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New research led by the University of Bristol has found the protein p53 plays a key role in epithelial migration and tissue repair. The findings could improve our understanding of the processes used by cells to repair tissues, and be used to identify interventions that could accelerate and improve wound repair.
Epithelial tissues are the linings that protect the body’s external skin and internal cavities, and their ability to repair themself is important. ?It is known that wounded epithelia repair themself thanks to the ability of the remaining cells to start migrating, collectively, to seal the breach. Specialised migratory cells called leader cells arise from damaged epithelia, promoting epithelial migration. However, it’s unclear what molecules and signals in epithelial cells make them become migratory leaders and how some wounded cells develop leader behaviour whilst some do not.
The study, funded by CRUK and Wellcome Trust and published in Scienceon [11 February], found that, when epithelial cells are damaged, the damage activates a molecular program that turns cells into migratory leader cells so that the breach can be repaired quickly. The same molecular program also makes sure that these highly migratory cells are removed when the breach is closed, so that the tissue restores its normal epithelial tissue structure.
Using a simplified model of a wound, epithelial sheets that were scratched in vitro to injure the epithelial monolayer, the researchers identified the molecular signal that makes leader cells emerge.
The study found that, following injury, cells at the border of the epithelial gap elevate p53 and p21, suggesting that the injury triggers the migratory program. Once the breach was repaired, leader cells were eliminated from the population by their healthy epithelial neighbours. The cells damaged by the wound were able to cause wound closure, but are then sacrificed to maintain a functional tissue with normal epithelial morphology.
Eugenia Piddini, Professorial Research Fellow in Cell Biology and Wellcome Trust Senior Research Fellow in the School of Cellular and Molecular Medicine (CMM) at the University of Bristol and lead senior author of this work, said: “Our findings improve our understanding of the mechanisms used by cells to repair tissues, and could be used to develop systems that accelerate wound healing.
“p53 plays two critical roles in epithelial repair. It starts leader driven epithelial closure and once the epithelium has been repaired, p53 induces leader cell clearance.”
Dr Giulia Pilia, Research Associate in CMM at the University of Bristol and co-first author, added: “Collective migration is important in other areas, for example in cancer, where groups of cells move together from the primary tumour to create metastases. It would be important to know if the same proteins that we identified in the wound model are at play in this situation, so that current therapeutic treatments could be modified.”
Next steps for the research will be to test whether the mechanisms that have been found in the in vitro epithelium also apply in vivo. If this is the case, the research team would like to test if they can selectively and safely induce leaders in vivo, to promote migration and tissue repair. This new-found knowledge of how leaders work could also be used to develop new therapeutic approaches that could help block the unwanted migration of metastatic cells.
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A recent study explains an essential component for proper mitochondrial function: The protein complexes MICOS and ATP synthase can communicate with each other. Dr. Heike Rampelt andProf. Dr. Nikolaus Pfanner at the Institute of Biochemistry and Molecular Biology of the University of Freiburg have uncovered an important mechanism that ensures efficient metabolic adaptation of mitochondria. The research is a collaboration with the groups of Prof. Dr. Martin van der Laan of Saarland University, Prof. Dr. Claudine Kraft of the University of Freiburg and Prof. Dr. Ida van der Klei of the University Groningen / Netherlands and combines biochemical approaches with fluorescence microscopy of living cells as well as electron microscopy to visualize mitochondrial membrane architecture. The study has been published in the journal Cell Reports.
Cellular respiration of the inner mitochondrial membrane
Mitochondria, the power plants of the cell, make massive contributions to the energy supply of the body by burning metabolites with the help of oxygen. This cellular respiration takes place in the inner of the two mitochondrial membranes that, in contrast to the outer membrane, is strongly folded. The structure and topology of these membrane folds, the so-called cristae membranes, has profound influence on the efficiency of respiration and is important for many mitochondrial functions. For this reason, cristae architecture is controlled precisely and adapted dynamically to changes in cellular metabolism. Defects in these processes result in severe human diseases.
Communication is key
Two protein complexes in the inner mitochondrial membrane that are required for a normal membrane architecture are the F1Fo-ATP synthase, an enzyme that also participates in energy conversion, and the MICOS complex (mitochondrial contact site and cristae organizing system). These complexes are regarded as antagonists; they are localized in different areas of the inner membrane and bend the membrane in opposite directions. It was unclear how the functions of these two protein complexes can be coordinated with each other. The team around Rampelt and Pfanner now demonstrate that MICOS and ATP synthase communicate with each other and that this is vital for healthy mitochondrial function. A MICOS subunit, Mic10, travels to the ATP synthase and stabilizes the association of several ATP synthases to large complexes. This new regulatory function of Mic10 is pivotal for efficient metabolic adaptation and respiratory growth. “Communication between the two complexes is likely key to the coordinated biogenesis of the inner mitochondrial membrane,” explains Rampelt.
