Individual response to COVID-19 'as important' as government action

March 6, 2020

Science Daily/University of Oxford

How individuals respond to government advice on preventing the spread of COVID-19 will be at least as important, if not more important, than government action, according to a new commentary from researchers at the University of Oxford and Imperial College London in the UK, and Utrecht University and the National Institute for Public Health and the Environment in the Netherlands.

As the UK moves into the "delay" phase of dealing with a possible COVID-19 epidemic, a new commentary, published today in The Lancet, looks at what we know so far about the new virus. The researchers, led by Professor Sir Roy Anderson at Imperial College and Professor Deirdre Hollingsworth at the University of Oxford's Big Data Institute, also suggest what can be done to minimise its spread and its impact.

Professor Hollingsworth said: 'Completely preventing infection and mortality is not possible, so this is about mitigation. Our knowledge and understanding of COVID-19 will change over time, as will the response. High quality data collection and analysis will form an essential part of the control effort. Government communication strategies to keep the public informed will be absolutely vital.'

Vaccine development is already underway, but it is likely to be at least a year before a vaccine can be mass-produced, even assuming all trials are successful. Social distancing is therefore the most important measure, with an individual's behaviour key. This includes early self-isolation and quarantine, seeking remote medical advice and not attending large gatherings or going to crowded places. The virus seems to largely affect older people and those with existing medical conditions, so targeted social distancing may be most effective.

Government actions will be important, including banning large events such as football matches, closing workplaces, schools and institutions where COVID-19 has been identified, and making sure that good diagnostic facilities and remotely accessed advice, like telephone helplines, are widely available. Ensuring the provision of specialist healthcare is also vital. The researchers warn, however, that large-scale measures may only be of limited effect without individual responsibility. All measures, of course, will have an economic impact, and some stricter measures, such as shutting down entire cities, as seen in Wuhan in China, may be less effective in Western democracies.

The aim of these social distancing measures is to "flatten the curve" of the infection, slowing the spread and avoiding a huge peak in the number of new infections.

Flattening the curve can avoid overwhelming health services, keep the impact on the economy to within manageable levels and effectively buy more time to develop and manufacture effective vaccines, treatments and anti-viral drug therapies.

Sir Roy said: 'Government needs to decide on the main objectives of mitigation -- is it minimising morbidity and associated mortality, avoiding an epidemic peak that overwhelms health-care services, keeping the effects on the economy within manageable levels, and flattening the epidemic curve to wait for vaccine development and manufacture on scale and antiviral drug therapies. We point out they cannot achieve all of these -- so choices must be made.'

The researchers highlight that wider support for the health service and health care workers during an epidemic is vital in any case -- during the Ebola epidemic in 2014-15, the death rate from other causes like malaria and childbirth rose sharply due to overwhelmed health services. The number of deaths indirectly caused by Ebola was higher than the number of deaths from Ebola itself.

While much has been made in the media of a number of "superspreading" events, where one infected individual has inadvertently spread the disease to many others, the authors warn that there are superspreading events in every epidemic, and care should be taken not to make too much of these.

Containing the spread of an infectious disease relies on keeping the "reproduction number," R0, the number of people infected by each infected person, below 1, when the pathogen will eventually die out. If R0 rises above 1, i.e. each infected person infects more than one other person, the pathogen will spread. Early data from China suggests that the R0 for COVID-19 could be as high as 2.5, implying that in an uncontained outbreak, 60% of the population could be infected. There are many unknowns in any new virus, however, and with COVID-19, it is not currently clear how long it takes for an infected person to become infectious to others, the duration of infectiousness, the fatality rate, and whether and for how long people are infectious before symptoms appear. It is also not currently clear if there are cases of COVID-19 which are non-symptomatic.

In comparisons with influenza-A (usual seasonal flu) and SARS, it currently seems likely that the epidemic will spread more slowly, but last longer, which has economic implications. Seasonal flu is generally limited by warmer weather, but as it is not known if this will affect COVID-19, the researchers say it will be important to monitor its spread in the Southern Hemisphere. Researchers will continue to collect and analyse data to monitor spread, while ongoing clinical research into treating seriously ill patients is also necessary.

