Publisher Health

Structural differences in lung airways between men and woman may be the cause of differences in chronic obstructive pulmonary disease (COPD) prevalence and outcomes between the sexes. According to a large, multicenter study published in the journal Radiology, researchers found that even among adults who have never smoked, or who have smoked less than 100 cigarettes in their lifetime, lung airways were smaller in women, which can lead to a higher risk for lung disease.
COPD refers to a group of diseases, such as emphysema and chronic bronchitis, that cause airflow blockage and breathing-related problems. More than 15 million Americans have COPD, according to the Centers for Disease Control and Prevention.
Overall, men have a higher rate of diagnosis and mortality, but with changes in smoking behavior and increasing urbanization, the prevalence of COPD in women is on the rise.
“The prevalence of COPD in women is fast approaching that seen in men, and airway disease may underlie some of the high COPD numbers in women that we are seeing,” said the study’s lead author, Surya P. Bhatt, M.D., M.S.P.H., associate professor of medicine, Division of Pulmonary, Allergy and Critical Care Medicine at the University of Alabama at Birmingham. “When airways narrow due to cigarette smoking, the impact on symptoms and survival is greater in women than in men.”
The assumption that women have smaller airways is based on comparisons of the trachea and main stem bronchi, but few studies have compared distal airways in normal individuals or accounted for differences in lung size.
For this study, researchers analyzed data from nearly 10,000 participants enrolled in Genetic Epidemiology of COPD (COPDGene), a prospective multicenter observational cohort study of current and former smokers, as well as never smokers, between the ages of 45 and 80 years, at 21 clinical centers across the United States. The researchers looked at data of never, current and former smokers enrolled in COPDGene from January 2008 to June 2011 and followed up longitudinally until November 2020.

New research from the University of Cincinnati shows early indications that light can be used as a treatment for certain diseases, including cancer.
Researchers from UC, the University of Illinois Urbana-Champaign and the University at Buffalo published the results of their study demonstrating light-activated proteins can help normalize dysfunction within cells in the journal Nature Communications July 25.
The research centers on the functions of mitochondria, organelles within a cell that act as the cell’s “power plant” and source of energy. Organelles are tiny specialized structures that perform various jobs inside cells.
Jiajie Diao, PhD, one of the study’s authors, said hundreds of mitochondria are constantly coming together (a process called fusion) and dividing into smaller parts (a process called fission) to stay balanced in healthy cells. But when mitochondria are not functioning properly, there is an imbalance of this process of fission and fusion.
This imbalance can lead to a number of mitochondrial diseases, including neurodegenerative diseases like dementia and certain cancers.
Diao said previous research found that another organelle within cells called a lysosome can play a role in mitochondria fission. When a mitochondria comes in contact with a lysosome, the lysosome can act like a pair of scissors and cut the mitochondria into smaller pieces.

A new study shows how mutation of the ADAR1 gene sets off biochemical pathways that produce an autoimmune response that harms the developing brain and other areas of the body.
The ADAR gene contains instructions for making proteins used by the immune system. Normally, the body’s immune system fights off pathogens, foreign bodies, and cancers. An RNA-editing enzyme produced by the ADAR1 gene steps in to stop abnormal immune activation when the body misidentifies its own RNA.
Mutations in the ADAR1 gene are common in people of northern European descent. When a second specific mutation is also present in an individual, together they can contribute to a condition in which an embryo, fetus or newborn appears to be over-zealously fighting off a viral infection, but no causative pathogens are present. In people the disease is called Aicardi-Goutieres Syndrome.
While most babies with the mutation do not have symptoms, the severe forms of the condition can lead to cognitive impairment, additional neurological problems, and damage to other organs, like the kidneys and liver, and it can be fatal. While the two disorders are not considered related, the syndrome shares a few features with another autoimmune disease, systemic lupus erythematosus.
Because it looks like the baby is trying to overcome a virulent virus, but no actual infection can be detected, the disease appears to mimic an infection acquired just before or soon after birth.
Studying the immunological repercussions of this mutation, in addition to increasing critical knowledge to improve medical understanding about this devastating disease, can provide broader insights into some aspects of genetic and biochemical activities and interactions culminating in abnormal inflammation.