Heike Rampelt, Nikolaus Pfanner and Claudine Kraft lead research groups at the Institute of Biochemistry and Molecular Biology of the Medical Faculty and perform research in the Excellence Cluster CIBSS of the University Freiburg in the area of biological signalling studies.
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A new Dartmouth-led study, published in the journal Environmental International, reveals how prenatal exposure to mixtures of commonly found metals can adversely affect fetal growth.
Fetal growth is linked to future health — infants who are born small for their gestational age experience greater rates of neonatal mortality and are at a higher risk of developing neurocognitive impairment in childhood and cardiometabolic disease later in life.
A growing number of studies have established that toxic metals, coming from sources such as contaminated food and drinking water and polluted air and dust, are prevalent in the environment, and many of these metals can cross the placenta or alter placental function, contributing to reduced fetal growth.
But prior research looking at metal impacts on fetal growth have typically looked at one metal at a time and within an individual population.
“The limitation of that is usually we’re exposed to a complex mixture of multiple metals simultaneously that might interact with each other, and exposure ranges can be narrow in just one population for a given metal,” explains lead author Caitlin Howe, PhD, an assistant professor of epidemiology at Dartmouth’s Geisel School of Medicine whose research focuses on toxic metal exposures and their impacts on maternal and child health.
“So, our goal was to look across multiple diverse populations with different types of exposures, so we could get a better sense of the full dose response relationship for some of these chemicals in the context of the larger mixture,” she says.

Asymptomatic COVID-19 cases are the bane of computer modelers’ existences — they throw off the modeling data to an unknown degree. You can’t measure what you can’t detect, right? A new approach from Los Alamos National Laboratory’s Theoretical Division, however, explores using historic epidemic data from eight different countries to estimate the transmission rate and fraction of under-reported cases.
“Asymptomatic cases are the ‘dark matter’ of epidemics,” said Nick Hengartner, one of the authors on the report published today in the journal PLOS ONE. “We see only the indirect evidence that more people are sick than reported, and if we don’t account for them, we may wrongly conclude that the epidemic is under control. So we changed the model to focus on the observed counts instead of trying to model the ‘perfect’ world. By looking back through the time series of historical data, we can see from their dynamics what’s missing.”
The importance of capturing the undocumented cases is significant, especially in a disease such as COVID-19, where asymptomatic individuals have accounted for 20-70 percent of all infections.
Co-author Imelda Trejo, a postdoctoral fellow at Los Alamos noted, “This is a new extension of the standard SIR (susceptible-infected-recovered) epidemiological models to study the underreported incidence of infectious disease. The new model reveals that trying to fit an SIR model type directly to raw incidence data will underestimate the true infectious rate. This could actually lead decisionmakers to declare the epidemic under control prematurely.” Instead, the team presented a Bayesian method (a statistical model using probability to represent all uncertainty within the model) to estimate the transmission rate and fraction of underreported cases.
As tested against the data of eight countries (Argentina, Brazil, Chile, Colombia, Mexico, Panama, Peru and the U.S.), the new approach directly describes the dynamics of the observed, under-reported cases. “We use the local dynamics of the observed cases to propose a model that gives us a conditional expectation of new cases, based on the observed history,” Trejo said.
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Around the world, more people are growing older. According to the World Health Organisation, 1 in 6 people in the world will be aged 60 years or over by 2030. By 2050, the world’s population of people aged 60 years and older will double to 2.1 billion. The number of persons aged 80 years or older is expected to triple between 2020 and 2050 to reach 426 million.
In line with the growing number of seniors, the number of people living with age-related diseases such as dementia, including Alzheimer’s Disease and Parkinson’s Disease is also expected to increase exponentially. These age-related diseases are an emerging impediment to healthy and functional aging.
A class of medicine used in the treatment of neuro-cognitive diseases and other neurological ailments (migraines, headaches, etc) are currently obtained from extracts of the ergot fungus. However, continued cultivation of the ergot fungus for medicine is not sustainable as industrial agriculture is one of the largest contributors to carbon emissions worldwide.
