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We must all realize, that a rouge nation, who hates America, can obtain the technology to
administer a Swine flu, or Sars virus, and release such Viruses in America.
What is the American millitary doing about such a situation.?
This is no laughing matter Mr. Bootneckstrap.We must all realize, that a rouge nation, who hates America, can obtain the technology to
administer a Swine flu, or Sars virus, and release such Viruses in America.
What is the American millitary doing about such a situation.?
Pissing themselves laughing at your post I should think.
At the University of Texas Medical School at Houston, Jun Liu uses a powerful electron microscope to examine E. coli bacteria and the tiny T-7 virus that infects them. Liu says until now, scientists could only speculate on how this virus injected its genetic material into another cell, because it happens in an instant. Before they inject in, they do not have a channel. After they inject in, they actually degrade the channel, so you never have a chance to see it, Liu said.
But in a collaborative study with other University of Texas colleagues, Liu used the electron microscope to examine quick-frozen solutions full of bacteria and viruses. Because when you freeze it, it is kind of like a snapshot that captures some intermediate stage. This is one of the highlights of this study, because we captured this intermediate stage that nobody had seen before, Liu said. This sophisticated technology was applied to a particular virus in this study, but what the researchers found could be useful in studying other viruses in the future, viruses that cause many diseases, such as influenza, or AIDS.
That is the hope of study participant Ian Molineux, professor of biology at the University of Texas main campus in Austin, who prepared the virus samples used in the study. If we can find a way of blocking any of multiple steps towards the final internalization of the genetic material, it provides the potential for finding more anti-viral drugs, Molineux said.
An animation, produced for Science magazine by the American Association for the Advancement of Science, shows how the virus puts out tendrils to, in effect, walk on the cell surface. "Then it stops moving and all the legs come down and get fixed on the cell surface, and the infection begins to initiate," Molineux said.
Molineux says the collaborative effort with Liu and others paid off, with each member of the team bringing his own area of expertise into play. We have a very strong collaboration. We are looking at other viruses now, Molineux said. He says each advance in understanding how viruses function brings researchers closer to finding ways to defeat them - and save lives.
High-Tech Images Show How Viruses Infect Cells
Viruses are strange things. Though there is some scientific question about whether viruses are alive or not, they do have a basic genetic structure that allows them to be biologically active. But they don't have the built-in reproductive capacity of bacteria -- tiny, living organisms which, once they have infected a human host, can make copies of themselves using their own DNA. John Connor, a virologist at Boston University in Massachusetts, explains that in order for viruses to reproduce and become a disease threat, they must first hijack the genetic machinery of a living cell: “They’re parasites," said Connor. "They get inside our cells and use a lot of our machinery in order to make extra copies of themselves. And so that poses a really delicate question of how do you destroy the virus without getting yourself.”
A laboratory specialist examines specimens of the Ebola virus at the Uganda virus research centre in Entebbe, 40km (25 miles) south from capital Kampala May 17, 2011.
Connor and his colleagues screened thousands of chemical compounds, looking for ones that showed strong antiviral activity. They identified several small molecules that interfere with the replication of a class of pathogens known as NNS viruses, which cause the deadly Marburg and Ebola infections, as well as measles and mumps. Once they have invaded a host cell, NNS viruses use their own genetic molecule -- known as RNA -- to hijack the host cell's DNA and force it to make copies of the virus. The most effective compounds discovered by the Boston researchers shut down that replication process -- at least in cell-culture experiments -- by limiting the viruses' RNA production.
The compounds do not thwart all viruses -- they have no effect, for example, on HIV, the virus that causes AIDS -- because of differences in the way viral pathogens enter and commandeer cells. Just as antibiotics are effective against many bacterial illnesses, Connor says he hopes this discovery leads to the development of broad-spectrum antiviral drugs to treat a variety of currently incurable viral infections. “Basically, one of the things my lab is interested in is trying to find 'monkey wrenches' [disruptive agents] to throw into viral replication machinery so it doesn’t work anymore," said Connor. "And the idea there is, if we find good ways of keeping viruses from doing their basic replication, we can ideally develop a new drug to treat these viruses.” An article by Boston University’s John Connor and colleagues on the discovery of compounds to combat Ebola, Marburg and other viral infections is published in the journal Chemistry and Biology.
Source
Scientists say the new malaria medicine may have a decisive edge against this persistent tropical-world killer. Michael Riscoe of Oregon Health and Science University, in the U.S. Northwest, says the new drug, known as ELQ-300, targets the mitochondria -- energy-producing structures in the parasite’s cells -- and the DNA building blocks they produce. “So the Plasmodium mitochondrion serves as a factory to make these DNA building blocks, but this is completely blocked by ELQ-300," explains Riscoe. "Studies show that the drug acts very quickly to shut down this process. In fact, (in) only about 10 minutes.”
Perhaps the biggest obstacle in the fight against malaria, Riscoe adds, is the Plasmodium parasite’s ability to mutate and develop resistance to each new drug used against the disease. In tests using laboratory animals, he notes, the parasite did not develop resistant to ELQ-300. “These findings suggest that if the drug is eventually developed for human use, then it could enjoy a long, useful clinical life before resistance emerges in the field.” That would be good news, because Riscoe says the new drug seems to be much more effective than current anti-malaria medicines. “ELQ-300 is about 30 times more effective at curing malaria in mice as compared to atovaquone, a drug that’s in clinical use today.”
Riscoe and his colleagues cite other advantages to ELQ-300: it may be cheaper to make than existing drugs, and it may be effective at lower doses. They suggest it could be used in combination with another drug to cure malaria with just one dose of medicine. After successful tests on laboratory mice, ELQ-300 is heading for human trials, starting with tests for safety. Michael Riscoe was interviewed in a podcast by Science Translational Medicine, the journal which published his research.
