New Disinfectant Protects Against Covid for Up 7 Days

An alum and several researchers at the University of Central Florida (UCF) have used nanotechnology to develop the cleaning agent, which protects against seven viruses for up to seven days.

UCF researchers have developed a nanoparticle-based disinfectant that can continuously kill viruses on a surface for up to seven days – a discovery that could be a powerful weapon against COVID-19 and other emerging pathogenic viruses. The findings, by a multidisciplinary team of the university’s virus and engineering experts and the leader of an Orlando technology firm, were published this week in  ACS Nano, a journal of the American Chemical Society.

Christina Drake ’07PhD, founder of Kismet Technologies, was inspired to develop the disinfectant after making a trip to the grocery store in the early days of the pandemic. There she saw a worker spraying disinfectant on a refrigerator handle, then wiping off the spray immediately.

Initially my thought was to develop a fast-acting disinfectant,” she says, “but we spoke to consumers, such as doctors and dentists, to find out what they really wanted from a disinfectant. What mattered the most to them was something long-lasting that would continue to disinfect high-touch areas like doorhandles and floors long after application.”

Drake partnered with Sudipta Seal, a UCF materials engineer and nanoscience expert, and Griff Parks, a College of Medicine virologist who is also associate dean of research and director of the Burnett School of Biomedical Sciences. With funding from the U.S. National Science Foundation, Kismet Tech and the Florida High Tech Corridor, the researchers created a nanoparticle-engineered disinfectant.

Its active ingredient is an engineered nanostructure called cerium oxide, which is known for its regenerative antioxidant properties. The cerium oxide nanoparticles are modified with small amounts of silver to make them more potent against pathogens.

It works both chemically and mechanically,” says Seal, who has been studying nanotechnology for more than 20 years. “The nanoparticles emit electrons that oxidize the virus, rendering it inactive. Mechanically, they also attach themselves to the virus and rupture the surface, almost like popping a balloon.”

Most disinfecting wipes or sprays will disinfect a surface within three to six minutes of application but have no residual effects. This means surfaces need to be wiped down repeatedly to stay clean from a number of viruses, like COVID-19. The nanoparticle formulation maintains its ability to inactivate microbes and continues to disinfect a surface for up to seven days after a single application.

The disinfectant has shown tremendous antiviral activity against seven different viruses,” says Parks, whose lab was responsible for testing the formulation against “a dictionary” of viruses. “Not only did it show antiviral properties toward coronavirus and rhinovirus, but it also proved effective against a wide range of other viruses with different structures and complexities. We are hopeful that with this amazing range of killing capacity, this disinfectant will also be a highly effective tool against other new emerging viruses.

The scientists are confident the solution will have a major impact in health care settings in particular, reducing the rate of hospital acquired infections, such as Methicillin-resistant Staphylococcus Aureus (MRSA), Pseudomonas aeruginosa and Clostridium difficile – which affect more than one in 30 patients admitted to U.S. hospitals. And unlike many commercial disinfectants, the formulation has no harmful chemicals, which indicates it will be safe to use on any surface. Regulatory testing for irritancy on skin and eye cells, as required by the U.S. Environmental Protection Agency, showed no harmful effects.

Many household disinfectants currently available contain chemicals that can be harmful to the body with repeated exposure,” Drake says. “Our nanoparticle-based product will have a high safety rating will play a major role in reducing overall chemical exposure for humans.”


How To Reverse Cell Aging

A team of scientists has found why elderly people are more susceptible to COVID-19 and are working to reverse the aging process of the body’s immune system.

Scientists from the Technion-Israel Institute of Technology say they have found a way to rejuvenate the aging process of the body’s immune system. Prof. Doron Melamed and doctoral student Reem Dowery sought to understand why the elderly population is more susceptible to severe cases of COVID-19 and why the vaccines seem to be less effective and wane faster among this population. The results of their work were published this month in the peer-reviewed, online medical journal Blood.
The secret begins with B cells, also known as B lymphocytes. These are the cells that produce antibodies against any pathogen that enters the body. They play a key role in protecting people from viruses and diseases.
B cells do not just disappear. They turn into “memoryB cells so that if the body is exposed to a previous pathogen, the individual will not get sick. That is because the immune response will be fast and robust, and it will eliminate the pathogen, often without the individual knowing he or she had been exposed to it.

Imagine you are growing into adulthood, and you become an adult and then an older person,” Melamed said. “You accumulate in your body many memory cells. You are exposed all the time to pathogens, and hence you make more and more memory cells. Because these are so long-lived, there is no room left for new B cells.
What happens when a new pathogen, such as the coronavirus, comes along? There are no young B cells that can recognize it. That is one of the reasons why older people are more susceptible to severe COVID-19 and many other diseases. As noted, this happens because of the body’s need for homeostasis, something that Melamed’s lab discovered a decade ago. But this year, they took the discovery another step and figured out a mechanism to override the system.
We found specific hormonal signals produced by the old B cells, the memory cells, that inhibit the bone marrow from producing new B cells,” Melamed said. “This is a huge discovery. It is like finding a needle in a haystack.”

It also means that, over time, specific drugs or treatments can be found to inhibit one of the hormones in the signaling pathway and get the bone marrow to produce new B cells.


