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An all Indiana University School of Medicine team of researchers led by, Rajiv Agarwal, MD, professor of medicine and staff physician at the Roudebush VA, and including Arjun Sinha, MD, associate professor of clinical medicine and renal section chief at the Roudebush VA, and Wanzhu Tu, PhD, professor of biostatistics and health data sciences and research scientist at Regenstrief Institute, found that chlorthalidone was effective in lowering blood pressure in individuals with advanced kidney disease.
The double-blind, placebo-controlled and randomized study, funded by the National Institutes of Health’s National Heart, Lung, and Blood Institute, titled Chlorthalidone in Chronic Kidney Disease (CLICK) was presented as part of a news conference and High Impact Clinical Trials session at the recent international meeting of the American Society of Nephrology and simultaneously published in the New England Journal of Medicine.
“Kidneys are key regulators of blood pressure. When an individual has chronic kidney disease, the kidneys are unable to control blood pressure,” said Agarwal. “If a person suffers from chronic kidney disease and high blood pressure, it is more likely their kidney disease will advance even further and lead to other health issues such as heart failure.”
The CLICK Study randomly assigned patients with stage 4 chronic kidney disease (CKD) to either a placebo or chlorthalidone group, with dosing at 12.5 mg daily. The dose was increased every four weeks, if needed, to a maximum of 50 mg per day for patients in the chlorthalidone group. The study was designed to see if blood pressure decreased in the patients treated with chlorthalidone from baseline to twelve weeks, when monitored using a state-of-the-art device called a 24-hour ambulatory blood pressure monitor.
Chlorthalidone was approved by the FDA in 1960 for treatment of high blood pressure or hypertension. However, it was largely believed to be ineffective in treating high blood pressure in people with advanced chronic kidney disease.
Results from the CLICK study showed chlorthalidone lowered blood pressure by a significant 11 mm Hg at 12 weeks as compared to 0.5 mm Hg reduction with placebo. There was a 50% reduction in albuminuria, a protein that appears in the urine of those suffering from kidney disease, which Agarwal says is remarkable and suggests that chlorthalidone has the potential to reduce kidney failure progression and hospitalizations for heart failure in these patients.
“These results show chlorthalidone is a low-cost solution for the treatment of hypertension in people with chronic kidney disease, ” said Agarwal.” These are people who are already taking a variety of medicines, so to have one that is cheap and effective is incredibly meaningful. However, the drug is potent, so the lowest therapeutic dose and careful monitoring is needed to avoid complications.”
This study was also funded by the Indiana Institute of Medical Research.
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Good news for pregnant coffee lovers: Consuming a low amount of caffeine during pregnancy could help to reduce gestational diabetes risk, according to researchers in the Perelman School of Medicine at the University of Pennsylvania and the National Institutes of Health. The findings were published Monday in JAMA Network Open.
“While we were not able to study the association of consumption above the recommended limit, we now know that low-to-moderate caffeine is not associated with an increased risk of gestational diabetes, preeclampsia, or hypertension for expecting mothers,” said the study’s lead author Stefanie Hinkle, PhD, an assistant professor of Epidemiology at Penn.
The American College of Obstetricians and Gynecologists (ACOG) recommends that pregnant women limit their caffeine consumption to less than 200 mg (about two, six-ounce cups) per day. The recommendations are based on studies that suggest potential associations with pregnancy loss and fetal growth at higher caffeine levels. However, there remains limited data on the link between caffeine and maternal health outcomes.
To better understand this association, researchers studied prospective data from 2,529 pregnant participants who were enrolled in the National Institute of Child Health and Human Development (NICHD) Fetal Growth Studies-Singleton Cohort at 12 U.S. clinical centers between 2009 and 2013.
At enrollment and at each office visit thereafter, women reported their weekly intake of caffeinated coffee, caffeinated tea, soda, and energy drinks. Concentrations of caffeine were also measured in the participants’ plasma at 10 to 13 weeks into their pregnancies. The researchers then matched their caffeine consumption with primary outcomes: clinical diagnoses of gestational diabetes, gestational hypertension, and preeclampsia.
The research team found that caffeinated beverage intake at 10 to 13 weeks gestation was not related to gestational diabetes risk. During the second trimester, drinking up to 100 mg of caffeine per day was associated with a 47 percent reduction in diabetes risk. There were no statistically significant differences in blood pressure, preeclampsia, or hypertension between those who did and did not drink caffeine during pregnancy.
