Tag: 19/5/23

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Monkeypox Virus can Linger for up to a Month on Surfaces

On By ModernMedia
Monkeypox virus. Source: NIH

According to a study published in the Journal of Infectious Diseases, the monkeypox virus remains infectious on steel surfaces for up to 30 days, especially in cold conditions, but can be effectively inactivated by alcohol-based disinfectants.

Smallpox viruses are notorious for their ability to remain infectious in the environment for a very long time. A study conducted by the Department of Molecular and Medical Virology at Ruhr University Bochum, Germany, has shown that temperature is a major factor in this process: at room temperature, a monkeypox virus that is capable of replicating can survive on a stainless steel surface for up to 11 days, and at 4°C for up to a month. Consequently, it’s very important to disinfect surfaces. According to the study, alcohol-based disinfectants are very effective against monkeypox viruses, whereas hydrogen peroxide-based disinfectants have proved inadequate.

Weeks of monitoring

Since 2022, the monkeypox virus has been transmitted more and more frequently from one human host to another. Although infections primarily result from direct physical contact, it’s also possible to contract the virus through contaminated surfaces, for example in the household or in hospital rooms. “Smallpox viruses are notorious for their ability to remain infectious in the environment for a very long time,” explains Dr Toni Meister from the Department for Molecular and Medical Virology at Ruhr University Bochum. “For monkeypox, however, we didn’t know the exact time frames until now.”

The researchers therefore studied them by applying the virus to sanitised stainless steel plates and storing them at different temperatures: at 4°C, at 22°C, which roughly corresponds to room temperature, and at 37°C. They determined the amount of infectious virus after different periods of time, ranging from 15 minutes to several days to weeks.

Viruses remain infectious for a long time

Regardless of the temperature, there was little change in the amount of infectious virus during the first few days. At 22 and 37°C, the virus concentration dropped significantly only after five days. At 37°C, no virus capable of reproducing was detected after six to seven days, at 22°C it took 10–11 days until infection was no longer possible. At 4°C, the amount of virus only dropped sharply after 20 days, and after 30 days there was no longer any danger of infection. “This is consistent with our experience that people can still contract monkeypox from surfaces in the household after almost two weeks,” points out Professor Eike Steinmann, Head of the Department for Molecular and Medical Virology.

In order to reduce the risk of infection in the event of an outbreak, it is therefore extremely important to disinfect surfaces. This is why the researchers tested the effectiveness of five common disinfectants. They found that alcohol-based or aldehyde-based disinfectants reliably reduced the risk of infection. A hydrogen peroxide-based disinfectant, however, didn’t inactivate the virus effectively enough in the study. “Our results support the WHO’s recommendation to use alcohol-based surface disinfectants,” concludes Toni Meister.

Source: Ruhr-University Bochum

Categories : Metabolic DisordersTags : 1 Comment

Quarter of Teens with Obesity Treated with Semaglutide Fell to Normal Weight

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Photo by Andres Ayrton on Pexels

A secondary analysis of a trial of 2.4mg semaglutide (Wegovy) found nearly half of the teenage participants with obesity returned to normal weight or fell below the obesity threshold. The trial, results of which were published in Obesity, added semaglutide to dietary advice and a daily goal of 60 minutes of moderate- to high-intensity physical activity.

During the 68-week STEP TEENS trial, 44.9% of participants (aged 12–18 with obesity) returned to either normal weight or went down to the overweight category while on treatment compared with only 12.1% of those on placebo. At the end of the trial, 25% of the treatment group dropped to normal weight compared to just 2% for placebo.

“These results underscore the high degree of clinical effectiveness of semaglutide in adolescents with obesity,” said first author Aaron S. Kelly, PhD, in a statement. “In a practical sense, we see that semaglutide reduced weight to a level below what is defined as clinical obesity in nearly 50% of the teens in our trial, which is historically unprecedented with treatments other than bariatric surgery.”

An ‘important piece to the puzzle’ of the obesity problem

“A question I get a lot is, ‘Is this going to solve the obesity problem? Should we just give it to everybody’?” said Kelly, who is at the University of Minesota. “No and no. It’s not going to solve the obesity problem, but it’s an important piece to the puzzle in helping to solve it, especially for those who already have obesity.”

The trial’s initial results saw a an average BMI reduction 16.1% with semaglutide compared with a 0.6% increase with placebo at week 68. On average, participants on semaglutide lost 15.3 kg, while those on placebo gained 2.4 kg.