The findings of the research, conducted in mouse models, appear July 28 in the print edition of Nature. The study took place in the University of Washington School of Medicine immunology labs of Andrew Oberst, Daniel Stetson and Ram Savan. It was led by Nicholas W. Hubbard, Joshua M. Ames and Megan Maurano.
They learned that a point mutation in a particular domain of the ADAR1 gene can lead to the activation of a mammalian protein known as ZBP1. This protein can trigger programmed cell death and as well as the orchestration of other gene activities in a dramatic response to a supposed threat.
The scientists found that ablating ZBP1 got rid of the apparent damaging effects from the ADAR1 mutation without eliminating the mutation’s underlying inflammatory program. The loss of one of the genes involved in cell death also had some protective effects. However, the scientists were surprised to see that, if they deleted it along with several other enzymes involved in cell death, the multiple deletions paradoxically made matters worse.
These findings suggest that RNA from within our own cells is altered by ADAR1, and that when this does not happen normally the result is activation of ZBP1. Unexpectedly, the study found that the damage that results from this ZBP1 activation is not related to activating cell death, the previously described function of ZBP1. Rather, their study suggests that mutation of the ADAR1 gene allows ZBP1 to signal for inflammatory responses that make the body attack its own tissues, even though there are no pathogens present to encourage a fight to take place.
In addition, the results from this study also point to a dual function of the enzyme caspase-8 as both an agent of programmed cell death as well as a suppressor of ZBP1 cell death and inflammation.
“Indeed, both the presence and absence of caspase-8 may drive pathology in ADAR1-mutant mice,” the scientists wrote in their Nature paper. They scientists think that two different types of programmed cell self-destruction, as well as the production of inflammation signals, may all contribute. These could occur in varying degrees, depending on cell and tissue types, to cause organ damage in animals that carry the two genes associated with the autoimmune disease under investigation.

There’s a common perception that autistic individuals are poor at recognising others’ emotions and have little insight into how effectively they do so.
But autistic adults are only slightly less accurate at reading people’s facial emotions compared to their non-autistic peers, according to new Australian research.
Recent research published in two papers in the leading international journal Autism Research shows we may need to revise widely accepted notions that adults diagnosed with autism experience difficulties when it comes to recognising social emotions and have little insight into their processing of others’ face emotions.
63 people diagnosed with autism and 67 non-autistic adults (with IQs ranging from 85 to 143) participated in a Flinders University study, with participants taking part in 3- 5-hour sessions comparing their recognition of 12 human face emotion expressions such as anger and sadness.
Dr Marie Georgopoulos collected a wide range of data during the course of her PhD, with subsequent reanalyses by the research team providing the basis for a series of research articles.
The results could mean social difficulties linked with autism may actually reflect differences that only become apparent in certain social interactions or high-pressure scenarios, challenging the perspective that autistic adults can’t adequately read facial emotion expressions.

Disease of the microscopic blood vessels that feed the white matter of our brain is associated with worse cognitive function and memory deficits in individuals with Alzheimer’s, scientists report.
“The main message of this paper is the mixed pathology as we call it — microvascular disease and Alzheimer’s — is associated with more brain damage, more white matter damage and more inflammation,” says Dr. Zsolt Bagi, vascular biologist in the Department of Physiology at the Medical College of Georgia at Augusta University.
Theirs and other recent findings suggest that some people with Alzheimer’s who have brain changes widely associated with the condition, like amyloid plaques, may not develop dementia without this underlying vascular dysfunction, the researchers write in the journal GeroScience.
“We are proposing that if you prevent development of the microvascular component, you may at least add several years of more normal functioning to individuals with Alzheimer’s,” Bagi says.
He and by Dr. Stephen Back, pediatric neurologist, Clyde and Elda Munson Professor of Pediatric Research and an expert in white matter injury and repair in the developing and adult brain at Oregon Health & Science University, are co-corresponding authors of the new study.
The good news is that vascular disease is potentially modifiable, Bagi says, by reducing major contributors like hypertension, obesity, diabetes and inactivity.

No other infectious disease has killed more people than tuberculosis. Currently, only one vaccine is available to prevent severe courses: Bacillus Calmette Guérin (BCG). However, it is not equally effective against all types of tuberculosis. Especially infants and immunocompromised patients are therefore in urgent need for more effective tuberculosis vaccines. A clinical trial in South Africa has now shown that the new vaccine candidate VPM1002, developed by Max Planck researcher Stefan H.E. Kaufmann and his team, is equally safe for newborns with and without HIV exposure and has fewer side effects compared to BCG.