To meet the global demand for such medication, between 10-15 tons of D-lysergic acid (DLA), an ingredient used in producing the medicine, are produced each year. The ergot fungi are parasites to cereal crops such as rye, and their cultivation entails growing them on top of fields of such crops that could otherwise be used for food production. In order to reduce the use of arable land to produce such medicine, a group of researchers from the Yong Loo Lin School of Medicine at the National University of Singapore (NUS Medicine) and Imperial College London have trialled an alternative way of producing DLA.
Using yeast commonly known to make bread, and synthetic biology techniques, the team introduced the enzymes from the ergot fungus into baker’s yeast, which also happens to be another fungus. Through a process known as fermentation, the modified yeast was then grown using sugar to produce DLA. Natural fermentation has been used throughout human history for food production, most notably in the production of bread and beer. Just like how baker’s yeast has been used to produce the alcohol and flavours in beer, fermentation using the modified yeast can now produce DLA.
The study was published in Nature Communications on 7 Feb 2022.
“It is possible to produce up to five tons of DLA annually using the current yeast strain; and with further optimisation, commercial production levels could be attainable,” explained Associate Professor Yew Wen Shan from the Department of Biochemistry at NUS Medicine and the co-lead Principal Investigator of the study. “This research builds upon the growing body of work that use microbes such as yeast for the sustainable production of medicine and functional food ingredients.”
Professor Paul Freemont, from the Department of Infectious Disease at Imperial College London, said: “Yeast has been a key part of human civilization for thousands of years, helping us to make bread and brew beer. But our relationship with this familiar microbe is evolving. Through this exciting collaboration we have been able to harness fungal cells to act as miniature factories to produce raw compounds for medicines. This is an example of how something seemingly small and inconsequential has the potential to change human lives, providing the drugs which will enable us to age better and reduce the environmental impact of industrial drug production.”
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The cellular proteins that hold cells and tissues together also perform critical functions when they experience increased tension. A new University of Illinois Urbana-Champaign study observed that when tugged upon in a controlled manner, these proteins — called cadherins — communicate with growth factors to influence in vitro tumor growth in human carcinoma cells.
The study, led by chemical and biomolecular engineering professor Deborah Leckband, found that cadherins that bond with growth factor receptors can sense mechanical force and respond by altering cell communication and growth.
The findings are published in the Proceedings of the National Academy of Sciences.
When bound to cadherin molecules in normal tissue, growth factor receptors cannot communicate with growth factor proteins — the substance they need to promote tissue growth. However, the study shows that changes in tensional stress on cadherin bonds disrupt the cadherin-growth factor interaction to switch on growth signals in tissues.
To demonstrate how tension influences tissue growth, the researchers set up an experiment to observe how in vitro human carcinoma cells convert mechanical information into biochemical signals, Leckband said.
The team used a self-built “cell stretcher” in which the carcinoma cells are grown in a thin layer on the surface of a flexible medium. When the cells are stretched, the researchers observed changes that could increase tissue growth and tumorigenesis.
“This study confirms that cadherins use force to switch on biochemical growth signaling,” Leckband said. “By confirming these force-induced disruptions, we may be able to find a way to mutate cadherin molecules in order to prevent certain types of tissue growth, such as metastatic transformation and tumorigenesis.”
The team has observed the cadherin-growth factor receptor complex in human epithelial tissue and plans to expand this concept by working with in vitro human breast tissue.
Illinois graduate students Brendan Sullivan and Vinh Vu; undergraduate student Adrian Kapustka; and researchers from Johns Hopkins University contributed to this study.
Leckband also is a professor of chemistry and of bioengineering, and is affiliated with the Beckman Institute for Advanced Science and Technology, the Carl R. Woese Institute for Genomic Biology and the Nick Holonyak Micro and Nanotechnology Laboratory.
The National Institutes of Health supported this study.
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A number of existing strains of SARS-CoV-2, as well as other future variants that could arise, have the potential to escape the immune system’s cytotoxic T cell response in some portion of the population. That’s the conclusion of a new modeling study publishing Feb. 10 in PLOS Computational Biology by Antonio Martín-Galiano of the Carlos III Health Institute, Spain, and colleagues.
The T cell response in humans is genetically encoded by HLA molecules — this means different individuals have different HLAs, programmed to recognize invading pathogens based on different parts, or “epitopes” of the pathogens. With thousands of different HLA molecules in the human population and thousands of possible epitopes in any given virus, the experimental evaluation of the immune response of every human HLA allele to every viral variant is not feasible. However, computational methods can facilitate this task.