The researchers note that the findings are consistent with studies that have found that caffeine has been associated with improved energy balance and decreased fat mass. They also say that they cannot rule out that these findings are due to other constituents of coffee and tea such as phytochemicals, which may impact inflammation and insulin resistance, leading to a lower risk for gestational diabetes.
However, past studies from the same group have shown that caffeine consumption during pregnancy, even in amounts less than the recommended 200 mg per day, was associated with smaller neonatal anthropometric measurements, according to Hinkle.
“It would not be advised for women who are non-drinkers to initiate caffeinated beverage consumption for the purpose of lowering gestational diabetes risk,” she said. “But our findings may provide some reassurance to women who already are consuming low to moderate levels of caffeine that such consumption likely will not increase their maternal health risks.”
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It’s become clear throughout the COVID-19 pandemic that airborne transmission of infectious respiratory particles plays an important role in how the virus spreads. The performing arts — from Broadway to Colorado State University’s University Center for the Arts — took a brutal hit early on, as it was suspected that singing, talking, and playing instruments in packed venues could put both performers and audience members at high risk of exposure.
Those suspicions were borne out in a CSU study that measured respiratory particles produced from people singing or playing instruments. Is singing worse than talking when it comes to how many particles are being emitted? Yes, according to the study. And the louder one talks or sings, the worse the emissions. A person’s age and whether they are male or female also affects their respiratory emissions, with males and adults emitting more airborne particles, on average, than females and minors.
The study was called Reducing Bioaerosol Emission and Exposures in the Performing Arts: A Scientific Roadmap for a Safe Return from COVID-19. Launched early in the pandemic before vaccines were widely available, it was led by John Volckens, professor in the Department of Mechanical Engineering with appointments in the CSU Energy Institute, the Colorado School of Public Health, the School of Biomedical Engineering, and the Department of Environmental and Radiological Health Sciences. His team partnered with Dan Goble, director of the CSU School of Music, Theatre and Dance, to determine the extent to which singers, musicians and actors emit aerosols (tiny airborne particles less than 100 microns in size), and whether those emissions could be quantified.
The collaboration’s first peer-reviewed paper, published this week in Environmental Science and Technology Letters via open access, confirmed what the engineers had suspected about airborne particle emissions that pertain to certain activities. Singing produced 77% more aerosols than talking; adults produced 62% more aerosols than minors; and males produced 34% more aerosols than females. The recent paper only contains results from the study’s singing and talking experiments; results from wind instrument-playing are pending further data analysis and peer review.
Goble and colleagues raised nearly $100,000 in support of the study, including gifts from the United States Institute for Theatre Technology, Conn-Selmer and the Yamaha Corp.
The centerpiece technology of the study was an aerosol testing chamber in Volckens’ Powerhouse Energy Campus lab, only a few of which exist in the U.S. About 100 volunteers ranging in age from 12 to 61 sat or stood in the chamber and sang, talked or played instruments while sophisticated equipment captured and measured the respiratory particles they were producing. They took measurements while subjects were both masked and unmasked.

Nanoscale machinery has many uses, including drug delivery, single-atom transistor technology, or memory storage. However, the machinery must be assembled at the nanoscale which is a considerable challenge for researchers.
For nanotechnology engineers the ultimate goal is to be able to assemble functional machinery part-by-part at the nanoscale. In the macroscopic world, we can simply grab items to assemble them. It is not impossible to “grab” single molecules anymore, but their quantum nature makes their response to manipulation unpredictable, limiting the ability to assemble molecules one by one. This prospect is now a step closer to reality thanks to an international effort led by the Research Centre Jülich of the Helmholtz society in Germany including researchers from the Department of Chemistry at the University of Warwick.
In the paper, ‘The stabilization potential of a standing molecule’, published on the 10th November 2021 in the journal Science Advances, an international team of researchers have been able to reveal the generic stabilisation mechanism of a single standing molecule, which can be used in the rational design and construction of three-dimensional molecular devices at surfaces.
The scanning probe microscope (SPM) has brought the vision of molecular-scale fabrication closer to reality, because it offers the capability to rearrange atoms and molecules on surfaces, thereby allowing the creation of metastable structures that do not form spontaneously. Using SPM, Dr Christian Wagner and his team were able to interact with a single standing molecule, perylene-tetracarboxylic dianhydride (PTCDA) on a surface to study the thermal stability and temperature at which the molecule would cease to be stable and would drop back into its natural state where it adsorbs flat on the surface. This temperature stands at -259.15 Celsius, only 14 degrees above the absolute zero-temperature point.
