Low humidity environments are a key factor in getting the flu and perhaps even dying from it

via Yale News – Yale University

Yale researchers have pinpointed a key reason why people are more likely to get sick and even die from flu during winter months: low humidity.

While experts know that cold temperatures and low humidity promote transmission of the flu virus, less is understood about the effect of decreased humidity on the immune system’s defenses against flu infection.

The Yale research team, led by Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology, explored the question using mice genetically modified to resist viral infection as humans do. The mice were all housed in chambers at the same temperature, but with either low or normal humidity. They were then exposed to the influenza A virus.

The researchers found that low humidity hindered the immune response of the animals in three ways. It prevented cilia, which are hair-like structures in airways cells, from removing viral particles and mucus. It also reduced the ability of airway cells to repair damage caused by the virus in the lungs. The third mechanism involved interferons, or signaling proteins released by virus-infected cells to alert neighboring cells to the viral threat. In the low-humidity environment, this innate immune defense system failed.

The study offers insight into why the flu is more prevalent when the air is dry. “It’s well known that where humidity drops, a spike in flu incidence and mortality occurs. If our findings in mice hold up in humans, our study provides a possible mechanism underlying this seasonal nature of flu disease,” said Iwasaki.

While the researchers emphasized that humidity is not the only factor in flu outbreaks, it is an important one that should be considered during the winter season. Increasing water vapor in the air with humidifiers at home, school, work, and even hospital environments is a potential strategy to reduce flu symptoms and speed recovery, they said.

Learn more: Flu virus’ best friend: Low humidity

 

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New anti-influenza drugs

(Image: courtesy of the National Museum of Health and Medicine, Armed Forces Institute of Pathology, Washington, D.C., United States.) [CC BY 2.5 (https://creativecommons.org/licenses/by/2.5)], via Wikimedia Commons

Researchers at LSTM and Imperial College London have designed drugs which could help combat any potential new flu pandemic, by targeting the receptors of the cells by which the virus gains entry to the human body.

In a paper published today(link is external) in the Journal of Immunology the team, led by LSTM’s Professor Richard Pleass, show that by engineering a part of an antibody they can target the viral proteins that allow flu to mutate and become so deadly to humans.

Last year marked the centenary of the 1918 influenza pandemic that claimed nearly 100 million lives worldwide, thus becoming the deadliest disease outbreak in recorded history. Global annual influenza outbreaks account for 300,000-650,000 respiratory deaths, mostly in children and the elderly.

Professor Pleass explained: “Influenza vaccines have limited public health impact during pandemics, and current influenza vaccines are less efficacious than vaccines for many other infectious diseases. This is because influenza viruses that circulate in human and animal populations mutate two key viral surface proteins, haemagglutinin (HA) and neuraminidase (NA), thus allowing them to escape from protective antibodies produced through natural infection or vaccination”

Both HA and NA target a sugar called sialic acid, that is found in abundance on the receptors of cells lining the mammalian respiratory tract, which the virus uses to gain entry into the body. The sialic acid-binding contacts on HA and NA do not mutate readily, otherwise the virus would not be able to infect human cells.

The team has engineered antibody Fc fragments with enhanced sialic acid that target these conserved parts of both HA and NA, binding influenza viruses and thus blocking their interactions with human cells.

By targeting sialic acid, these engineered biologicals may also be useful in the control of other pathogens, such as group B streptococci, Streptococcus pneumoniaeMycoplasma genitalium, and Newcastle Disease Virus.

“Better anti-influenza therapeutics are urgently needed.” Continued Professor Pleass: “The transfer of antibodies from people recovering from influenza during the 1918 and 2009 pandemics reduced mortality from influenza by 50% and 26% respectively. However, to be useful, these antibody medicines (also called FLU-IVIG) need to be manufactured in advance of future epidemics, which is obviously problematic as there may be modest or little neutralising activity against newly emerging strains. Therefore, combinations of existing medicines, including FLU-IVIG, with sialic acid blockers could increase their efficacy while future-proofing against the next pandemic.”

Professor Sara Marshall, Head of Clinical and Physiological Sciences at the Wellcome Trust, who provided funding for this work, said: “This is a fascinating project, and one which could have really far-reaching impact not only for influenza but as a platform technology to develop new medicines for many other diseases that are currently treated by antibodies.”

The technology described is available for licensing.

Learn more: LSTM and Imperial College Researchers design new anti-influenza drugs

 

 

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A biomarker that can predict who will be most susceptible to influenza

Purvesh Khatri
via Stanford Medicine – Stanford University

Scientists at Stanford are believed to be the first to have discovered a biomarker that can predict who will be most susceptible to influenza.

