A electron microscope image of a coronavirus is seen in this undated picture provided by the Health Protection Agency in London February 19, 2013.

LONDON | Wed Mar 13, 2013 4:38pm EDT

LONDON (Reuters) - Scientists have worked out how a deadly new virus which was unknown in humans until last year is able to infect human cells and cause severe, potentially fatal damage to the lungs.

In one of the first detailed studies of the virus - which emerged in the Middle East and has so far infected 15 people worldwide, killing nine of them - Dutch researchers identified a cell surface protein it uses to enter and infect human cells.

The finding, published in the journal Nature, came as the World Health Organization (WHO) confirmed the 15th case of the virus, known as novel coronavirus or NCoV, in a male patient in Saudi Arabia who died on March 2.

Other cases have been in Jordan and Qatar, and in patients in Germany and Britain linked to travel in the Middle East.

NCoV is from the same family of viruses as those that cause common colds and the one that caused the deadly outbreak of Severe Acute Respiratory Syndrome (SARS) that first emerged in Asia in 2003.

The WHO first issued an international alert about it in September after it was identified in a Qatari man in Britain who had recently been in Saudi Arabia.

A study published last month found that NCoV was well adapted to infecting human cells and may be treatable with medicines similar to the ones used for SARS, which killed a tenth of the 8,000 people it infected.

In this latest study, led by Bart Haagmans at the Erasmus Medical Center in The Netherlands, researchers set out to find how the virus got into cells - which receptors it used - and then to find out where in the body those receptors were common.

POTENTIAL VACCINES

"Once you can identify the receptor and you know the distribution of the receptor in the body, then you can get more information on the pathogenesis (the way it infects people) of the virus and the possibility for transmission," Haagmans said in a telephone interview.

Researchers identified the key receptor for the disease as a cell surface protein called dipeptidyl peptidase 4 (DPP4).

They also found cells containing DPP4 receptors were common in the lower respiratory tract but not in the upper respiratory tract - giving clues to why the virus causes illness in the lungs rather than in the nose and throat as a cold virus would.

The findings should help researchers find ways of developing potential drugs or vaccines to block the DPP4 receptors and prevent infection, Haagmans said.

A few drugs that block DPP4 receptors are already on the market, licensed for use in diabetes, but Haagmans said his team already tried using those to stop the virus in laboratory tests and found they did not work.

He said, however, that the team was working with other molecules that might block the receptors and could form the basis for developing a potential vaccine.

Initial analysis by scientists at Britain's Health Protection Agency last year found that NCoV's closest relatives were most probably bat viruses.

Yet further work by a research team in Germany suggests NCoV may have come through an intermediary - possibly goats.

Haagmans said since DPP4 receptors were also present in other species, including bats, his findings showed it was feasible the virus came from bats. He said the idea that goats may have been an intermediary also looked feasible.

(Reporting by Kate Kelland; Editing by Pravin Char)

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It's a familar scene at clinics across the United States but despite an upsurge in vaccinations, the flu has reached epidemic proportions. There's not much more authorities can do, although scientists at Colombia University in New York believe that in the future, they will be far better equipped to spread the word about the spread of the flu. Using web-based estimates from six recent flu seasons in New York City to retrospectively generate weekly flu forecasts, Dr. Jeffrey Shaman was able to pinpoint the peak timing of outbreaks more than seven weeks before they occurred. He says the concept can be applied to future predictions. (SOUNDBITE) (English) JEFFREY SHAMAN, ASSISTANT PROFESSOR OF ENVIRONMENTAL HEALTH SCIENCES AT COLUMBIA UNIVERSITY, SAYING: "We've been doing this at the municipal scale because the Google Flu Trend Observations are at the municipal scale so we can run the models at a municipal scale: it can run for New York city, we can run it for Miami, Dallas, Phoenix, Seattle, what have you. And so, the idea there is that we can predict within those localities when the peak timing of influenza will take place. We can also predict total number of cases, perhaps; we can also try to predict the magnitude of the peak - how many cases there are at the peak, that's the type of information we could potentially provide." And when combined with real time data, such as the number of flu-related search qeries from a given area and regional outbreak estimates from health authorities, Shaman says the public can be better informed. He foresees a day when flu warnings are issued much like weather reports. (SOUNDBITE) (English) JEFFREY SHAMAN, ASSISTANT PROFESSOR OF ENVIRONMENTAL HEALTH SCIENCES AT COLUMBIA UNIVERSITY, SAYING: "You hear there's an eighty percent chance of rain, you're a lot more likely to take an umbrella that day than if you hear there's a twenty percent chance of rain, okay? So if you have that kind of information that you hear the influenza outbreak is coming, you'll prepare: you're more likely to get vaccinated, perhaps; you're more likely to take other preventative measures; you're more likely if you hear a child's sick and you were going to have a play day with that child, for instance, say 'let's not do it right now, let's do it in a couple weeks.' So, it's that kind of information that I think would be beneficial and people have a right to know." ..and that "right to know", could translate into fewer cases of flu. It's an idea that Shaman believes has the potential to go viral.