One of the main priorities for researchers and policymakers will be contact tracing, with models suggesting that 70% of people an individual has come into contact with will need to be traced to control the early spread of the disease. The authors say other priorities include shortening the time from symptom onset to isolation, supporting home treatment and diagnosis, and developing strategies to deal with the economic consequences of extended absence from work.

Author Professor Hans Heesterbeek from the Department of Population Health Sciences at the University of Utrecht said: 'Social distancing measures are societally and economically disruptive and a balance has to be sought in how long they can be held in place. The models show that stopping measures after a few months could lead to a new peak later in the year. It would be good to investigate this further.'

https://www.sciencedaily.com/releases/2020/03/200306183353.htm

Risk of coronavirus importation in Africa

February 20, 2020

Science Daily/INSERM (Institut national de la santé et de la recherche médicale)

Egypt, Algeria and Republic of South Africa are the African countries most at risk for coronavirus COVID-19 importation in the continent, due to high air traffic with the contaminated Chinese provinces. But these countries are also among the best equipped on the continent to quickly detect and deal with new cases. In other African countries, the risk of importation is lower, but health organization deficiencies raise concerns about rapid spread.

The COVID-19 coronavirus continues to spread in China and cases have been reported in more than 25 countries. The African continent was spared for a long time until a first case was recently reported in Egypt. Vittoria Colizza, research director at Inserm (French Institute for Health and Medical Research), and her team from Unit 1136 Pierre Louis Institute of Epidemiology and Public Health (Inserm / Sorbonne University), in collaboration with the Université libre de Bruxelles, the Oxford Martin Programme on Pandemic Genomics and the University of California Los Angeles, assessed the risk of importing the virus into Africa, country by country, and the capacities of each of them to detect and deal with it.

The researchers evaluated the risk of the virus importation according to the number of cases declared by each chinese province and according to air traffic between the three main airports of each of these provinces (except Hubei due to flights suspension) and each African country. Moreover, they analyzed the potential of each country to face the risk of the spread of a contagious disease using WHO data and official data.

Each country makes a mandatory annual declaration to the WHO of its resources to deal with an epidemic (State Parties self-assessment Annual Reporting SPAR). It includes twenty-four items weighted into an overall score between 0 and 100, 100 showing a strong preparedness to face an epidemic.

These indicators are legislation, adherence to WHO standards, laboratory skills, medical staff, emergency organization, food safety, level of equipment in healthcare centers and public communication.

The researchers also took into account the IDVI score (for Infectious Disease Vulnerability Index), also noted out of 100, 0 corresponding to an extreme vulnerability and 100 to the lowest vulnerability. The IDVI takes into account factors not directly linked to the health system but which can influence the response to an epidemic: the size of the population, the socio-economic level or even political stability. Thus, high IDVI and SPAR scores are predictive to an efficient response in case of virus importation.

The results show that Egypt, Algeria and Republic of South Africa are the countries most at risk of importing the virus to Africa due to high trade exchanges with China. On the other hand, their SPAR and IDVI scores are among the best on the continent, letting expect effective detection and containment of the virus. Other countries as Nigeria, Ethiopia, Sudan, Angola, Tanzania, Ghana and Kenya, are at lower risk of virus importation but their SPAR and IDVI scores are lower, raising fears of the nondetection of possible imported cases and of local or even national spread.

Finally, the researchers clustered the African countries at risk into three groups according to the influence of the Chinese provinces in these countries. Thus, a first group including 18 countries will be more vulnerable in the event of a major epidemic in the province of Beijing, a second comprising 7 countries will be more exposed in the event of a strong growth of the epidemic in the province of Guangdong and a third group of two countries is risking virus importation only from Fujian province.

"This work will allow the international community to make projections and plans according to the evolution in China. It also alerts the countries most exposed to the need of being prepared for the possible introduction of the virus. We can see how hard it is to quickly detect imported cases, as even well prepared developed countries missed some of them. For several poorly equipped African countries, the risks are significant of not having sufficient organization and infrastructure for detection, containment and urgent care, raising fears of a risk of epidemic on the continent," concludes Vittoria Colizza.

https://www.sciencedaily.com/releases/2020/02/200220104049.htm

Breakthrough in coronavirus research results in new map to support vaccine design

February 19, 2020

Science Daily/University of Texas at Austin

Researchers have made a critical breakthrough toward developing a vaccine for the 2019 novel coronavirus by creating the first 3D atomic scale map of the part of the virus that attaches to and infects human cells. Mapping this part, called the spike protein, is an essential step so researchers around the world can develop vaccines and antiviral drugs to combat the virus.

