. Currently, emergency committees can only declare that something is or isn’t a global emergency.The UN should create an independent accountability commission that assesses response to major disease outbreaks.Governments, NGOs, the scientific community, and industry should develop rules for conducting research during an outbreak and a program for accelerating research between crises.Research funders should set up a facility to finance development of vaccines, drugs, disease tests, and other necessary medical equipment for diseases which the pharmaceutical industry won’t develop on its own.A global health committee should be set up as part of the UN Security Council to bring high-level attention to health issues and crises.The WHO should return its focus to its core functions, concentrating on efforts that only the WHO can undertake.The WHO’s executive board should establish a freedom of information policy; countries should stop earmarking the funding they provide the WHO; and countries should demand a WHO director general strong enough to stand up to the most powerful governments.Ebola’s deadly tallyVolume 90%Press shift question mark to access a list of keyboard shortcutsKeyboard ShortcutsEnabledDisabledPlay/PauseSPACEIncrease Volume↑Decrease Volume↓Seek Forward→Seek Backward←Captions On/OffcFullscreen/Exit FullscreenfMute/UnmutemSeek %0-9 facebook twitter Email Linkhttps://www.statnews.com/2015/11/22/ebola-panel-health-recommendations/?jwsource=clCopied EmbedCopiedLive00:0000:3700:37 HealthReport: 10 ways to protect against a global health catastrophe @HelenBranswell Tags Ebolaglobal healthWorld Health Organization About the Author Reprints Helen Branswell
About the Author Reprints The reason that doesn’t happen in some 80 percent of cancer patients is that their tumors don’t have enough neoantigens to attract T cells. The total number of neoantigens roughly predicts whether cancer patients respond to immune-blockade drugs like Keytruda and Opdivo, a similar agent from Bristol-Myers Squibb, but the connection isn’t perfect.“You see cases with a lot of neoantigens who don’t respond, and some with few neoantigens who do respond,” said Dr. Eliezer Van Allen, a clinician-scientist at the Dana-Farber Cancer Institute in Boston and an author of the new study, which was published in Science.The number of neoantigens is only part of the story. This study goes beyond previous ones in showing that when neoantigens are found throughout a tumor rather than in some cells only, patients have the best shot at benefitting from immunotherapy. And that’s true even if there are relatively few neoantigens.For instance, 12 out of 13 study participants whose lung cancers responded to Keytruda not only had a lot of neoantigens (more than 70), most of those neoantigens were present throughout the tumor. They attracted tumor-attacking T cells, which Keytruda let in, destroying enough of the cancer to send the patients into remission.In contrast, 16 of 18 lung cancer patients who did not benefit from Keytruda either did not have many neoantigens or had neoantigens that were present in only some tumor cells. Even a patient with a huge number of neoantigens relapsed after only two months; more than 80 percent of his mutations were found in only some tumor cells.“The tumors that we think will respond the best [to Keytruda and similar drugs] have a certain neoantigen burden, but those neoantigens have to be in almost every tumor cell,” said Dr. Charles Swanton, a cancer geneticist at the Francis Crick Institute in London, who, with immunologist Sergio Quezada of University College London, led the study. Swanton, Quezada, and three other coauthors also filed several patents that cover methods for identifying neoantigens and predicting the prognosis of cancer patients accordingly. Sharon Begley The scientists got similar results in melanoma: The fewer total neoantigens, and the more scattered around a tumor they were, the less patients responded to Yervoy, an immunotherapy drug from Bristol-Myers Squibb.Notably, melanoma patients who had already received chemotherapy drugs or radiation had large numbers of neoantigens, apparently induced by those treatments, but each one was found in only a few tumor cells. Standard cancer therapies “may be causing changes in tumors that might not be helpful” in terms of making patients respond to subsequent immunotherapy, Swanton said.The evidence is too preliminary for doctors to act upon, but the findings suggest that some patients might be better off skipping slash-and-burn chemo and going right to immune-modulating agents. Plus, physicians may be able to tell, by analyzing neoantigens in cells taken via standard biopsy, whether a patient has a good chance of being helped by those drugs.The study results can also “be used to inform the development of personalized cancer vaccines,” said Van Allen. These experimental treatments, which are tailor-made to a patient’s neoantigen profile, are being tested in clinical trials now. They are designed to stimulate the immune system to attack neoantigens on tumors, but scientists hadn’t been sure which neoantigens would make the best vaccines.“This is a very important paper,” said Dr. Elizabeth Jaffee, of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, who was not involved in the study. “It addresses a critical question in this field: Are all [neoantigens] equally important to the immune system or is there a way to sort this out?”The suggestion that the best neoantigens are found throughout the tumor “makes the case that we need to sample more of the tumor before predicting which expressed mutations are most relevant for immune targeting,” Jaffee said. ‘I want what Jimmy Carter had’: Patients clamor for the president’s cancer drug When neoantigens are found throughout a tumor, patients have the best shot at benefitting from immunotherapy drugs like Keytruda and Yervoy. Cancer Research UK/Phospho Biomedical Animation Related: The key to both — identifying patients likely to respond to the new immunotherapy drugs and producing tumor-attacking, individualized vaccines — lies in deciphering the crazy quilt of mutations a particular patient has.Only about one-fifth of cancer patients respond to immunotherapies like Keytruda, which is credited with helping Carter survive an advanced form of skin cancer. What makes “responders” different, previous studies in melanoma and lung cancer have suggested, is that