Researchers at the Stanford University School of Medicine have found a way to predict whether someone exposed to the flu virus is likely to become ill.

Purvesh Khatri, PhD, associate professor of medicine and of biomedical data science, and his team used a computational approach to pinpoint a blood-based genetic biomarker to determine an individual’s susceptibility to the disease.

“We’ve been after this for about four years,” Khatri said. “To our knowledge, it’s the first biomarker that shows susceptibility to influenza, across multiple strains.”

The biomarker is a gene called KLRD1, and it essentially acts as a proxy for the presence of a special type of immune cell that may be a key to stamping out nascent flu infection. Put simply: the more of this cell type found in a person’s blood, the lower their flu susceptibility. The research even hints at new avenues for pursuing a broadly applicable flu vaccine.

A paper describing the work will be published online June 14 in Genome Medicine. Khatri is the senior author. Graduate student Erika Bongen is the lead author.

The secret’s in the cell type

At the start of their study, Khatri and his group ran gene expression analyses that sifted through the collection of human genes, looking for a sign that one might be particularly important for fighting off the flu. But the sheer number of genes in a small number of samples overshadowed any potential signal, so Khatri turned to a different approach that repurposed immune cell data collected from more than 150 studies that monitored gene expression in the immune cells of more than 6,000 samples.

“The idea was, instead of looking at 20,000 variables [or genes], let’s bring it down to 20 ¾ let’s only look at 20 immune cell types and see if any of these shows a consistent pattern in regard to H1N1 or H3N2 flu infection, and then we’ll look at genes that are related to that cell type only,” Khatri said. “And that turned out to be the answer.”

Using a computational approach developed in his lab, Khatri and his team parsed the identity and proportion of cells present in participants of two studies — one conducted at Harvard University, the other at Duke University — comprising a total of 52 individuals who volunteered to sniff up live influenza in the name of science. The researchers were looking only at types of immune cells present in each individual just before they were infected with the flu.

“We found that a type of immune cell called a natural killer cell was consistently low at baseline in individuals who got infected,” Bongen said. Those who had a higher proportion of natural killer cells had better immune defenses and fought off illness.

“So we asked, ‘What are the genes that represent natural killer cells?’ And there turned out to be this one gene, KLRD1, that seemed to be a good target,” Bongen said.

Old data, new tricks

KLRD1, when expressed, manifests as a receptor on the surface of natural killer cells. KLRD1 is basically a counting chip. When the score was tallied, Khatri saw that, on the whole, those whose immune cells consisted of 10-13 percent natural killers did not succumb to the flu, whereas those whose natural killer cells fell short of 10 percent wound up ill. It’s a fine line, Khatri said, but the distinction between the groups is quite clear: Everyone who had 10 percent or more natural killer cells stood strong against the infection and showed no symptoms.

Khatri said his findings could help health professionals understand who’s at the highest risk for flu infection. “If, for example, there’s a flu epidemic going on, and Tamiflu supplies are limited, this data could help identify who should be prophylactically treated first,” Khatri said.

Khatri emphasizes that for now, the link between KLRD1 levels and influenza susceptibility is only an association. The next step, he said, is to find the mechanism.

“It will be crucial to understand the role of natural killer cells’ protection so that we can potentially leverage that in designing better flu vaccines,” he said. “Since we see that natural killer cells are protective across different strains, maybe that would be a path to a universal flu vaccine.”

More broadly, Khatri said that this research exemplifies the power of “data repurposing.”

“Our work shows how you can use data that exists from previous studies to answer questions that those studies alone would not have been able to answer,” Khatri said. “But by aggregating the data, we were able to find a signal across both studies and use that to discover something new.”

Learn more: Stanford scientists discover biomarker for flu susceptibility

 

 

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A new target for influenza could offer broad protection against various influenza virus strains and lessen the severity of illness

Credit: NIH
The virus surface (yellow) is covered with proteins called hemagglutinin (blue) and neuraminidase (red).

Influenza vaccines that better target the influenza surface protein called neuraminidase (NA) could offer broad protection against various influenza virus strains and lessen the severity of illness, according to new research published in Cell.

Current seasonal influenza vaccines mainly target a different, more abundant influenza surface protein called hemagglutinin (HA). However, because influenza vaccines offer varying and sometimes limited protection, scientists are exploring ways to improve vaccine effectiveness. The new research builds on previous studies of NA and was conducted by a team of scientists including investigators from the Centers of Excellence for Influenza Research and Surveillance (CEIRS)program, which is organized and funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.