Jan. 15 - As the flu outbreak reaches epidemic levels in the U.S., scientists are turning to weather modeling to help forecast the future seasonal spread of the virus. Rob Muir reports.

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Paramedics dressed in protective attire walk in front of the ship, the Bellriva, in Wiesbaden December 8, 2012. The Bellriva has been quarantined after at least 30 passengers were found to be suffering from diarrhoea and vomiting. Authorities believed it is caused by the Norovirus, a virus that is spread from person-to-person and causes flu-like symptoms.

LONDON | Mon Dec 31, 2012 8:53am EST

LONDON (Reuters) - Poor Larry isn't looking too good. He's pale and clammy and he's been projectile vomiting over and over again while his carers just stand by and watch.

Yet their lack of concern for Larry is made up for by their intense interest in how far splashes of his vomit can fly, and how effectively they evade attempts to clean them up.

Larry is a "humanoid simulated vomiting system" designed to help scientists analyze contagion. And like millions around the world right now, he's struggling with norovirus - a disease one British expert describes as "the Ferrari of the virus world".

"Norovirus is one of the most infectious viruses of man," said Ian Goodfellow, a professor of virology at the department of pathology at Britain's University of Cambridge, who has been studying noroviruses for 10 years.

"It takes fewer than 20 virus particles to infect someone. So each droplet of vomit or gram of feces from an infected person can contain enough virus to infect more than 100,000 people."

Norovirus is hitting hard this year - and earlier too.

In Britain so far this season, more than a million people are thought to have suffered the violent vomiting and diarrhea it can bring. The Health Protection Agency (HPA) said this high rate of infection relatively early in the winter mirrors trends seen in Japan and Europe.

"In Australia the norovirus season also peaks during the winter, but this season it has gone on longer than usual and they are seeing cases into their summer," it said in a statement.

In the United States, the Centers for Disease Control and Prevention (CDC) say norovirus causes 21 million illnesses annually. Of those who get the virus, some 70,000 require hospitalization and around 800 die each year.

PROFUSE AND PROJECTILE

Norovirus dates back more than 40 years and takes its name from the U.S. city of Norwalk, Ohio, where there was an outbreak of acute gastroenteritis in school children in November 1968.

Symptoms include a sudden onset of vomiting, which can be projectile, and diarrhea, which may be profuse and watery. Some victims also suffer fevers, headaches and stomach cramps.

John Harris, an expert on the virus at Britain's HPA, puts it simply: "Norovirus is very contagious and very unpleasant."

What makes this such a formidable enemy is its ability to evade death from cleaning and to survive long periods outside a human host. Scientists have found norovirus can remain alive and well for 12 hours on hard surfaces and up to 12 days on contaminated fabrics such as carpets and upholstery. In still water, it can survive for months, maybe even years.

At the Health and Safety Laboratory in Derbyshire, northern England, where researcher Catherine Makison developed the humanoid simulated vomiting system and nicknamed him "Vomiting Larry", scientists analyzing his reach found that small droplets of sick can spread over three meters.

"The dramatic nature of the vomiting episodes produces a lot of aerosolized vomit, much of which is invisible to the naked eye," Goodfellow told Reuters.

Larry's projections were easy to spot because he had been primed with a "vomitus substitute", scientists explain, which included a fluorescent marker to help distinguish even small splashes - but they would not be at all easily visible under standard white hospital lighting.

Add the fact that norovirus is particularly resistant to normal household disinfectants and even alcohol hand gels, and it's little wonder the sickness wreaks such havoc in hospitals, schools, nursing homes, cruise ships and hotels.

During the two weeks up to December 23, there were 70 hospital outbreaks of norovirus reported in Britain, and last week a cruise ship that sails between New York and Britain's Southampton docked in the Caribbean with about 200 people on board suffering suspected norovirus.