Quantum chemical calculations performed in collaboration with Dr. Reinhard Maurer from the Department of Chemistry at the University of Warwick were able to reveal that the subtle stability of the molecule stems from the competition of two strong counteracting quantum forces, namely the long-range attraction from the surface and the short-range restoring force arising from the anchor point between molecule and the surface.
Dr Reinhard Maurer, from the Department of Chemistry at the University of Warwick comments:
“The balance of interactions that keeps the molecule from falling over is very subtle and a true challenge for our quantum chemical simulation methods. In addition to teaching us about the fundamental mechanisms that stabilise such unusual nanostructures, the project also helped us to assess and improve the capabilities of our methods.”
Dr Christian Wagner from the Peter Grünberg Institute for Quantum Nanoscience (PGI-3) at Research Centre Jülich comments:
“To make technological use of the fascinating quantum properties of individual molecules, we need to find the right balance: They must be immobilized on a surface, but without fixing them too strongly, otherwise they would lose these properties. Standing molecules are ideal in that respect. To measure how stable they actually are, we had to stand them up over and over again with a sharp metal needle and time how long they survived at different temperatures.”
Now that the interactions that give rise to a stable standing molecule are known, future research can work towards designing better molecules and molecule-surface links to tune those quantum interactions. This can help to increase stability and the temperature at which molecules can be switched into standing arrays towards workable conditions. This raises the prospect of nanofabrication of machinery at the nanoscale.
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Exposure to PFAS — a class of synthetic chemicals utilized in food wrappers, nonstick cookware and other products — reprograms the metabolism of benign and malignant human prostate cells to a more energy efficient state that enables the cells to proliferate at three times the rate of nonexposed cells, a new study in mice found.
However, consuming a high-fat diet significantly accelerated development of tumors in the PFAS-exposed mice, said the scientists at the University of Illinois Urbana-Champaign and the U. of I. Chicago who conducted the research. PFAS is an abbreviation for perfluoroalkyl and polyfluoroalkyl substances, often described as “forever chemicals” because they don’t degrade naturally and persist as environmental pollutants. Studies have associated PFAS with harmful effects in laboratory animals.
“Our data suggest that exposure to PFAS synergizes with dietary fat to activate the protein-coding gene PPARa, altering cells’ metabolism in ways that escalate the carcinogenic risk in normal prostate cells while driving tumor progression in malignant cells,” said food science and human nutrition professor Zeynep Madak-Erdogan, the principal investigator on the project.
“These alterations in cell metabolism that occur downstream of PPARa activation may underpin the increased prostate cancer risk observed in men who are exposed to PFAS,” said Madak-Erdogan, who also holds an appointment as a health innovation professor with the Carle Illinois College of Medicine.
In their analyses of gene transcription activity, the scientists found that PPARa was expressed at significantly greater levels in the tumor cells of the PFAS-exposed mice that ate the high-fat diet. PPARa controls cell proliferation and differentiation, aids in immune and inflammatory responses and has been found to play a key role in the development of liver and kidney cancers, according to the study.
Previous studies, including some conducted in humans, linked PFAS with a range of serious health problems such as prostate cancer, the most common male cancer in the U.S.

The 24-hour news cycle and social media bombardment often resulting in conflicting messages about health issues might be making it harder than ever for people to make critical decisions, according to a Rutgers-led study.
The study, published in Journal of Behavioral Medicine, examined how contradictory health information impacts responses to new information and feelings toward the recommendations and experts providing them.
“People are regularly expected to interpret complex health recommendations, especially in the wake of the COVID-19 pandemic,” said lead author Patrick Barnwell, a graduate student at Rutgers-New Brunswick. “Conflicting health-related recommendations are increasingly common due to the speed at which 24-hour news cycles and social media can spread information.”
According to the study, conflicting information can be two or more statements about a health-related issue inconsistent with one another, from several sources like an expert or non-expert and shared in various ways like in-person or on the internet.
The researchersconducted an online study where one group read a conflicting article about the benefits of eating whole-grain foods while the other group read an article with consistent information on the same topic. The participants then performed a computerized task to measure their attention and reported the effort it took to complete.
Those who read the article with conflicting information were more confused, made more errors and responded slower on the attention task, and had more negative feelings about research and scientists. They also said it took them more effort to complete the attention task than those who read the article with no conflicting messaging, even though they did not perform as well on the task.