“The degree of body weight reduction is unprecedented,” lead study author Daniel Weghuber, MD, of Paracelsus Medical University, told MedPage Today at the ObesityWeek meeting, when the results were presented. “After years of frustration, all of a sudden patients were actually losing weight. They’d never seen that before.”

These results led to the approval for ages 12 and older by the FDA in December 2022, after being approved for adults in June 2021. The study also found a slightly superior but non-significant effect in females than males, despite not being set up to measure sex differences. The same was true for ages 12–14 vs 15–18.

Source: MedPage Today

Categories : Environmental EffectsTags :

Ultra-protective Sunscreens May One Day be Based on Our Own Melanin

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Photo by Rfstudio on Pexels

Our body’s own melanin has long held potential as an inspiration for ultra-protective sunscreens, but has been too unstable to properly study. In Nature Chemistry, researchers report a major advance in understanding the fundamental structure of melanin and one of its subunits that turns light into heat, protecting the body from sun damage.

Melanin is the body’s natural pigment that is its first and best natural defence against the damaging effect of ultraviolet radiation. Cosmetics companies have long tried to harness the protective powers of natural and synthetic melanin for use in chemical sunscreens and other personal care products. For example, melanin could, in theory, be used to produce a radiation barrier that augments skin care products by matching a more diverse range of natural skin tones. But melanin is so notoriously unstable and difficult to study that, thus far, scientists have not been able to see what it looks like at the molecular level, resulting in a slow, trial-and-error approach to its potential use in personal care products.

“As we gain a better understanding of the structure of melanin, we should be able to predictably make alternatives that perform better than what is currently available,” said Jean-Philip Lumb, one of the lead authors of the paper. The study found that the melanin component converted light into heat from all wavelengths, spanning the ultraviolet to the infrared, offering a broad spectrum of protection. The molecule was also remarkably small, which the researchers say has practical benefits because the number of atoms needed to provide this level of sun protection is fewer than anything reported up to now. “We’ve taken a major step forward in understanding a new mechanism for how melanin can serve as a sunscreen,” Lumb said.

Source: McGill University

Categories : Neurodegenerative DiseasesTags :

Epstein–Barr Virus Antibodies may Trigger Multiple Sclerosis

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Source: CC0

Researchers at Karolinska Institutet have found further links between Epstein–Barr virus and multiple sclerosis. A study published in Science Advances shows that some individuals have antibodies against the virus that mistakenly attack a protein in the brain and spinal cord.

Many years ago, the Epstein–Barr virus (EBV), which infects most people early in life and then usually lies dormant was linked to multiple sclerosis (MS) but the reason remained a mystery. Increasing evidence, including two papers published in Science and Nature last year, suggests that EBV infection precedes MS and that antibodies against the virus may be involved. However, the molecular mechanisms seem to vary between patients and remain largely unknown.

“MS is an incredibly complex disease, but our study provides an important piece in the puzzle and could explain why some people develop the disease,” says Olivia Thomas, postdoctoral researcher at the Department of Clinical Neuroscience, Karolinska Institutet and shared first author of the paper. “We have discovered that certain antibodies against the Epstein-Barr virus, which would normally fight the infection, can mistakenly target the brain and spinal cord and cause damage.”

The researchers analysed blood samples from more than 700 patients with MS and 700 healthy controls. They found that antibodies that bind to a certain protein in the Epstein-Barr virus, EBNA1, can also bind to a similar protein in the brain and spinal cord called CRYAB, whose role is to prevent protein aggregation during conditions of cellular stress such as inflammation. These misdirected, cross-reactive antibodies may damage the nervous system and cause severe symptoms in MS patients, including problems with balance, mobility and fatigue. The antibodies were present in about 23 percent of MS patients and 7% of control individuals.

“This shows that, whilst these antibody responses are not required for disease development, they may be involved in disease in up to a quarter of MS patients,” says Olivia Thomas. “This also demonstrates the high variation between patients, highlighting the need for personalised therapies. Current therapies are effective at reducing relapses in MS but unfortunately, none can prevent disease progression.”

“We are now expanding our research to investigate how T cells fight EBV infection and how these immune cells may damage the nervous system in multiple sclerosis and contribute to disease progression,” says joint first author of the paper Mattias Bronge, affiliated researcher at the Department of Clinical Neuroscience, Karolinska Institutet.

Source: Karolinska Institutet