Investigators analyzed blood samples from people vaccinated against influenza and people diagnosed with either the 2009 H1N1 influenza virus or H3N2 influenza viruses. The volunteers were recruited for this study or had taken part in prior influenza research studies. The analyses indicate that influenza vaccines rarely induce NA-reactive antibodies, whereas natural influenza infection induces these types of antibodies at least as often as they induce HA-reactive antibodies. Additional studies in mice reinforced the human data, indicating that current influenza vaccines do not induce NA-reactive antibodies efficiently.

Additional laboratory experiments show that the NA-reactive antibodies induced during natural influenza infection are broadly reactive, meaning they could potentially protect against diverse strains of influenza. To test this theory, scientists isolated NA-reactive monoclonal antibodies from the H3N2 and H1N1 influenza patients (N2-reactive antibodies and N1-reactive antibodies, respectively). They administered 13 N2-reactive antibodies to mice and subsequently infected the mice with a different H3N2 virus strain. Eleven of the 13 N2-reactive antibodies partially or fully protected the mice. They also administered eight N1-reactive antibodies to mice and subsequently infected the mice with a similar H1N1 virus strain or an H5N1-like virus strain. Four of the eight antibodies completely protected the mice against both virus strains.

The authors note that the findings suggest that influenza vaccines should be optimized to better target NA for broad protection against diverse influenza strains. In this regard, NIAID is supporting research to characterize NA responses in infected and vaccinated individuals and to determine the mechanism of action of NA protection. NIAID also supports “NAction!” a CEIRS working group that identifies knowledge gaps in our understanding of NA and sets NA research priorities for improved influenza vaccines. These efforts contribute to NIAID’s larger plan to develop a universal influenza vaccine—a vaccine that can durably protect all age groups against multiple influenza virus strains.

Learn more: Research Offers Clues for Improved Influenza Vaccine Design

 

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Safe for human exposure, far-UVC light may offer low-cost solution to eradicating airborne viruses in indoor public spaces

Continuous low doses of far ultraviolet C (far-UVC) light can kill airborne flu viruses without harming human tissues, according to a new study at the Center for Radiological Research at Columbia University Irving Medical Center (CUIMC). The findings suggest that use of overhead far-UVC light in hospitals, doctors’ offices, schools, airports, airplanes, and other public spaces could provide a powerful check on seasonal influenza epidemics, as well as influenza pandemics.

The study was published online today in Scientific Reports.

Scientists have known for decades that broad-spectrum UVC light, which has a wavelength of between 200 to 400 nanometers, or nm), is highly effective at killing bacteria and viruses by destroying the molecular bonds that hold their DNA together. This conventional UV light is routinely used to decontaminate surgical equipment.

“Unfortunately, conventional germicidal UV light is also a human health hazard and can lead to skin cancer and cataracts, which prevents its use in public spaces,” said study leader David J. Brenner, PhD, the Higgins Professor of Radiation Biophysics at the Vagelos College of Physicians and Surgeons and director of the Center for Radiological Research at Columbia.

Several years ago, Brenner and his colleagues hypothesized that a narrow spectrum of ultraviolet light called far-UVC could kill microbes without damaging healthy tissue. “Far-UVC light has a very limited range and cannot penetrate through the outer dead-cell layer of human skin or the tear layer in the eye, so it’s not a human health hazard. But because viruses and bacteria are much smaller than human cells, far-UVC light can reach their DNA and kill them,” said Brenner, who is also a professor of environmental health sciences at Columbia’s Mailman School of Public Health.

Previously shown to kill MRSA

In their earlier studies, Brenner’s team demonstrated that far-UVC light was effective at killing MRSA (methicillin-resistant S. aureus) bacteria, a common cause of surgical wound infections but not harm human or mouse skin.

Influenza virus spreads from person to person mainly through fine liquid droplets, or aerosols, that become airborne when people with flu cough, sneeze, or talk. The new study was designed to test if far-UVC light could efficiently kill aerosolized influenza virus in the air, in a setting similar to a public space.

In the study, aerosolized H1N1 virus—a common strain of flu virus—was released into a test chamber and exposed to very low doses of 222 nm far-UVC light. A control group of aerosolized virus was not exposed to the UVC light. The far-UVC light efficiently inactivated the flu viruses, with about the same efficiency as conventional germicidal UV light.

“If our results are confirmed in other settings, it follows that the use of overhead low-level far-UVC light in public locations would be a safe and efficient method for limiting the transmission and spread of airborne-mediated microbial diseases, such as influenza and tuberculosis,” Brenner said.

At a price of less than $1,000 per lamp—a cost that would surely decrease if the lamps were mass produced—far-UVC lights are relatively inexpensive. “And unlike flu vaccines, far-UVC is likely to be effective against all airborne microbes, even newly emerging strains,” Brenner added.

Learn more: Can UV Light Fight the Spread of Influenza?

 

 

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