Researchers say these reactions may undermine the effectiveness of and satisfaction with public health and disease management. Ultimately, patients may have difficulty making and implementing appropriate health-related decisions, and those decisions may be uninformed or misinformed.
Researchers suggest health professionals make sure messaging is consistent so that patients focus on the information and their specific decisions, rather than exerting attention to decipher the ambiguity in information.
“Consistent messaging is particularly important now given the amount of information public health officials are disseminating on vaccination,” said Richard Contrada, a professor of psychology and director of the Rutgers Social, Health and Interdisciplinary Psychophysiology Lab. “Since we regularly read an abundance of conflicting information, it may be valuable for educational programs or webinars to integrate strategies people can utilize to help understand and potentially resolve discrepancies contained in health-related messaging.”
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A first-of-its-kind study led by researchers at Georgia State reveals surprising new information about the relationship between neuron activity and blood flow deep in the brain, as well as how the brain is affected by salt consumption.
When neurons are activated, it typically produces a rapid increase of blood flow to the area. This relationship is known as neurovascular coupling, or functional hyperemia, and it occurs via dilation of blood vessels in the brain called arterioles. Functional magnetic resource imaging (fMRI) is based on the concept of neurovascular coupling: experts look for areas of weak blood flow to diagnose brain disorders.
However, previous studies of neurovascular coupling have been limited to superficial areas of the brain (such as the cerebral cortex) and scientists have mostly examined how blood flow changes in response to sensory stimuli coming from the environment (such as visual or auditory stimuli). Little is known about whether the same principles apply to deeper brain regions attuned to stimuli produced by the body itself, known as interoceptive signals.
To study this relationship in deep brain regions, an interdisciplinary team of scientists led by Dr. Javier Stern, professor of neuroscience at Georgia State and director of the university’s Center for Neuroinflammation and Cardiometabolic Diseases, developed a novel approach that combines surgical techniques and state-of-the-art neuroimaging. The team focused on the hypothalamus, a deep brain region involved in critical body functions including drinking, eating, body temperature regulation and reproduction. The study, published in the journal Cell Reports, examined how blood flow to the hypothalamus changed in response to salt intake.
“We chose salt because the body needs to control sodium levels very precisely. We even have specific cells that detect how much salt is in your blood,” said Stern. “When you ingest salty food, the brain senses it and activates a series of compensatory mechanisms to bring sodium levels back down.”
The body does this in part by activating neurons that trigger the release of vasopressin, an antidiuretic hormone that plays a key role in maintaining the proper concentration of salt. In contrast to previous studies that have observed a positive link between neuron activity and increased blood flow, the researchers found a decrease in blood flow as the neurons became activated in the hypothalamus.
“The findings took us by surprise because we saw vasoconstriction, which is the opposite of what most people described in the cortex in response to a sensory stimulus,” said Stern. “Reduced blood flow is normally observed in the cortex in the case of diseases like Alzheimer’s or after a stroke or ischemia.”
The team dubbed the phenomenon “inverse neurovascular coupling,” or a decrease in blood flow that produces hypoxia. They also observed other differences: In the cortex, vascular responses to stimuli are very localized and the dilation occurs rapidly. In the hypothalamus, the response was diffuse and took place slowly, over a long period of time.
“When we eat a lot of salt, our sodium levels stay elevated for a long time,” said Stern. “We believe the hypoxia is a mechanism that strengthens the neurons’ ability to respond to the sustained salt stimulation, allowing them to remain active for a prolonged period.”
The findings raise interesting questions about how hypertension may affect the brain. Between 50 and 60 percent of hypertension is believed to be salt-dependent — triggered by excess salt consumption. The research team plans to study this inverse neurovascular coupling mechanism in animal models to determine whether it contributes to the pathology of salt-dependent hypertension. In addition, they hope to use their approach to study other brain regions and diseases, including depression, obesity and neurodegenerative conditions.
“If you chronically ingest a lot of salt, you’ll have hyperactivation of vasopressin neurons. This mechanism can then induce excessive hypoxia, which could lead to tissue damage in the brain,” said Stern. “If we can better understand this process, we can devise novel targets to stop this hypoxia-dependent activation and perhaps improve the outcomes of people with salt-dependent high blood pressure.”