At least 20 million people worldwide suffer from tuberculosis, according to World Health Organization (WHO), with 10 million new cases every year and about 1.5 million deaths annually. The disease is caused by mycobacteria, which predominantly affect the lungs, but can also infect any other organ. Tuberculosis is particularly common in low income countries. Here, the WHO recommends that newborns be immunized against it as soon as possible.
First used 100 years ago, the BCG vaccine against the disease contains attenuated pathogens of cattle tuberculosis. “We know that BCG can prevent so-called tuberculous meningitis and miliary tuberculosis in infants with a 75 to 86 percent effectiveness rate. But this is not the case for the most common form of the disease, pulmonary tuberculosis, in all age groups. Here, BCG is only insufficiently effective,” explains Kaufmann, Emeritus Director at the Max Planck Institute for Multidisciplinary Sciences in Göttingen and the Max Planck Institute for Infection Biology in Berlin.
Since the 1990s, the infection biologist and his team have been working on an improved next-generation vaccine, called VPM1002. To achieve this, the researchers genetically modified the attenuated BCG vaccine strain so that immune cells can better recognize the pathogens. “We developed VPM1002 in no small part to combine increased safety with improved efficacy for immunocompromised children,” the Max Planck researcher reports.
Vaccine candidate VPM1002 is safe
The group of immunocompromised children includes, for example, HIV-exposed infants born to HIV-positive mothers. In a clinical trial in South Africa, an international research consortium including Kaufmann has now compared VPM1002 with BCG in HIV-exposed and non-HIV-exposed newborns. The study examined both the safety and the immune response induced — called immunogenicity — associated with the formation of immune cells and immunostimulatory proteins. The conclusion of the study: VPM1002 is safe in both HIV-exposed and non-HIV-exposed newborns, has fewer side effects than BCG, and elicits a similar immune response.
In the randomized phase II double-blind study in South Africa, 416 eligible newborns were randomly selected and vaccinated before day 12 of life. 312 of them received VPM1002, and 104 received the BCG vaccine. As the study showed, VPM1002 triggered fewer vaccine-related adverse reactions than BCG. This was true for reactions occurring at the injection site, such as scarring and abscess formation, as well as enlargement of lymph nodes. This finding is important because local and regional reactions after vaccination are among the limitations of the BCG vaccine, Kaufmann points out.
Newborns with or without HIV exposure showed similar immunogenicity with both vaccines. However, starting at six weeks of age, the BCG-triggered immune response was greater than in even younger infants.
Phase III study investigates protection
“Studies such as those described here examine a vaccine’s immunogenicity, but not its protection. For the latter, we have already developed a larger phase III clinical trial and have successfully enrolled mothers with their newborns to participate. Now the clock is ticking,” Kaufmann said. The infectious biologist expects initial results showing whether VPM1002 can provide comparable or better protection than existing BCG vaccines in about three years. In addition, the VPM1002 vaccine is currently evaluated in adults in two other phase III clinical trials in India for protection against tuberculosis. These trials are expected to be completed in 2023 and 2024, respectively.
The Max Planck Society licensed the VPM1002 vaccine to the company Vakzine Projekt Management (VPM) in 2004. Starting in 2012, the company continued to develop the vaccine in collaboration with the Serum Institute of India, one of the world’s largest vaccine manufacturers. “Serum Institute of India is giving access to a unique solution for tuberculosis elimination by detect-treat-prevent strategy. VPM1002 is a unique component of this strategy, and it will help in preventing infection and disease. The ongoing phase III trial is one of the key trials in order to strengthen our scientific rationale. Pleased to see that we have completed recruitment of all infants in such an important trial,” said Umesh Shaligram, Executive Director R&D of Serum Institute of India.

A new, non-invasive ocular imaging method may be able to detect an early indicator of glaucoma in time to prevent disease progression and vision loss, according to a new study from New York Eye and Ear Infirmary of Mount Sinai (NYEE). The study was published in the July/August issue of Ophthalmology Glaucoma.