Mapping this part, called the spike protein, is an essential step so researchers around the world can develop vaccines and antiviral drugs to combat the virus. The paper is publishing Wednesday, Feb. 19 in the journal Science.

The scientific team is also working on a related viable vaccine candidate stemming from the research.

Jason McLellan, associate professor at UT Austin who led the research, and his colleagues have spent many years studying other coronaviruses, including SARS-CoV and MERS-CoV. They had already developed methods for locking coronavirus spike proteins into a shape that made them easier to analyze and could effectively turn them into candidates for vaccines. This experience gave them an advantage over other research teams studying the novel virus.

"As soon as we knew this was a coronavirus, we felt we had to jump at it," McLellan said, "because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this, because we've already shown these mutations work for a bunch of other coronaviruses."

The bulk of the research was carried out by the study's co-first authors, Ph.D. student Daniel Wrapp and research associate Nianshuang Wang, both at UT Austin.

Just two weeks after receiving the genome sequence of the virus from Chinese researchers, the team had designed and produced samples of their stabilized spike protein. It took about 12 more days to reconstruct the 3D atomic scale map, called a molecular structure, of the spike protein and submit a manuscript to Science, which expedited its peer review process. The many steps involved in this process would typically take months to accomplish.

Critical to the success was state-of-the-art technology known as cryogenic electron microscopy (cryo-EM) in UT Austin's new Sauer Laboratory for Structural Biology. Cryo-EM allows researchers to make atomic-scale 3D models of cellular structures, molecules and viruses.

"We ended up being the first ones in part due to the infrastructure at the Sauer Lab," McLellan said. "It highlights the importance of funding basic research facilities."

The molecule the team produced, and for which they obtained a structure, represents only the extracellular portion of the spike protein, but it is enough to elicit an immune response in people, and thus serve as a vaccine.

Next, McLellan's team plans to use their molecule to pursue another line of attack against the virus that causes COVID-19, using the molecule as a "probe" to isolate naturally produced antibodies from patients who have been infected with the novel coronavirus and successfully recovered. In large enough quantities, these antibodies could help treat a coronavirus infection soon after exposure. For example, the antibodies could protect soldiers or health care workers sent into an area with high infection rates on too short notice for the immunity from a vaccine to take effect.

https://www.sciencedaily.com/releases/2020/02/200219152850.htm

New 'universal' target for antiviral treatment

New 'universal' target for antiviral treatment

February 11, 2020

Science Daily/Massachusetts General Hospital

Researchers have uncovered a novel potential antiviral drug target that could lead to treatments protecting against a host of infectious diseases

As the coronavirus outbreak shows, viruses are a constant threat to humanity. Vaccines are regularly developed and deployed against specific viruses, but that process takes a lot of time, doesn't help everyone who needs protection, and still leaves people exposed to new outbreaks and new viruses.

Now, researchers at Massachusetts General Hospital (MGH) have uncovered a novel potential antiviral drug target that could lead to treatments protecting against a host of infectious diseases -- creating a pan, or universal, treatment. Their work suggests that the protein Argonaute 4 (AGO4) is an "Achilles heel" for viruses.

AGO4 is one of a family of AGO proteins. Until now, there has been little evidence of why they are important. The researchers, led by Kate L. Jeffrey, PhD, and her collaborators found that AGO4 plays a key role protecting cells against viral infections.

Specifically, this protein is uniquely antiviral in mammalian immune cells. The group studied the anti-viral effects of several Argonaute proteins, and found that only cells that were deficient in AGO4 were "hyper-susceptible" to viral infection. In other words, low levels of AGO4 make mammalian cells more likely to become infected.

This study was published today by Cell Reports.