they have a huge number of mutated genes producing molecules that find their way to the surface of the tumor cell. There, the aberrant molecules, known as neoantigens, stick out like pushpins in a corkboard.advertisement By Sharon Begley March 3, 2016 Reprints Turning your cancer against itselfVolume 90%Press shift question mark to access a list of keyboard shortcutsKeyboard ShortcutsEnabledDisabledPlay/PauseSPACEIncrease Volume↑Decrease Volume↓Seek Forward→Seek Backward←Captions On/OffcFullscreen/Exit FullscreenfMute/UnmutemSeek %0-9 facebook twitter Email Linkhttps://www.statnews.com/2016/03/03/cancer-immunotherapy-neoantigens/?jwsource=clCopied EmbedCopiedLive00:0002:0202:02 Personalized cancer vaccines rally the immune system to identify and kill cancerous cells based on genetic information from the patient’s own tumors. Alex Hogan and Hyacinth Empinado/STAT Because those neoantigens are newcomers, the immune system should recognize them as foreign and attack, destroying the cancer cell — which is where drugs like Merck’s Keytruda come in. They lift molecular blockades that tumors use to keep the immune system’s T cells out. As a result, T cells charge in and destroy the tumor. Senior Writer, Science and Discovery (1956-2021) Sharon covered science and discovery. [email protected] Related: Watch: Turning your cancer against itself For cancer patients, the promise of new immune-modulating drugs like the one that apparently helped former President Jimmy Carter comes with a sobering downside: very few get any benefit from them.But if a new study published on Thursday is right, physicians might be able to figure out which patients those are, sparing others an expensive but useless treatment.The research also offers clues for how to make a promising but unproven treatment, personalized cancer vaccines, more likely to succeed.advertisement In the LabThe newest cancer therapies don’t work on everyone. Now, doctors have a clue why @sxbegle Tags cancercancer vaccinesKeytruda
Ed Silverman Daily reporting and analysis The most comprehensive industry coverage from a powerhouse team of reporters Subscriber-only newsletters Daily newsletters to brief you on the most important industry news of the day STAT+ Conversations Weekly opportunities to engage with our reporters and leading industry experts in live video conversations Exclusive industry events Premium access to subscriber-only networking events around the country The best reporters in the industry The most trusted and well-connected newsroom in the health care industry And much more Exclusive interviews with industry leaders, profiles, and premium tools, like our CRISPR Trackr. Pharmalot By Ed Silverman May 11, 2018 Reprints What’s included? Tags pharmaceuticalsSTAT+Trump [email protected] Pharmalot Columnist, Senior Writer Ed covers the pharmaceutical industry. About the Author Reprints Sen. Ron Wyden, D-Ore. Susan Walsh/AP Democratic senator opens probe into Novartis over its dealings with Trump’s attorney A lawmaker is opening an investigation into Novartis for paying $1.2 million to President Trump’s personal attorney, Michael Cohen, in an attempt to gain access to the White House, a disclosure that has prompted widespread criticism of the drug maker.The company has said it agreed to a one-year contract, beginning in February 2017, with Cohen’s firm, Essential Consultants, in order to create a direct channel to the Trump administration about “health care policy matters.” The arrangement, however, has been widely derided because Cohen is not a lobbyist or an expert in health care matters. And Novartis said it let the contract lapse when it expired. GET STARTED STAT+ is STAT’s premium subscription service for in-depth biotech, pharma, policy, and life science coverage and analysis. Our award-winning team covers news on Wall Street, policy developments in Washington, early science breakthroughs and clinical trial results, and health care disruption in Silicon Valley and beyond. Unlock this article — plus daily coverage and analysis of the pharma industry — by subscribing to STAT+. First 30 days free. GET STARTED Log In | Learn More @Pharmalot What is it?
Daily reporting and analysis The most comprehensive industry coverage from a powerhouse team of reporters Subscriber-only newsletters Daily newsletters to brief you on the most important industry news of the day STAT+ Conversations Weekly opportunities to engage with our reporters and leading industry experts in live video conversations Exclusive industry events Premium access to subscriber-only networking events around the country The best reporters in the industry The most trusted and well-connected newsroom in the health care industry And much more Exclusive interviews with industry leaders, profiles, and premium tools, like our CRISPR Trackr. By Jonathan Saltzman — Boston Globe Dec. 4, 2018 Reprints Unlock this article — plus daily coverage and analysis of the biotech sector — by subscribing to STAT+. First 30 days free. GET STARTED What is it? CAMBRIDGE — John White, a retired North Attleborough bioengineer, was diagnosed in early 2015 with aggressive prostate cancer. It had spread to his bladder and pelvic lymph nodes. It didn’t respond to hormone therapy and chemotherapy. His oncologist feared White might have only a year to live.Then scientists at Foundation Medicine, a Cambridge, Mass., biotech, ran a new diagnostic test to sequence the DNA of cancer cells in his prostate gland, which had been surgically removed. The bad news was that he had a rare form of the disease, marked by an extraordinary number of genetic changes in the cancerous cells. The good news: The new test showed that he might respond to any of three new immunotherapy drugs. What’s included? STAT+ is STAT’s premium subscription service for in-depth biotech, pharma, policy, and life science coverage and analysis. Our award-winning team covers news on Wall Street, policy developments in Washington, early science breakthroughs and clinical trial results, and health care disruption in Silicon Valley and beyond. Jonathan Saltzman — Boston Globe Log In | Learn More Tags biotechnologyBostoncancerdiagnosticsgeneticsprecision medicineSTAT+ About the Author Reprints GET STARTED “I was only given months to live four years ago . . . I am still thriving,” said John White. Aram Boghosian for the Boston Globe Biotech For one cancer patient, biotech’s genetic test turns out to be a ‘lifesaver’