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Scientists have developed EP67, a new spray that helps boost the immune system can fight off flu in just two hours – even before symptoms.

The drug, delivered by a nasal spray, contains a synthetic protein that triggers the immune system to fight the flu before the body normally would.

Once a person is exposed to the flu, current treatments are designed to target the current circulating strain exactly, but the virus can sometimes develop a resistance against them.

This new treatment doesn’t need to match the virus exactly and gets the immune system to react almost immediately to the threat before the body normally would.

Scientists have developed EP67, a new spray that helps boost the immune system can fight off flu in just two hours

Scientists have developed EP67, a new spray that helps boost the immune system can fight off flu in just two hours

Flu is potentially fatal to people with a low immune system as they struggle to shake off the infection and can also be lethal to the elderly.

Researchers at San Diego State University in America focused the study on the protein EP67, which has previously been used as something added to a vaccine to help activate the immune response, but they wanted to see if it would work on its own.

They tested EP67 on mice by infecting them with a flu virus – finding those given a dose within 24 hours did not get sick, or as sick, as those not treated with the protein.

The level of illness in mice is measured by weight loss – typically mice lose about 20% of their weight when infected with the flu, but those treated with EP67 lost an average of 6%.

The researchers also found mice who were treated a day after being infected with a lethal dose of influenza did not die.

EP67 is active in animals, including birds, so the finding could also have huge implications for veterinary applications.

It could also be used if there is a new strain of the infectious disease, before the actual pathogen has been identified, like in SARS or the 2009 H1N1 influenza outbreak.

Future research will examine the effect EP67 has in the presence of a number of other pathogens and look closer at exactly how EP67 functions within different cells in the body.

Although this study, published in science journal PLoS ONE, focuses on the flu, EP67 has the potential to work on other respiratory diseases and fungal infections and could have huge potential for emergency therapeutics.

Professor Joy Phillips, of San Diego State University, said: “The flu virus is very sneaky and actively keeps the immune system from detecting it for a few days until you are getting symptoms.

“Our research showed that by introducing EP67 into the body within 24 hours of exposure to the flu virus caused the immune system to react almost immediately to the threat, well before your body normally would.

“When you find out you’ve been exposed to the flu, the only treatments available now target the virus directly but they are not reliable and often the virus develops a resistance against them.

“EP67 could potentially be a therapeutic that someone would take when they know they’ve been exposed that would help the body fight off the virus before you get sick.”

 

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An international research team has shown how some cells in the body can repel attacks from HIV by starving the virus of the building blocks of life.

Viruses cannot replicate on their own; they must hijack other cells and turn them into virus production factories.

The study, published in Nature Immunology, showed how some parts of the immune system destroy their own raw materials, stopping HIV.

It is uncertain whether this could be used in therapy, experts caution.

HIV attacks the immune system and can weaken the body’s defenses to the point that everyday infections become fatal.

However, not all parts of the immune system become subverted to the virus’ cause. Macrophages and dendritic cells, which have important roles in orchestrating the immune response, seem to be more resistant.

In 2011, researchers identified the protein SAMHD1 as being a critical part of this resistance. Now scientists believe they know how it works.

The scientists have shown that SAMHD1 breaks down the building blocks of DNA. So if a cell needs to make a copy of itself it will have a pool of these building blocks – deoxynucleoside triphosphates or dNTPs – which make the new copies of the DNA. However, they can also be used by viruses.

The study, by an international team of researchers, showed that SAMHD1 lowered the levels of dNTPs below that needed to build viral DNA and prevented infection. When they removed SAMHD1 then those cells had higher levels of dNTPs and were infected by HIV.

The report said: “By depleting the pool of available dNTPs, SAMHD1 effectively starves the virus of a building block that is central to its replication strategy.”

HIV attacks the immune system and can weaken the body's defenses to the point that everyday infections become fatal

HIV attacks the immune system and can weaken the body's defenses to the point that everyday infections become fatal

It is possible for macrophages and dendritic cells to produce SAMHD1 as they are “mature cells” which do not go on to produce new cells.

Prof. Baek Kim, one of the researchers from the University of Rochester Medical Center, said: “It makes sense that a mechanism like this is active in macrophages.

“Macrophages literally eat up dangerous organisms, and you don’t want those organisms to have available the cellular machinery needed to replicate and macrophages themselves don’t need it, because they don’t replicate.

“So macrophages have SAMHD1 to get rid of the raw material those organisms need to copy themselves. It’s a great host defense.”

Dr. Jonathan Stoye, virologist at the Medical Research Council National Institute of Medical Research, was part of the team which determined the chemical structure of SAMHD1 last year and predicted that it would attack the dNTPs.

“We hypothesized that it works in this fashion and the paper tells us we were right. It is depleting cells of these dNTPs, in cells which are not proliferating (dividing).”

However, some cells do need to divide to boost numbers as part of the immune defence. Such as CD4 cells which are the prime target for HIV infection.

“Cells which are proliferating would be in trouble if we took dNTPs away,” Dr. Jonathan Stoye said.

He added: “How we can use the anti-retroviral action of this protein is not clear to me.”

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