The study authors include Ranjan Roy and Ferdinand Althammer, postdoctoral researchers in the Center for Neuroinflammation and Cardiometabolic Diseases, Jordan Hamm, assistant professor of neuroscience at Georgia State, and colleagues at the University of Otago in New Zealand, Augusta University and Auburn University. The research was supported by the National Institute of Neurological Disorders and Stroke.

For hard-to-treat leukemias, lymphomas and other blood cancers, stem cell transplantation is the gold standard of care. The procedure involves replacing a patient’s own blood-forming stem cells with a donor’s stem cells and, in the process, eradicating cancer cells in the blood, lymph nodes and bone marrow.
But many patients with such deadly blood cancers are too fragile to undergo stem cell transplants. That’s because a patient’s stem cells first must be destroyed by intensive chemotherapy and sometimes total body radiation before a donor’s stem cells are infused. This so-called conditioning regimen makes space for incoming donor stem cells, helps to remove cancer cells remaining in the body, and depletes the patient’s immune system so it can’t attack the donor’s stem cells. However, toxicities and suppression of the immune system caused by conditioning regimens puts patients at high risk of infections, organ damage and other life-threatening side effects.
Now, studying mice, researchers at Washington University School of Medicine in St. Louis have developed a method of stem cell transplantation that does not require radiation or chemotherapy. Instead, the strategy takes an immunotherapeutic approach, combining the targeted elimination of blood-forming stem cells in the bone marrow with immune-modulating drugs to prevent the immune system from rejecting the new donor stem cells. With the new technique, mice underwent successful stem cell transplants from unrelated mice without evidence of dangerously low blood cell counts that are a hallmark of the traditional procedure. The data also suggested that such stem cell transplants can be effective against leukemia.
The study, available online in the Journal of Clinical Investigation, opens the door to safer stem cell transplantation, meaning more patients with various types of blood cancers could receive this potentially curative therapy, and it could be considered as a treatment for other diseases, such as sickle cell anemia or other genetic disorders, that are less life-threatening.
“To be able to do a stem cell transplant without having to give radiation or chemotherapy would be transformative,” said senior author and medical oncologist John F. DiPersio, MD, PhD, the Virginia E. & Sam J. Golman Professor of Medicine and chief of the Division of Oncology at Washington University School of Medicine. “It could eliminate the dangerously low blood cell counts, bleeding complications, organ damage, and infections. It has particular implications for conducting bone marrow transplantation or gene therapy for patients with noncancerous diseases such as sickle cell anemia, where the toxicities of chemotherapy- or radiation-associated conditioning are important to avoid. We have more work to do before we’re ready to translate these findings to people, but we’re encouraged by the results of this study.”
As an alternative to high-dose chemotherapy and whole-body radiation, DiPersio, who also directs the Center for Gene & Cellular Immunotherapy, and his colleagues harnessed drugs that are toxic to cells, and attached these drugs to antibodies that target specific surface proteins that are expressed primarily on bone marrow stem cells. Only when these antibody-drug conjugates (ADCs) bind to those specific proteins are they then internalized by the stem cells, which leads to release of the drug payload inside the cell and, ultimately, cell death. Using the ricin derivative saporin as the drug payload, the researchers generated two different ADCs to target two specific proteins found on the surface of blood stem cells, which minimizes the potential for them to cause damage to other cell types.

Breast cancers that have an overactive PI3K enzyme, involved in cell growth and division, tend to be more aggressive and to spread and divide more like stem cells. But a new study by Ralitsa Madsen of University College London and colleagues publishing Nov. 11 in the journal PLOS Genetics uncovers a surprising relationship between PI3K activity and mutations in the PIK3CA gene that codes for the enzyme. Breast cancer tumors with one mutant copy of the PIK3CA gene tend to have lower PI3K activity. In comparison, patients with two or more copies often had higher PI3K? activity, resulting in more aggressive tumors and a poorer prognosis for patients with certain types of breast cancer.
Experiments in the lab previously showed that two but not one mutant PIK3CA gene can promote a persistent stem cell state — a quality called “stemness.” But until now, there was no evidence from human patients to support this idea. In the new study, researchers investigate the relationship among PI3K mutations, PI3K activity and stemness in breast cancer. They used publicly available data from nearly 3,000 breast cancer tumors and applied computational methods to infer PI3K activity and stemness. They discovered that aggressive tumors had more PI3K activity and a higher degree of stemness. However, they were surprised to find that cancer cells with only one mutant copy of PIK3CA had lower levels of stemness and are potentially less aggressive.
