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WHO Declares Pandemic In Response To Ongoing Global Spread Of Novel Influenza A (H1N1) Virus

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PCR diagnostic test to detect novel H1N1 virus.
On June 11, 2009, the World Health Organization (WHO) raised the worldwide pandemic alert level to Phase 6 in response to the ongoing global spread of the novel influenza A (H1N1) virus, which causes swine flu. A Phase 6 designation indicates that a global pandemic is underway.More than 70 countries are now reporting cases of human infection with novel H1N1 flu. This number has been increasing over the past few weeks, but many of the cases reportedly had links to travel or were localized outbreaks without community spread. The WHO designation of a pandemic alert Phase 6 reflects the fact that there are now ongoing community level outbreaks in multiple parts of world.

WHO’s decision to raise the pandemic alert level to Phase 6 is a reflection of the spread of the virus, not the severity of illness caused by the virus. It’s uncertain at this time how serious or severe this novel H1N1 pandemic will be in terms of how many people infected will develop serious complications or die from novel H1N1 infection. Experience with this virus so far is limited and influenza is unpredictable. However, because novel H1N1 is a new virus, many people may have little or no immunity against it, and illness may be more severe and widespread as a result. In addition, currently there is no vaccine to protect against novel H1N1 virus.

In the United States, most people who have become ill with the newly declared pandemic virus have recovered without requiring medical treatment, however, CDC anticipates that there will be more cases, more hospitalizations and more deaths associated with this pandemic in the coming days and weeks. In addition, this virus could cause significant illness with associated hospitalizations and deaths in the fall and winter during the U.S. influenza season.

Background

Novel influenza A (H1N1) is a new flu virus of swine origin that first caused illness in Mexico and the United States in March and April, 2009. It’s thought that novel influenza A (H1N1) flu spreads in the same way that regular seasonal influenza viruses spread, mainly through the coughs and sneezes of people who are sick with the virus, but it may also be spread by touching infected objects and then touching your nose or mouth. Novel H1N1 infection has been reported to cause a wide range of flu-like symptoms, including fever, cough, sore throat, body aches, headache, chills and fatigue. In addition, many people also have reported nausea, vomiting and/or diarrhea.

The first novel H1N1 patient in the United States was confirmed by laboratory testing at CDC on April 15, 2009. The second patient was confirmed on April 17, 2009. It was quickly determined that the virus was spreading from person-to-person. On April 22, CDC activated its Emergency Operations Center to better coordinate the public health response. On April 26, 2009, the United States Government declared a public health emergency and has been actively and aggressively implementing the nation’s pandemic response plan.

Since the outbreak was first detected, an increasing number of U.S. states have reported cases of novel H1N1 influenza with associated hospitalizations and deaths. By June 3, 2009, all 50 states in the United States and the District of Columbia and Puerto Rico were reporting cases of novel H1N1 infection. While nationwide U.S. influenza surveillance systems indicate that overall influenza activity is decreasing in the country at this time, novel H1N1 outbreaks are ongoing in parts of the U.S., in some cases with intense activity.

CDC is continuing to watch the situation carefully, to support the public health response and to gather information about this virus and its characteristics. The Southern Hemisphere is just beginning its influenza season and the experience there may provide valuable clues about what may occur in the Northern Hemisphere this fall and winter.

Buckyball Computer Simulations Help Team Find Molecular Key To Combating HIV

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Rice University's Andrew Barron and his group, working with labs in Italy, Germany and Greece, have identified specific molecules that could block the means by which HIV -- the deadly virus that causes AIDS -- spreads by taking away its ability to bind with other proteins.Using computer simulations, researchers tested more than 100 carbon fullerene, or C60 ("buckyball"), derivatives initially developed at Rice for other purposes to see if they could be used to inhibit a strain of the virus, HIV-1 PR, by attaching themselves to its binding pocket.

"There are a lot of people doing this kind of research, but it tends to be one group or one pharmaceutical company taking a shotgun approach -- make a molecule and try it out, then make another molecule and try it out," said Barron, Rice's Charles W. Duncan Jr.-Welch Professor of Chemistry and professor of materials science. "This is interesting because we're tackling an important problem in a very rational way."

The groups reported their findings in a paper published on the American Chemical Society's Journal of Chemical Information and Modeling web site last week.