In the new study, researchers first determined the full set of epitopes from an original reference strain of SARS-CoV-2 from Wuhan, China. The team discovered 1,222 epitopes of SARS-CoV-2 that were associated with major HLA subtypes, covering about 90% of the human population; at least 9 out of every 10 people can launch a T cell response to COVID-19 based on these 1,222 epitopes.
Then, the researchers computationally analyzed whether any of 118,000 different SARS-CoV-2 isolates from around the world, described in a National Center for Biotechnology Information (NCBI) dataset, had mutations in these epitopes. 47% of the epitopes, they showed, were mutated in at least one existing isolate. In some cases, existing isolates had mutations in multiple epitope regions, but cumulative mutations never affected more than 15% of epitopes for any given HLA allele type. When the team analyzed susceptible alleles and the geographic origin of their respective escape isolates, the team found that they co-existed in some geographical regions — including sub-Saharan Africa and East and Southeast Asia — , suggesting potential genetic pressure on the cytotoxic T cell response in these areas.
“The accumulation of these changes in independent isolates is still too low to threaten the global human population,” the authors say. “Our protocol has identified mutations that may be relevant for specific populations and warrant deeper surveillance.”
However, Martín-Galiano notes that “unnoticed SARS-CoV-2 mutations” might in future “threaten the cytotoxic T response in human subpopulations.”
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While in high school in 1972, she was raped and became pregnant. Her illegal abortion paved the way for France to decriminalize the procedure in 1975.Marie-Claire Chevalier was 16 when she was raped by a high school classmate and became pregnant. She then had an abortion, which was illegal at the time unless the woman’s life was in danger.Her classmate was later arrested on unrelated charges of auto theft. In a bid to avoid prosecution, he revealed Ms. Chevalier’s abortion to the authorities; he was released, and she was arrested and imprisoned.In a sensational 1972 trial, she was represented by Gisèle Halimi, one of Frances’s most renowned lawyers and a prominent feminist. She won Ms. Chevalier’s acquittal, and the landmark case helped pave the way for the decriminalization of abortion in France.While many in France celebrated the outcome, Ms. Chevalier was traumatized by the whole experience. She changed her first name to Catherine after the trial to try to regain her anonymity and lived the rest of her life out of the public eye.Ms. Chevalier died on Jan. 23 in a hospital in Orléans, south of Paris. She was 66. The cause was brain cancer, her mother, Michèle Chevalier, said.In predominantly Roman Catholic France, abortion was long considered a mortal sin and was officially banned by the Napoleonic Code of 1810, which threatened women who had abortions with imprisonment. During the German occupation in World War II, the procedure was deemed a capital crime, and some women who underwent abortions or performed them were executed, often by guillotine. The last such execution was in 1943.By the late 1960s and early ’70s, a series of legal challenges focused increasing attention on the abortion statute. Perhaps the most prominent of these challenges was that of Ms. Chevalier, whose mother had sought out Ms. Halimi to represent her.Ms. Halimi agreed to do so with the goal of politicizing the case and legalizing abortion. Some of France’s leading intellectuals, including Simone de Beauvoir, joined the cause.The trial took place in the Paris suburb of Bobigny when Ms. Chevalier was 17. Ms. Halimi declared in her opening argument that she, too, had had an abortion. “I say it gentlemen, I am a lawyer who broke the law,” she declared in court. She received a disciplinary summons but maintained in subsequent appearances that she had done the right thing, saying, “Sometimes it is necessary to break the law to move forward and bring about a change in society.”When the verdict was rendered, Ms. Chevalier was fined 500 francs and released, while activists chanted her name in the streets. Four others, including her mother, had been charged as accomplices and were absolved.The case, with its young protagonist and its high-profile lawyer, became a cause célèbre and a catalyst in the feminist campaign to overturn the law. Among those who joined was Simone Veil, the French health minister and a survivor of Auschwitz. She endured an avalanche of personal attacks but kept pushing for change. And on Jan. 17, 1975, France enacted the Veil Law, decriminalizing abortion.This was two years after the U.S. Supreme Court had legalized abortion in the United States Roe v. Wade. As in France, it had taken