The MGH researchers suggest that boosting levels of AGO4 could shore up the immune system to protect against multiple viruses. "The goal is to understand how our immune system works so we can create treatments that work against a range of viruses, rather than just vaccines against a particular one," says Jeffrey.

Mammals have four Argonaute proteins (1-4), which act by silencing genes and which are remarkably conserved throughout multiple living things, including plants. These are RNAi and microRNA effector proteins and RNAi is the major antiviral defense strategy in plants and invertebrates. Studies of influenza infected mice have shown that AGO4-deficient animals have significantly higher levels of the virus.

The next steps are to "determine how broad spectrum this is to any virus type," says Jeffrey. "Then we need to discover how to boost AGO4 to ramp up protection against viral infections."

https://www.sciencedaily.com/releases/2020/02/200211170106.htm

Coronavirus outbreak raises question: Why are bat viruses so deadly?

Bats' fierce immune systems drive viruses to higher virulence, making them deadlier in humans

February 10, 2020

Science Daily/University of California - Berkeley

A study of cultured bat cells shows that their strong immune responses, constantly primed to respond to viruses, can drive viruses to greater virulence. Modelling bat immune systems on a computer, the researchers showed that when bat cells quickly release interferon upon infection, other cells quickly wall themselves off. This drives viruses to faster reproduction. The increased virulence and infectivity wreak havoc when these viruses infect animals with tamer immune systems, like humans.

It's no coincidence that some of the worst viral disease outbreaks in recent years -- SARS, MERS, Ebola, Marburg and likely the newly arrived 2019-nCoV virus -- originated in bats.

A new University of California, Berkeley, study finds that bats' fierce immune response to viruses could drive viruses to replicate faster, so that when they jump to mammals with average immune systems, such as humans, the viruses wreak deadly havoc.

Some bats -- including those known to be the original source of human infections -- have been shown to host immune systems that are perpetually primed to mount defenses against viruses. Viral infection in these bats leads to a swift response that walls the virus out of cells. While this may protect the bats from getting infected with high viral loads, it encourages these viruses to reproduce more quickly within a host before a defense can be mounted.

This makes bats a unique reservoir of rapidly reproducing and highly transmissible viruses. While the bats can tolerate viruses like these, when these bat viruses then move into animals that lack a fast-response immune system, the viruses quickly overwhelm their new hosts, leading to high fatality rates.

"Some bats are able to mount this robust antiviral response, but also balance it with an anti-inflammation response," said Cara Brook, a postdoctoral Miller Fellow at UC Berkeley and the first author of the study. "Our immune system would generate widespread inflammation if attempting this same antiviral strategy. But bats appear uniquely suited to avoiding the threat of immunopathology."

The researchers note that disrupting bat habitat appears to stress the animals and makes them shed even more virus in their saliva, urine and feces that can infect other animals.

"Heightened environmental threats to bats may add to the threat of zoonosis," said Brook, who works with a bat monitoring program funded by DARPA (the U.S. Defense Advanced Research Projects Agency) that is currently underway in Madagascar, Bangladesh, Ghana and Australia. The project, Bat One Health, explores the link between loss of bat habitat and the spillover of bat viruses into other animals and humans.

"The bottom line is that bats are potentially special when it comes to hosting viruses," said Mike Boots, a disease ecologist and UC Berkeley professor of integrative biology. "It is not random that a lot of these viruses are coming from bats. Bats are not even that closely related to us, so we would not expect them to host many human viruses. But this work demonstrates how bat immune systems could drive the virulence that overcomes this."

The new study by Brook, Boots and their colleagues was published this month in the journal eLife.

Boots and UC Berkeley colleague Wayne Getz are among 23 Chinese and American co-authors of a paper published last week in the journal EcoHealth that argues for better collaboration between U.S. and Chinese scientists who are focused on disease ecology and emerging infections.

Vigorous flight leads to longer lifespan -- and perhaps viral tolerance

As the only flying mammal, bats elevate their metabolic rates in flight to a level that doubles that achieved by similarly sized rodents when running.

Generally, vigorous physical activity and high metabolic rates lead to higher tissue damage due to an accumulation of reactive molecules, primarily free radicals. But to enable flight, bats seem to have developed physiological mechanisms to efficiently mop up these destructive molecules.