MOVING TARGET

The good news, for some, is that not everyone appears to be equally susceptible to norovirus infection. According to Goodfellow, around 20 percent of Europeans have a mutation in a gene called FUT2 that makes them resistant.

For the rest the only likely good news will have to wait for the results of trials of a potential norovirus vaccine developed by U.S. drugmaker LigoCyte Pharmaceuticals Inc, or from one of several research teams around the world working on possible new antiviral drugs to treat the infection.

Early tests in 2011 indicated that around half of people vaccinated with the experimental shot, now owned by Japan's Takeda Pharmaceutical Co, were protected from symptomatic norovirus infection.

The bad news, virologists say, is that the virus changes constantly, making it a moving target for drug developers. There is also evidence that humans' immune response to infection is short-lived, so people can become re-infected by the same virus within just a year or two.

"There are many strains, and the virus changes very rapidly - it undergoes something virologists call genetic drift," Harris said in a telephone interview. "When it makes copies of itself, it makes mistakes in those copies - so each time you encounter the virus you may be encountering a slightly different one."

This means that even if a vaccine were to be fully developed - still a big 'if' - it would probably need to be tweaked and repeated in a slightly different formula each year to prevent people getting sick.

Until any effective drugs or vaccines are developed, experts reckon that like the common cold, norovirus will be an unwelcome guest for many winters to come. Their advice is to stay away from anyone with the virus, and use soap and water liberally.

"One of the reasons norovirus spreads so fast is that the majority of people don't wash their hands for long enough," said Goodfellow. "We'd suggest people count to 15 while washing their hands and ensure their hands are dried completely."

(Reporting by Kate Kelland; Editing by Will Waterman)

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Malaysian soldiers prepare their protective gear prior to the slaughter of pigs at a farm in Sungai Nipah, 60 miles southwest of Kuala Lumpur, after an outbreak of the virus that later came to be known as Nipah virus. March 20, 1999.

HONG KONG | Fri Aug 3, 2012 5:47pm EDT

HONG KONG (Reuters) - A virus that is very similar to the deadly Nipah and Hendra viruses has been discovered in fruit bats in Australia and researchers are hoping it can help them find ways to fight those highly dangerous cousins.

The Nipah virus kills 40-75 percent of the people it infects while the Hendra virus, which normally affects horses, kills more than 50 percent of the people it infects.

But the newly discovered Cedar virus, with 90 percent of its genes identical to those of Hendra and Nipah, failed to cause any disease when researchers injected it into rats, guinea pigs and ferrets, they wrote in a paper published on Friday in the journal PLoS Pathogens (Public Library of Science).

They are now comparing the DNA of all three viruses to tease out genes that are responsible for the deadliness of the Nipah and Hendra, said lead author Gary Crameri, at the Commonwealth Scientific and Industrial Research Organisation's Australian Animal Health Laboratory.

"We have already done genetic analyses and identified those things that are different between Hendra/Nipah and the Cedar," Crameri said in a telephone interview.

"Our plan now is to genetically engineer these viruses so we can take some parts of the Hendra genome that don't appear in Cedar but play some role in how deadly they are, put them into Cedar and then do infection trials with the new hybrid virus and see if it is as deadly."

Researchers hope to home in on the rogue genes to find cures for Nipah and Hendra, which are also found in bats.

"There is no secret that the pathogenicity of the Hendra and Nipah lie in their genes and this will help us narrow down some of the options. From there, we can start to think about therapeutic approaches, new drugs that we can use to target these viruses so that when people get infected, we can treat them, something we don't have now," Crameri said.

Bats are a natural reservoir for many viruses, including highly pathogenic ones like rabies, Ebola, SARS, Hendra and Nipah. Although Cedar appears not to cause any disease in the few animal species that researchers tested the virus on, it is not known if it causes disease in people.

A Nipah outbreak in 1998 killed at least 105 pig farmers in Malaysia and one abattoir worker in Singapore. There have been numerous outbreaks since in Bangladesh and India.

While the cases in Malaysia and Singapore were due to contact with infected pigs, the South Asian outbreaks were mostly due to consumption of raw date palm juice that had been contaminated with urine or droppings from infected fruit bats.

The Hendra virus kills 75 percent of the horses it infects. While it rarely jumps from horse to people, four of the 7 human cases recorded since 1994 in Australia have resulted in death.

(Editing by Robert Birsel)

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