The study focused on measuring flavoprotein fluorescence (FPF) in the eye. Mitochondria — which are responsible for generating energy in cells — produce FPF when they are stressed, and levels of FPF are elevated in people with glaucoma compared to those with normal eyes. Mitochondrial dysfunction in the optic nerve, which sends light signals to the brain and is critical for vision, can eventually lead to loss of cells and tissue damage, causing multiple eye diseases such as glaucoma, and macular degeneration, as well as other retinal damage. This is the first comprehensive study to look at FPF changes in the optic nerves in patients with different stages of glaucoma compared to healthy eyes.
“Glaucoma is difficult to diagnose in early stages, and often physicians agonize to confirm subtle signs of progression in advanced stages. Once structural damage to the optic nerve has occurred, it is currently not possible to reverse. The better we become at identifying early or ongoing degeneration, the more proactive we can be at implementing protective therapy,” says principal investigator Richard B. Rosen, MD, Vice Chair and Director of Ophthalmology Research at NYEE and Chief of the Retina Service for the Mount Sinai Health System. “Our study shows FPF may be useful as an objective measure for predicting glaucoma progression earlier than measuring structural damage, with similar sensitivity to visual field changes but easier and potentially more consistently.”
A team of researchers used the OcuMet Beacon — a fundus camera with special filters that specifically isolates the fluorescence, developed by OcuSciences Inc. — to analyze 86 eyes. Fifty of the eyes had glaucoma, based upon thinning of the retinal fiber layer, and 36 had no disease. They found FPF, an indicator of mitochondrial oxidative stress, was significantly higher in glaucoma eyes compared to normal eyes,especially in early-stage glaucoma cases where damage is difficult to detect. Levels of FPF correlated with other means of detecting glaucoma including visual field mean deviation, visual field pattern deviation, and retinal nerve fiber layer thickness.
These results suggest that FPF could be used clinically to reliably and objectively detect metabolic evidence of injury due to glaucoma, limiting the need for frequent visual field testing, the gold standard for measuring visual function. In fact, the researchers say, FPF may be a more accurate measurement, as visual fields have a number of downsides — they are subjective, fluctuate with a patient’s attention, and patients can lose concentration during this assessment.
“Previous studies have demonstrated that when the mitochondrial oxidative stress is relieved by medication or surgery, the flavoprotein fluorescence levels go down. This makes the technique very attractive as a sensitive way of monitoring response to therapy,” explains Dr. Rosen. “This measurement could potentially be used as a first-line indicator to monitor of glaucoma progression for the patient and the physician.”
Researchers say their next step is to see if FPF can reliably monitor the effect of therapy for glaucoma patients, to see when treatment has flattened the risk curve of progression in advanced cases, as well as identifying patients who require early glaucoma intervention.

Liver cancer’s rapid growth leads to a vulnerability in its energy-production and cell-building processes that may be potently exploited with a new combination-treatment strategy, according to a study from researchers at the Perelman School of Medicine at the University of Pennsylvania.
In the study, published August 2 in Cell Metabolism, the researchers discovered that the main type of primary liver cancer, hepatocellular carcinoma (HCC), modifies its metabolism in a way that leaves it susceptible to disruptions in the supply of a key molecule, arginine. This arginine vulnerability, they found, is present in all HCC cancers regardless of the specific genetic mutations that gave rise to them.
The researchers showed in preclinical tests that starving HCC tumors of arginine, and also blocking the survival-promoting response that results, leaves HCC tumors in a no-growth, “senescent” state — in which they can be killed off with a new class of drugs that target senescent cells.
“Essentially we identified a metabolic property of most liver cancers that offers the possibility of treating these cancers effectively, using drugs that are already approved or in development,” said study senior author Celeste Simon PhD, the Arthur H. Rubenstein, MBBCh Professor in the Department of Cell and Developmental Biology, and scientific director of the Abramson Family Cancer Research Institute at Penn Medicine.
HCC is the most common form of liver cancer in adults. According to the National Cancer Institute, it accounts for roughly 80 percent of primary liver tumors — tumors that originate in the liver instead of spreading there from other organs. HCC occurs in about 29,000 Americans annually, nearly a million are detected worldwide, and it is thought to be caused by chronic liver inflammation due to hepatitis viruses, alcoholism, and obesity. The disease is seldom cured, because it tends to be diagnosed only after it has advanced beyond the possibility of surgical removal. Furthermore, liver transplants, which can cure benign disease, are often unavailable to advanced HCC patients. Drug treatments for HCC are limited and almost never result in cures. Thus, there is an urgent need for new treatment strategies.