This has the side benefit of efficiently mopping up damaging molecules produced by inflammation of any cause, which may explain bats' uniquely long lifespans. Smaller animals with faster heart rates and metabolism typically have shorter lifespans than larger animals with slower heartbeats and slower metabolism, presumably because high metabolism leads to more destructive free radicals. But bats are unique in having far longer lifespans than other mammals of the same size: Some bats can live 40 years, whereas a rodent of the same size may live two years.

This rapid tamping down of inflammation may also have another perk: tamping down inflammation related to antiviral immune response. One key trick of many bats' immune systems is the hair-trigger release of a signaling molecule called interferon-alpha, which tells other cells to "man the battle stations" before a virus invades.

Brook was curious how bats' rapid immune response affects the evolution of the viruses they host, so she conducted experiments on cultured cells from two bats and, as a control, one monkey. One bat, the Egyptian fruit bat (Rousettus aegyptiacus), a natural host of Marburg virus, requires a direct viral attack before transcribing its interferon-alpha gene to flood the body with interferon. This technique is slightly slower than that of the Australian black flying fox (Pteropus alecto), a reservoir of Hendra virus, which is primed to fight virus infections with interferon-alpha RNA that is transcribed and ready to turn into protein. The African green monkey (Vero) cell line does not produce interferon at all.

When challenged by viruses mimicking Ebola and Marburg, the different responses of these cell lines were striking. While the green monkey cell line was rapidly overwhelmed and killed by the viruses, a subset of the rousette bat cells successfully walled themselves off from viral infection, thanks to interferon early warning.

In the Australian black flying fox cells, the immune response was even more successful, with the viral infection slowed substantially over that in the rousette cell line. In addition, these bat interferon responses seemed to allow the infections to last longer.

"Think of viruses on a cell monolayer like a fire burning through a forest. Some of the communities -- cells -- have emergency blankets, and the fire washes through without harming them, but at the end of the day you still have smoldering coals in the system -- there are still some viral cells," Brook said. The surviving communities of cells can reproduce, providing new targets for the the virus and setting up a smoldering infection that persists across the bat's lifespan.

Brook and Boots created a simple model of the bats' immune systems to recreate their experiments in a computer.

"This suggests that having a really robust interferon system would help these viruses persist within the host," Brook said. "When you have a higher immune response, you get these cells that are protected from infection, so the virus can actually ramp up its replication rate without causing damage to its host. But when it spills over into something like a human, we don't have those same sorts of antiviral mechanism, and we could experience a lot of pathology."

The researchers noted that many of the bat viruses jump to humans through an animal intermediary. SARS got to humans through the Asian palm civet; MERS via camels; Ebola via gorillas and chimpanzees; Nipah via pigs; Hendra via horses and Marburg through African green monkeys. Nonetheless, these viruses still remain extremely virulent and deadly upon making the final jump into humans.

Brook and Boots are designing a more formal model of disease evolution within bats in order to better understand virus spillover into other animals and humans.

"It is really important to understand the trajectory of an infection in order to be able to predict emergence and spread and transmission," Brook said.

https://www.sciencedaily.com/releases/2020/02/200210144854.htm

First childhood flu helps explain why virus hits some people harder than others

Researchers also report that travel-related screening for coronavirus will identify less than half of those infected

February 4, 2020

Science Daily/University of California - Los Angeles

Why are some people better able to fight off the flu than others? Part of the answer, according to a new study, is related to the first flu strain we encounter in childhood.

Scientists from UCLA and the University of Arizona have found that people's ability to fight off the flu virus is determined not only by the subtypes of flu they have had throughout their lives, but also by the sequence in which they are been infected by the viruses. Their study is published in the open-access journal PLoS Pathogens.

The research offers an explanation for why some people fare much worse than others when infected with the same strain of the flu virus, and the findings could help inform strategies for minimizing the effects of the seasonal flu.

In addition, UCLA scientists, including Professor James Lloyd-Smith, who also was a senior author of the PLoS Pathogens research, recently completed a study that analyzes travel-related screening for the new novel coronavirus 2019-nCoV.