another pregnant woman, a Dallas waitress named Norma McCorvey — under the pseudonym “Jane Roe” — to challenge the law and achieve a major victory for women.Although Ms. Chevalier was proud of the effect her case had had, she loathed the publicity and shunned the notion of exploiting it for fame or profit. “It’s not my style to build on what has screwed me up,” she said in a rare interview in 2019 with the French newspaper “Libération.”Still, her story has been packaged and repackaged for public consumption by the media, in a radio series, a television movie and theatrical productions, including a play in 2019 at the Comédie-Française, called “Hors la Loi” (“Outlaw”). A blue metal footbridge in front of the Bobigny court was dedicated in her name.But she remained haunted by the experience, from the rape and abortion to the trial.“Time has passed, and yet it’s still there, buried in my memory,” she said in the 2019 interview. “All it takes is a tiny little thing to wake it up.”Marie-Claire Chevalier was born on July 12, 1955, into a working-class family in Meung-sur-Loire, near Orléans.Her father was never part of the picture. Her mother, who was a ticket inspector for the RATP, the state-owned transportation company, raised her and her two younger sisters by herself.In the 2019 interview, Ms. Chevalier described her clandestine abortion as “a second rape,” a gruesome and painful procedure that she said led to her hemorrhaging and being rushed to a hospital, near death.She was in her 30s before she had sex again, she said. But she and her partner could not conceive, and she worried that the abortion had made her sterile. In 1988, she finally had a daughter.In addition to her mother, she is survived by her daughter, three grandchildren and her two sisters.She later worked as a child-care assistant and as a welder for the army. When she was about 40, she became a nurse, working in a hospital and a retirement home. In her final years, she lived alone with her many cats and two horses in the countryside.“She died without ever asking anyone for anything,” her mother said in an interview. “She needed help, and she never contacted us.”But she remains an inspiration to younger French feminists.“Marie-Claire Chevalier has made us the most beautiful gift,” Céline Piques, the spokeswoman for “Osez le féminisme!” (“Dare to be feminist!”), said in an interview. That gift, she said, was to take on the cause of abortion rights “and to agree to be publicly exposed, with the consequences I assume it had on her personal life.”

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesLuc Montagnier, the French virologist credited as a co-discoverer of the human immunodeficiency virus (HIV), has died aged 89.Montagnier was jointly awarded the 2008 Nobel Prize for his work in isolating the virus that causes Aids.He was lauded for this work, but later criticised for unscientific claims about autism and Covid-19.Local news site FranceSoir reported he died on Tuesday in Neuilly-sur-Seine “surrounded by his children”.The virologist first began working on the virus in the early 1980s while at France’s Pasteur Institute, a non-profit research foundation.Montagnier and his team – including Françoise Barré-Sinoussi, who would later win the Nobel Prize in Physiology or Medicine with him – examined tissue samples from patients with the mysterious new syndrome.They managed to isolate HIV in the lymph node of an Aids patient and published news of the discovery in the journal Science in 1983. In the same edition, US scientist Robert Gallo published similar findings, and later concluded that the virus caused Aids. The dispute over who first identified HIV caused years of heated debate. Gallo admitted in 1991 that the virus he found came from the Pasteur Institute the year before, and the two men publicly agreed in 2002 that Montagnier’s team discovered HIV, but that Gallo first showed its role in causing Aids.However, when Montagnier and Barré-Sinoussi were awarded the Nobel Prize in 2008 for their work – alongside Harald zur Hausen for his work on cervical cancer – the committee controversially did not mention Robert Gallo. Montagnier later generated huge criticism for a series of unscientific claims, including over the causes of autism and later over the origins of Covid-19.Born in 1932 in the central French town of Chabris, Montagnier began working at Paris’s Faculty of Sciences in 1955. He moved to the Pasteur Institute in 1972, and after his work on HIV led the foundation before moving to Queens College, City University of New York in 1997.French media first reported that he had died at the American hospital in Neuilly-sur-Seine on 8 February. Local authorities later officially confirmed his death.You may also be interested in:This video can not be playedTo play this video you need to enable JavaScript in your browser.