The approach taken by Simon and her team — targeting tumor metabolism — is one that cancer researchers have been exploring more and more in recent years. Cancer cells usually find ways to modify their energy-production and molecule-building processes to accommodate their rapid growth. These modifications create vulnerabilities for the cancer cells that may be found in all or virtually all cases of a given cancer type. The challenge has been to identify these susceptibilities in different cancers and develop viable strategies for targeting them in a way that avoids metabolic redundancies and plasticity.
In the new study, Simon’s team first established from existing cancer cell gene activity databases, and from tests on patient tumor samples and cancer cell lines, that virtually all HCCs turn up their metabolism by suppressing a biochemical process called the urea cycle. The urea cycle normally produces, among other things, an amino acid called arginine, which is a building-block of proteins and has many other important functions. The researchers showed that HCC cells compensate for their loss of internal, urea-cycle arginine production by importing arginine from their surroundings, mainly via a transporter protein called SLC7A1.
The researchers tried blocking SLC7A1 activity in HCC cells to starve them of arginine. This didn’t kill the HCC cells, though. Instead, arginine starvation triggered a stress response that threw the cells into a dormant, slow-growth mode — from which they could recover if arginine became available again. The researchers then tried blocking the stress response as well, and found that the HCC cells now were forced into a more profound and harder-to-reverse no-growth state called senescence.
The senescent state is one that many cells fall into during normal aging. So-called senolytic drugs to kill these cells are being developed by pharma companies, because removing senescent cells has been found to have a rejuvenating effect in animal models of aging. Simon’s team used one of these experimental senolytic compounds, ABT-263, and found that it killed senescent HCC cells and caused very strong tumor regression in animal models of HCC.
The findings thus point to the possibility of a three-part combination treatment — to starve HCC tumors of arginine, to block the ensuing stress response and induce senescence, and, lastly, to kill the resulting senescent HCC cells and stop tumor growth. Simon said it is possible that all three of these effects could be achieved with drugs that are already in use or being studied for other applications.
“Conceivably this type of combination treatment, if implemented properly, would also make many patients more responsive to other treatments such as immunotherapies,” Simon said.
The research was funded by the National Cancer Institute (T32 CA09140, P01 CA104838, R35 CA197602) and by the Belgian American Educational Foundation.

Researchers at the Terasaki Institute for Biomedical Innovation (TIBI) have developed and optimized a minimally invasive method for more targeted, efficient, and sustained delivery of immunotherapeutic treatments for cancer. Such a targeted approach cuts down on the higher dosages and possible deleterious side effects that are experienced when more systemic treatment methods are employed.
There are many ways by which the body responds to abnormal cells or foreign invaders. One mechanism involves the T-cells of the immune system, which have proteins on their surface called “checkpoint proteins.” These checkpoint proteins bind to proteins on the surface of other cells, and this can result in either stimulation or suppression of T-cell activity. Stimulation of the T-cells leads to the destruction of abnormal or invading cells, while suppression is a built-in mechanism to prevent the immune system from attacking the body’s own normal cells.
Tumor cells, however, can sometimes display surface proteins which outwit the immune system by binding to T-cells and suppressing their activity; this allows the tumor cells to grow and spread. In recent years, “immune checkpoint inhibitor” antibodies (ICIs) have been developed which will block tumor cell binding to the T-cells. In effect, this re-activates the T-cell’s immune response to destroy tumor cells. In the United States, ICIs have been used successfully to treat cancers in the kidney, bladder, liver and head or neck areas.
These ICIs are commonly administered through systemic injection, and although these antibodies have demonstrated efficacy, their effects vary among patients. For some patients, the nonspecific nature of this delivery can lead to excessive T-cell stimulation that can produce toxic side effects. Systemic drug delivery also dilutes the ICI’s effectiveness, necessitating higher dosages and higher costs.
The main feature of the TIBI team’s approach was an injectable gelatin biomaterial containing disc-shaped silicate nanoplatelets mixed in. The nanoplatelets contained charged surfaces which were optimal for protectively binding to ICIs, while using minimally invasive injection to deliver the ICI-loaded biomaterial to the tumor site.