The new study supports the idea that overactive PI3K enzymes are linked to more aggressive breast cancers. Additionally, the researchers warn that the number of copies of mutant PIK3CA mutations in a tumor may affect how it responds to cancer therapies. They conclude that this information, along with data on PI3K activity, should be considered when choosing patients to participate in clinical trials of new drugs.
Madsen adds, “Breast cancer stratification by PIK3CA mutant dose reveals a counterintuitive relationship with functional indices of PI3K pathway activity and tumor dedifferentiation.”
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A new study by researchers at The Wistar Institute, an international biomedical research leader in cancer, immunology, infectious disease, and vaccine development, shows how key features on the surface of HIV-infected cells help the disease evade detection by the immune system. It also shows how these features can be disabled. The findings, published in PLOS Pathogens, are a first step toward a new class of treatment aimed at not just suppressing virus replication, but killing cells harboring persistent virus that prevent us from curing HIV infection.
“We identified a glyco-immune checkpoint interaction as a novel mechanism that allows HIV-infected cells to evade immune surveillance,” said Mohamed Abdel-Mohsen, Ph.D., assistant professor in the Vaccine & Immunotherapy Center at The Wistar Institute and coauthor on the paper. “And we developed a novel approach that selectively targets these interactions on the surface of these infected cells.”
A cure or long-term remission remains the holy grail of HIV research. Current treatments can reduce HIV to undetectable levels, but they can’t eradicate it entirely. The disease typically returns quickly when treatment stops. And even when controlled, HIV increases risk for other health problems, including neurological disorders, cardiovascular disease, and cancer.
For the new study, researchers looked at a type of sugar molecule called sialic acid on the surface of HIV-infected cells. These sugars bind with special receptors called siglecs on the surface of disease-fighting “natural killer” immune cells. When activated, these receptors act as inhibitors, restraining the killer cells and causing them to stop killing. “We thought, ‘is it possible that these HIV-infected cells are using this interaction — covering themselves with these sugars to evade the natural killer immune surveillance?'” said Abdel-Mohsen.
The Abdel-Mohsen lab found that was indeed the case and these infected cells can take advantage of this inhibitory connection to evade immune surveillance. Researchers then investigated whether they could manipulate this connection to make the killer cells more effective at killing HIV-infected cells. First, they looked at whether disabling the inhibitors from the killer cells would unleash their full killing power. However, this can cause the immune cells to attack indiscriminately, destroying both healthy and unhealthy cells. The researchers then turned their attention to the HIV cells. They used an enzyme called sialidase to remove the sialic acid sugars that were activating the immune inhibitors. However, this again affected all cells, causing the killer cells to attack indiscriminately. Finally, they developed a sialidase conjugate linked to HIV antibodies. This antibody-sialidase conjugate only targeted sialic acid on HIV cells. With the sialic acid removed from these cells, the killer immune cells attacked and killed the HIV-infected cells, leaving healthy cells alone.
“The killer cells become a super killer for the HIV-infected cells and they now attack them in a selective manner,” said Abdel-Mohsen. “The discovery could be a missing link in the “shock and kill” approach to HIV treatment that has been a focus of research for the past several years,” he added. This two-step process involves first “shocking” the HIV out of latency so it can be detected, and then stimulating the immune system to “kill” the virus once and for all. However, while effective methods have been discovered to reverse latency, scientists haven’t yet found a way to make HIV-infected cells more killable once reactivated. “We may have the shock, but we don’t have yet the kill,” Abdel-Mohsen said. “Our method actually increases the susceptibility of HIV-infected cells to killing, which is one of the top unmet needs in the HIV field.”
First author Samson Adeniji, Ph.D., a postdoctoral fellow at Wistar, noted that the team’s approach could be tested in combination with broadly neutralizing antibody therapies currently being studied in clinical trials. “By combining approaches, we could turn these immune cells from a cop into a kind of Robocop,” he said.
The researchers also noted that, in addition to HIV, the approach could have a clinical application in treating other infectious diseases that may evade the immune system, including hepatitis and COVID. Next, the team is moving forward with animal studies to test their findings in vivo. They’re also investigating other sugar molecules on HIV that may play a similar role as sialic acid. “HIV-infected cells are likely evading immune surveillance through many potential glyco-immune checkpoints,” Abdel-Mohsen said. “We are investigating other mechanisms and how to break them.”
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