The researchers report that screening travelers is not very effective for the 2019 coronavirus -- that it will catch less than half of infected travelers, on average -- and that most infected travelers are undetectable, meaning that they have no symptoms yet, and are unaware that they have been exposed. So stopping the spread of the virus is not a matter of just enhancing screening methods at airports and other travel hubs.

"This puts the onus on government officials and public health officials to follow up with travelers after they arrive, to isolate them and trace their contacts if they get sick later," said Lloyd-Smith, a UCLA professor of ecology and evolutionary biology. Many governments have started to impose quarantines, or even travel bans, as they realize that screening is not sufficient to stop the spread of the coronavirus.

One major concern, Lloyd-Smith said, is that other countries, especially developing nations, lack the infrastructure and resources for those measures, and are therefore vulnerable to importing the disease.

"Much of the public health world is very concerned about the virus being introduced into Africa or India, where large populations exist do not have access to advanced medical care," he said.

The researchers, including scientists from the University of Chicago and the London School of Tropical Hygiene and Medicine, have developed a free online app where people can calculate the effectiveness of travel screening based on a range of parameters.

Solving a decades-old question

The PLoS Pathogens study may help solve a problem that had for decades vexed scientists and health care professionals: why the same strain of the flu virus affects people with various degrees of severity.

A team that included some of the same UCLA and Arizona scientists reported in 2016 that exposure to influenza viruses during childhood gives people partial protection for the rest of their lives against distantly related influenza viruses. Biologists call the idea that past exposure to the flu virus determines a person's future response to infections "immunological imprinting."

The 2016 research helped overturn a commonly held belief that previous exposure to a flu virus conferred little or no immunological protection against strains that can jump from animals into humans, such as those causing the strains known as swine flu or bird flu. Those strains, which have caused hundreds of spillover cases of severe illness and death in humans, are of global concern because they could gain mutations that allow them to readily jump not only from animal populations to humans, but also to spread rapidly from person to person.

In the new study, the researchers investigated whether immunological imprinting could explain people's response to flu strains already circulating in the human population and to what extent it could account for observed discrepancies in how severely the seasonal flu affects people in different age groups.

To track how different strains of the flu virus affect people at different ages, the team analyzed health records that the Arizona Department of Health Services obtains from hospitals and private physicians.

Two subtypes of influenza virus, H3N2 and H1N1, have been responsible for seasonal outbreaks of the flu over the past several decades. H3N2 causes the majority of severe cases in high-risk elderly people and the majority of deaths from the flu. H1N1 is more likely to affect young and middle-aged adults, and causes fewer deaths.

The health record data revealed a pattern: People first exposed to the less severe strain, H1N1, during childhood were less likely to end up hospitalized if they encountered H1N1 again later in life than people who were first exposed to H3N2. And people first exposed to H3N2 received extra protection against H3N2 later in life.

The researchers also analyzed the evolutionary relationships between the flu strains. H1N1 and H3N2, they learned, belong to two separate branches on the influenza "family tree," said James Lloyd-Smith, a UCLA professor of ecology and evolutionary biology and one of the study's senior authors. While infection with one does result in the immune system being better prepared to fight a future infection from the other, protection against future infections is much stronger when one is exposed to strains from the same group one has battled before, he said.

The records also revealed another pattern: People whose first childhood exposure was to H2N2, a close cousin of H1N1, did not have a protective advantage when they later encountered H1N1. That phenomenon was much more difficult to explain, because the two subtypes are in the same group, and the researchers' earlier work showed that exposure to one can, in some cases, grant considerable protection against the other.

"Our immune system often struggles to recognize and defend against closely related strains of seasonal flu, even though these are essentially the genetic sisters and brothers of strains that circulated just a few years ago," said lead author Katelyn Gostic, who was a UCLA doctoral student in Lloyd-Smith's laboratory when the study was conducted and is now a postdoctoral fellow at the University of Chicago. "This is perplexing because our research on bird flu shows that deep in our immune memory, we have some ability to recognize and defend against the distantly related, genetic third cousins of the strains we saw as children.

"We hope that by studying differences in immunity against bird flus -- where our immune system shows a natural ability to deploy broadly effective protection -- and against seasonal flus -- where our immune system seems to have bigger blind spots -- we can uncover clues useful to universal influenza vaccine development."