Their method of modeling ways to attack HIV may not be unique, but their collaboration is. Research groups from five institutions -- two in Greece, one in Germany, one in Italy and Barron's group at Rice -- came together through e-mail contacts and conversations over many months, each working on facets of the problem. "Not all the groups have ever met in person," Barron said. Most remarkable, he said, is that their research to date has been completely unfunded.

Using simulations to narrow down a collection of fullerenes to find the good ones is "the least time-consuming low-cost procedure for efficient, rational drug design," the team wrote.

"A long time ago, people noticed that C60 fits perfectly into the hydrophobic pocket in HIV, and it has an inhibition effect," Barron said. "It's not particularly strong, but there's potentially a very strong binding effect. The problem is, it's not the perfect unit." The objective was to find an existing fullerene derivative molecule that could be easily modified to become the perfect unit.

Rice got involved, he said, "because we make the molecules and the other guys had a great method for in-silico testing of molecules. They approached us and said, 'Do you think we could use some of these?' Then we started bouncing ideas around.

"We began thinking about a very simple experiment to calculate the binding efficiency of a molecule in the HIV pocket, then calculate that for a series of molecules, decide which one is best, make that molecule in real life and see if it correlates," Barron said. "If it does, then you've got a way to design your ultimate molecule. Our work was the first step in the process."

In fact, through their "in-silico," or computer-based, calculations, they found two good fits among the fullerene derivatives tested and are now working to enhance their binding properties to get that perfect molecule, one that sticks "like Velcro" to the virus and can be fine-tuned for various strains.

"This is just one component of the problem -- we're not going to cure HIV," Barron cautioned. The hope, he said, is to develop a method for the rapid creation of drugs to address various strains of HIV and other diseases.

Authors of the paper with Barron were Manthos Papadopoulos of the National Hellenic Research Foundation, Athens; Serdar Durdagi of the National Hellenic Research Foundation and the Freie Universitat, Berlin; Claudiu Supuran of the University of Florence, Italy; T. Amanda Strom, Nadjmeh Doostdar and Mananjali Kumar of Rice; and Thomas Mavromoustakos of the National Hellenic Research Foundation and the University of Athens.

The impromptu nature of the project intrigued Barron as much as the subject itself. "Here you've got computational people, experimental people, synthesis people, characterization people who've come together naturally as a collaboration and developed this protocol, developed their own methodologies.

"And no one's paid us to collaborate. Serdar Durdagi’s graduate fellowship was funded by the European Union. The fellowships of Rice graduate students Amanda Strom, Nadjmeh Doostdar and Mananjali Kumar were funded, in part, by Rice's Center for Biological and Environmental Nanotechnology. This is purely an academic collaboration." He said the group is working on a second paper and seeking funding to expand the project.

HIV's March Around Europe Mapped

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map depicts the spread of HIV in Europe.
hose travelling abroad should take seriously advice to pack their condoms and keep their needles to themselves. Research published in the open access journal Retrovirology shows that tourists, travellers and migrants from Greece, Portugal, Serbia and Spain actively export HIV-1 subtype B to other European nations.An international team of scientists used samples from 17 European countries to construct a viral phylogeography – a geographic pattern of genetic information taken from viruses at a number of locations that can be used to track how and when it spread (this technique has recently been applied to the bird flu virus H5N1.) HIV-1 subtype B is the most prevalent form of the HIV virus circulating in Europe today.

The results showed that for three countries (Austria, Poland and Luxembourg) no significant exporting migration was observed. Whereas Greece, Portugal, Serbia and Spain were a source of subtype B to other countries. Notably, the virus spread widely from Greece and Spain to seven and five target countries respectively. Other countries had narrower targets, with Italy exporting HIV to Austria, and Portugal passing the virus primarily to Luxembourg (some 13% of Luxembourg's population is Portuguese). Other nations such as Austria, Belgium, Denmark, Germany and Luxembourg showed only limited export of HIV-1 subtype B, while for Italy, Israel, Norway, the Netherlands, Sweden, Switzerland and the UK the authors inferred significant bidirectional migration. For Poland no significant migration was found.

According to the first author, Dimitrios Paraskevis, "Popular tourist destinations like Greece, Portugal and Spain probably spread HIV with tourists infected during their holidays. To a large extent HIV spread within Poland is due to injecting drug users, who make up around half of the HIV-infected population. Viruses move around with travellers – thus health programmes within countries should not only target the national populations, prevention efforts must also be aimed at migrants, travellers and tourists – who are both major sources and targets of HIV."