COVID: the Risk of Death is 70% Higher for Male than for Female Patients

Evidence increasingly indicates that male sex is a risk factor for more severe disease and death from COVID-19. Male bias in COVID-19 mortality is observed in nearly all countries with available sex-disaggregated data, and the risk of death in males is ∼1.7 times higher than in females. Aging is strongly associated with higher risk of death in both sexes, but at all ages above 30 years, males have a significantly higher mortality risk, rendering older males the most vulnerable group. Sex differences are intertwined with differences in gender roles socially and with behavioral factors, which also influence COVID-19 incidence and outcomes. However, there are also possible biological mechanisms of male sex bias that affect the severity of COVID-19, particularly with respect to immune responses.

Sex differences beyond sex organs are present across species and extend to physiological systems, including the immune system. Infection by different pathogens results in differential immune responses and disease outcomes by sex, and although the pattern depends on age and other host factors, male sex is more often associated with lower immune responses and higher susceptibility and/or vulnerability to infections in animals. This is generally also the case in humans: Male patients have higher viral loads for hepatitis B virus (HBV) and HIV. Conversely, females generally mount a more robust immune response to vaccines, such as influenza vaccines. However, the heightened immune responses in females can also lead to detrimental immunopathology in infections.

The physiological response to virus infection is initiated when virus replication is detected by pattern recognition receptors. This leads to two antiviral programs by the infected cells.

How To Intercept Coronavirus Infection

Nanoparticles cloaked in human lung cell membranes and human immune cell membranes can attract and neutralize the SARS-CoV-2 virus in cell culture, causing the virus to lose its ability to hijack host cells and reproduce. The first data describing this new direction for fighting COVID-19 were published on June 17, 2020 in the journal Nano Letters. The “nanosponges” were developed by engineers at the University of California San Diego (UC San Diego) and tested by researchers at Boston University. The UC San Diego researchers call their nano-scale particlesnanosponges” because they soak up harmful pathogens and toxins.

In lab experiments, both the lung cell and immune cell types of nanosponges caused the SARS-CoV-2 virus to lose nearly 90% of its “viral infectivity” in a dose-dependent manner. Viral infectivity is a measure of the ability of the virus to enter the host cell and exploit its resources to replicate and produce additional infectious viral particles.

Instead of targeting the virus itself, these nanosponges are designed to protect the healthy cells the virus invades.

Nanosponges attacking and neutralizing the SARS-COV-2 virus

Traditionally, drug developers for infectious diseases dive deep on the details of the pathogen in order to find druggable targets. Our approach is different. We only need to know what the target cells are. And then we aim to protect the targets by creating biomimetic decoys,” said Liangfang Zhang, a nanoengineering professor at the UC San Diego Jacobs School of Engineering.

His lab first created this biomimetic nanosponge platform more than a decade ago and has been developing it for a wide range of applications ever since. When the novel coronavirus appeared, the idea of using the nanosponge platform to fight it came to Zhang “almost immediately,” he said.

In addition to the encouraging data on neutralizing the virus in cell culture, the researchers note that nanosponges cloaked with fragments of the outer membranes of macrophages could have an added benefit: soaking up inflammatory cytokine proteins, which are implicated in some of the most dangerous aspects of COVID-19 and are driven by immune response to the infection.


Defective immune cells make us old

T cells are supposed to defend us from pathogens, but a new mouse study suggests they may also speed aging. Blocking inflammation caused by the cells or boosting their supply of a key metabolic molecule lessened the severity of some aging-related symptoms in rodents, raising the possibility these treatments could benefit older people. The discovery is “a fantastic result directly linking metabolism, inflammation, and aging,” says immunologist Kylie Quinn of RMIT University, Bundoora, in Australia. “They’ve done a really thorough job of making sure it’s the T cells” that are causing the mice to age quickly.

Our T cells let us down as we age, becoming weaker pathogen fighters. This decline helps explain why elderly people are more susceptible to infections and less responsive to vaccines. One reason T cells falter as we get older is that mitochondria, the structures that serve as power plants inside cells, begin to malfunction. But T cells might not just reflect aging. They could also promote it. Older people have chronic inflammation throughout the body, known as inflammaging, and researchers have proposed it spurs aging. T cells may stoke this process because they release inflammation-stimulating molecules.

To test that hypothesis, immunologist María Mittelbrunn of the University Hospital 12 October’s Health Research Institute and colleagues genetically modified mice to lack a protein in the mitochondria of their T cells. This alteration forces the cells to switch to a less efficient metabolic mechanism for obtaining energy.

By the time the rodents were 7 months old, typically the prime of life for a mouse, they already appeared to be in their dotage, the team reports today in Science. Compared with typical mice, the modified rodents were slow and sluggish. They had shrunken, weak muscles and were less resistant to infections. Like many elderly people, they suffered from weakened hearts and shed much of their body fatT cells from the altered mice poured out molecules that trigger inflammation, the team found, suggesting the cells could be partially responsible for the animals’ physical deterioration. “The immune system plays a role in increasing the velocity of aging,” Mittelbrunn says.

The scientists also tested whether they could slow the aging clock. First they dosed the mice with a drug that blocks tumour necrosis factor alpha (TNF-alpha), one of the inflammation-inducing molecules that T cells unleash; the treatment increased the animals’ grip strength, improved their performance in a maze, and boosted the heart’s pumping power.

Mittelbrunn and colleagues also gave the animals a compound that raises levels of nicotinamide adenine dinucleotide (NAD), a molecule that’s vital for metabolic reactions that enable cells to extract energy from food. NAD’s cellular concentrations typically decline with age, and the researchers found that ramping it up in the mice made them more active and strengthened their hearts.