Around the world, influenza remains a major killer. The past two flu seasons have been more severe than expected, said Michael Worobey, a co-author of the study and head of the University of Arizona's department of ecology and evolutionary biology. In the 2017-18 season, 80,000 people died in the U.S., more than in the swine flu pandemic of 2009, he said.

People who had their first bout of flu as children in 1955 -- when the H1N1 was circulating but the H3N2 virus was not -- were much more likely to be hospitalized with an H3N2 infection than an H1N1 infection last year, when both strains were circulating, Worobey said.

"The second subtype you're exposed to is not able to create an immune response that is as protective and durable as the first," he said.

The researchers hope that their findings could help predict which age groups might be severely affected during future flu seasons based on the subtype circulating. That information could also help health officials prepare their response, including decisions about who should receive certain vaccines that are only available in limited quantities.

The research was funded by the National Institutes of Health, the National Science Foundation, DARPA and the David and Lucile Packard Foundation. In 2018, the NIH's National Institute of Allergy and Infectious Diseases announced a strategic plan to develop a universal flu vaccine.

https://www.sciencedaily.com/releases/2020/02/200204094722.htm

Unique new antiviral treatment made using sugar

January 29, 2020

Science Daily/University of Manchester

New antiviral materials made from sugar have been developed to destroy viruses on contact and may help in the fight against viral outbreaks. This new development from a collaborative team of international scientists shows promise for the treatment of herpes simplex (cold sore virus), respiratory syncytial virus, hepatitis C, HIV, and Zika virus to name a few. The team have demonstrated success treating a range of viruses in the lab - including respiratory infections to genital herpes.

This new development from a collaborative team of international scientists shows promise for the treatment of herpes simplex (cold sore virus), respiratory syncytial virus, hepatitis C, HIV, and Zika virus to name a few. The team have demonstrated success treating a range of viruses in the lab -- including respiratory infections to genital herpes.

The research is a result of a collaboration between scientists from The University of Manchester, the University of Geneva (UNIGE) and the EPFL in Lausanne, Switzerland. Although at a very early stage of development, the broad spectrum activity of this new approach could also be effective against newly prevalent viral diseases such as the recent coronavirus outbreak.

So called 'virucidal' substances, such as bleach, are typically capable of destroying viruses on contact but are extremely toxic to humans and so cannot be taken or applied to the human body without causing severe harm. Developing virucides from sugar has allowed for the advent of a new type of antiviral drug, which destroys viruses yet is non-toxic to humans.

Current antiviral drugs work by inhibiting virus growth, but they are not always reliable as viruses can mutate and become resistant to these treatments.

Using modified sugar molecules the team showed that the outer shell of a virus can be disrupted, thereby destroying the infectious particles on contact, as oppose to simply restricting its growth. This new approach has also been shown to defend against drug resistance.

Publishing their work in the journal Science Advances the team showed that they successfully engineered new modified molecules using natural glucose derivatives, known as cyclodextrins. The molecules attract viruses before breaking them down on contact, destroying the virus and fighting the infection.

Dr Samuel Jones, from The University of Manchester and a member of the Henry Royce Institute for Advanced Materials, jointly led the pioneering research with Dr Valeria Cagno from the University of Geneva. "We have successfully engineered a new molecule, which is a modified sugar that shows broad-spectrum antiviral properties. The antiviral mechanism is virucidal meaning that viruses struggle to develop resistance. As this is a new type of antiviral and one of the first to ever show broad-spectrum efficacy, it has potential to be a game changer in treating viral infections." said Sam.

Professor Caroline Tapparel from the University of Geneva and Prof Francesco Stellacci from EPFL were both also senior authors of the study. Prof Tapparel declared: "We developed a powerful molecule able to work against very different viruses, therefore, we think this could be game changing also for emerging infections."

The molecule is patented and a spin-out company is being set up to continue pushing this new antiviral towards real-world use. With further testing the treatment could find a use in creams, ointments and nasal sprays or other similar treatments for viral infections. This exciting new material can work to break down multiple viruses making for cost-effective new treatments even for resistant viruses.

https://www.sciencedaily.com/releases/2020/01/200129143339.htm