The gelatin/nanoplatelet mixture was optimized for more effective ICI delivery and sustained drug release. The team also demonstrated that several factors such as nanoplatelet, gelatin and ICI concentration, pH and conditions for biomaterial degradation could be tuned for controlling ICI release appropriate for specific tumors.
The researchers conducted additional experiments to measure the efficacy of their shear-thinning biomaterial (STB), which deforms under stress during injection and quickly self-recovers afterward. These STB were used to inject ICIs into melanoma tumors in mice. Their findings showed that melanoma tumors in these mice showed the slowest tumor growth and smallest size, as well as clear margins between the tumor and skin layer and a lack of inflammation and necrotic tissue; these effects occurred to a much higher degree and were maintained over a longer period than the negative control samples, due to the sustained ICI release and delivery.
The number of T cells activated due to ICI delivery was quantified, and it was found that the samples with STB-delivered ICIs had over 44% more T helper cells and almost 36% more T killer cells than those of the negative controls.
Finally, tumor cell death was investigated. Experiments with different staining techniques showed that there was up to 13.2 times more tumor cell death in STB-delivered samples than in negative control samples.
“The results obtained here clearly demonstrate the effectiveness of targeted, controllable and sustainable antibody delivery to reinstate the body’s natural defense mechanisms against cancer,” said TIBI’s Director and CEO, Ali Khademhosseini, Ph.D. “Its potential in creating combination therapies further extends its impact.”
Authors are: Qingzhi Wu, Moyuan Qu, Han-Jun Kim, Xingwu Zhou, Xing Jian, Yi Chen, Jixiang Zhu, Li Ren, Tyler Wolter, Heemin Kang, Chun Xu, Zhen Gu, Wujin Sun, and Ali Khademhosseini.
This research was supported by the National Institutes of Health (EB024403, HL14095).

The appointment of Robert Fenton, a veteran emergency response official, comes as New York, California and Illinois declare states of emergency.WASHINGTON — President Biden named a veteran emergency response official on Tuesday to manage the U.S. government’s handling of the monkeypox outbreak as some of the nation’s largest states declare states of emergency.The official, Robert Fenton, a regional administrator for the Federal Emergency Management Agency and twice its acting head, will serve as the White House monkeypox coordinator. Alongside him, Dr. Demetre Daskalakis, director of the Division of H.I.V. Prevention at the Centers for Disease Control and Prevention, will serve as his deputy.An early-morning statement issued by the White House said that the two men would be charged with overseeing the effort “to combat the current monkeypox outbreak, including equitably increasing the availability of tests, vaccinations and treatments.”Mr. Biden had come under pressure to name someone with presidential backing to lead the response as cases continue to spread, particularly in the L.G.B.T.Q. community.The appointments came a day after Gov. Gavin Newsom of California declared a state of emergency to help address the monkeypox outbreak there. New York and Illinois have made similar declarations, as have the mayors of New York City and San Francisco.The C.D.C. has recorded nearly 6,000 cases of monkeypox since May, with nearly half in those three large states. No deaths have been reported so far — monkeypox is rarely fatal — but the virus can lead to intense pain. It is spread primarily through prolonged physical contact.The Biden administration has not declared a state of emergency, even though the World Health Organization did so late last month, but Xavier Becerra, the U.S. secretary of health and human services, is considering it.The White House said that 737,000 more vaccines were shipped out on Monday, bringing the total number of distributed doses to 1.1 million.“It’s very important as we’re trying to really have an aggressive approach to dealing with monkeypox,” Karine Jean-Pierre, the White House press secretary, told reporters on Monday. She added that 80,000 tests were being conducted per week. “That’s another important, significant way of making sure that people are getting tested so they know if they have monkeypox or not,” she noted.The two officials installed by Mr. Biden on Tuesday morning have wide experience. Mr. Fenton, who oversees the American West for FEMA, has managed responses to natural disasters, disease outbreaks and humanitarian operations and twice served as the agency’s acting administrator.Dr. Daskalakis is known as a national expert on health issues affecting the L.B.G.T.Q. community, having previously led infectious-disease management for New York City, including its response to Covid-19.“Bob Fenton and Dr. Daskalakis are proven, effective leaders that will lead a whole of government effort to implement President Biden’s comprehensive monkeypox response strategy with the urgency that this outbreak warrants,” Dr. Anthony S. Fauci, the president’s chief medical adviser, said in the White House statement.