He found the virus that causes AIDS, fell into a feud over it and later turned controversial, taking an anti-vaccine stance during the Covid-19 crisis.Luc Montagnier, a French virologist who shared a Nobel Prize for discovering the virus that causes AIDS, died on Tuesday in the Paris suburb of Neuilly-sur-Seine. He was 89.The town hall in Neuilly confirmed that a death certificate for Dr. Montagnier had been filed there.For all the glory Dr. Montagnier earned in discovering the virus, today known as H.I.V., in later years he distanced himself from colleagues by dabbling in maverick experiments that challenged the basic tenets of science. Most recently he was an outspoken opponent of coronavirus vaccines.The discovery of H.I.V. began in Paris on Jan. 3, 1983. That was the day that Dr. Montagnier (pronounced mon-tan-YAY), who directed the Viral Oncology Unit at the Pasteur Institute, received a piece of lymph node that had been removed from a 33-year-old man with AIDS.Dr. Willy Rozenbaum, the patient’s doctor, wanted the specimen to be examined by Dr. Montagnier, an expert in retroviruses. At that point, AIDS had no known cause, no diagnostic tests and no effective treatments. Many doctors, though, suspected that the disease was triggered by a retrovirus, a kind of germ that slips into the host cell’s DNA and takes control, in a reversal of the way viruses typically work; hence the name retro.From this sample Dr. Montagnier’s team spotted the culprit, a retrovirus that had never been seen before. They named it L.A.V., for lymphadenopathy associated virus.The Pasteur scientists reported their landmark finding in the May 20, 1983, issue of the journal Science, concluding that further studies were necessary to prove L.A.V. caused AIDS.The following year, the laboratory run by the American researcher Dr. Robert Gallo, at the National Institutes of Health, published four articles in one issue of Science confirming the link between a retrovirus and AIDS (for acquired immune deficiency syndrome). Dr. Gallo called his virus H.T.L.V.-III. There was some initial confusion as to whether the Montagnier team and the Gallo team had found the same virus or two different ones.When the two samples were found to have come from the same patient, scientists questioned whether Dr. Gallo had accidentally or deliberately got the virus from the Pasteur Institute.And what had once been camaraderie between those two leading scientists exploded into a global public feud, spilling out of scientific circles into the mainstream press. Arguments over the true discoverer and patent rights stunned a public that, for the most part, had been shielded from the fierce rivalries, petty jealousies and colossal egos in the research community that can disrupt scientific progress.Dr. Montagnier sued Dr. Gallo for using his discovery for a U.S. patent. The suit was settled out of court, mediated by Jonas Salk, who had years earlier been involved in a similar battle with Albert Sabin over the polio vaccine.Dr. Montagnier in 1984 holding images of the virus found to cause AIDS. The top one was discovered by an American team led by Dr. Robert Gallo; the bottom one was detected by Dr. Montagnier’s team in Paris. The samples were later found to have come from the same patient.Associated PressBoth Dr. Montagnier and Dr. Gallo shared many prestigious awards, among them the 1986 Albert Lasker Medical Research Award, which honored Dr. Montagnier for discovering the virus and Dr. Gallo for linking it to AIDS. That same year, the AIDS virus, known by Americans as H.T.L.V.-III and the French as L.A.V., was officially given one name, H.I.V., for human immunodeficiency virus.The following year, with the dispute between the doctors still raging, President Ronald Reagan and Prime Minister Jacques Chirac of France stepped into the fray and signed an agreement to share patent royalties, proclaiming both scientists co-discoverers of the virus.In 2002, the two scientists appeared to have resolved their rivalry, at least temporarily, when they announced that they would work together to develop an AIDS vaccine. Then came the announcement of the 2008 Nobel Prize for Medicine or Physiology.Dr. Gallo had long been credited with linking H.I.V. to AIDS, but the Nobel Committee for Physiology or Medicine singled out its discoverers, awarding half the prize jointly to Dr. Montagnier and Dr. Françoise Barré-Sinoussi, who had worked with him at the Pasteur Institute on the virus discovery. (The other half was awarded to Dr. Harald zur Hausen of Germany “for his discovery of human papilloma viruses causing cervical cancer.”)The Nobel committee said it had no doubt “as to who had made the fundamental discoveries” concerning H.I.V. Introducing the winners at the award ceremony in Sweden, Professor Björn Bennström, a committee member, said, “Never before had science advanced so quickly from finding the disease-causing agent to anti-viral agents.”In his acceptance speech, contrary to the views of other AIDS experts, Dr. Montagnier said he believed that H.I.V. relied on other factors to spark full-blown disease. “H.I.V. ,” he said, “is the main cause, but could also be helped by accomplices.” He was referring to other infections, perhaps from bacteria, and a weakened immune system.After his work with H.I.V., Dr. Montagnier veered into nontraditional experiments, shocking and infuriating colleagues. One experiment, published in 2009 in a journal he founded, claimed that DNA emitted electromagnetic radiation. He suggested that some bacterial DNA continue to emit signals long after an infection is cleared.The Coronavirus Pandemic: Key Things to KnowCard 1 of 3Some mask mandates ending.