Source
Granny says ask dat space alien how come dey been flingin' asteroids at us...
Discovery Could Lead to New Drugs to Block Deadly Viruses
March 25, 2013 - U.S. researchers have discovered a class of potent chemical compounds that could stop a host of viruses in their tracks, including the deadly Marburg and Ebola viruses and pathogens that cause rabies, mumps and measles. Drugs made from the compounds would stop infection by interfering with a virus ability to reproduce itself inside human cells.
Viruses are strange things. Though there is some scientific question about whether viruses are alive or not, they do have a basic genetic structure that allows them to be biologically active. But they don't have the built-in reproductive capacity of bacteria -- tiny, living organisms which, once they have infected a human host, can make copies of themselves using their own DNA. John Connor, a virologist at Boston University in Massachusetts, explains that in order for viruses to reproduce and become a disease threat, they must first hijack the genetic machinery of a living cell: Theyre parasites," said Connor. "They get inside our cells and use a lot of our machinery in order to make extra copies of themselves. And so that poses a really delicate question of how do you destroy the virus without getting yourself.
A laboratory specialist examines specimens of the Ebola virus at the Uganda virus research centre in Entebbe, 40km (25 miles) south from capital Kampala May 17, 2011.
Connor and his colleagues screened thousands of chemical compounds, looking for ones that showed strong antiviral activity. They identified several small molecules that interfere with the replication of a class of pathogens known as NNS viruses, which cause the deadly Marburg and Ebola infections, as well as measles and mumps. Once they have invaded a host cell, NNS viruses use their own genetic molecule -- known as RNA -- to hijack the host cell's DNA and force it to make copies of the virus. The most effective compounds discovered by the Boston researchers shut down that replication process -- at least in cell-culture experiments -- by limiting the viruses' RNA production.
The compounds do not thwart all viruses -- they have no effect, for example, on HIV, the virus that causes AIDS -- because of differences in the way viral pathogens enter and commandeer cells. Just as antibiotics are effective against many bacterial illnesses, Connor says he hopes this discovery leads to the development of broad-spectrum antiviral drugs to treat a variety of currently incurable viral infections. Basically, one of the things my lab is interested in is trying to find 'monkey wrenches' [disruptive agents] to throw into viral replication machinery so it doesnt work anymore," said Connor. "And the idea there is, if we find good ways of keeping viruses from doing their basic replication, we can ideally develop a new drug to treat these viruses. An article by Boston Universitys John Connor and colleagues on the discovery of compounds to combat Ebola, Marburg and other viral infections is published in the journal Chemistry and Biology.
Source
See also:
New Malaria Drug Shows Promise in Animal Tests
March 25, 2013 U.S. researchers have developed a new fast-acting drug against malaria that appears to avoid the problem with current medicines, which often lose their effectiveness against increasingly drug-resistant strains of malaria parasites, called Plasmodium.
Scientists say the new malaria medicine may have a decisive edge against this persistent tropical-world killer. Michael Riscoe of Oregon Health and Science University, in the U.S. Northwest, says the new drug, known as ELQ-300, targets the mitochondria -- energy-producing structures in the parasites cells -- and the DNA building blocks they produce. So the Plasmodium mitochondrion serves as a factory to make these DNA building blocks, but this is completely blocked by ELQ-300," explains Riscoe. "Studies show that the drug acts very quickly to shut down this process. In fact, (in) only about 10 minutes.
Perhaps the biggest obstacle in the fight against malaria, Riscoe adds, is the Plasmodium parasites ability to mutate and develop resistance to each new drug used against the disease. In tests using laboratory animals, he notes, the parasite did not develop resistant to ELQ-300. These findings suggest that if the drug is eventually developed for human use, then it could enjoy a long, useful clinical life before resistance emerges in the field. That would be good news, because Riscoe says the new drug seems to be much more effective than current anti-malaria medicines. ELQ-300 is about 30 times more effective at curing malaria in mice as compared to atovaquone, a drug thats in clinical use today.
Riscoe and his colleagues cite other advantages to ELQ-300: it may be cheaper to make than existing drugs, and it may be effective at lower doses. They suggest it could be used in combination with another drug to cure malaria with just one dose of medicine. After successful tests on laboratory mice, ELQ-300 is heading for human trials, starting with tests for safety. Michael Riscoe was interviewed in a podcast by Science Translational Medicine, the journal which published his research.
Source
In past years, this might have been occasion for panic. Yet chicken and pork sales have not plummeted, as they did during flus linked to swine and birds. Travel to Shanghai or Mecca has not been curtailed, nor have there been alarmist calls to close national borders. Is this relatively calm response in order? Or does the simultaneous emergence of two new diseases suggest something more dire?
Actually, experts say, the answer to both questions may well be yes. “We’ve done a great job globally in the last 10 years,” said Dr. William B. Karesh, a wildlife veterinarian and chief of health policy for the EcoHealth Alliance, which tracks animal-human outbreaks. “Compared to H5N1 and SARS, we’re getting on top of these diseases much, much faster.” But he added that “people have become desensitized over time — it’s ‘Oh, O.K., another one.’ ” And scientists say the world cannot afford to relax. The threat is real. New diseases are emerging faster than ever.
A man in Saudi Arabia wore a mask last week to protect against a virus that has killed 22 since it was found there last year.
Peter Daszak, a parasitologist and president of the EcoHealth Alliance, has even put a number on it: 5.3 new ones each year, based on a study using data from 1940 to 2004. He and his co-authors blamed population growth, deforestation, antibiotic overuse, factory farming, live animal markets, bush meat hunting, jet travel and other factors. Some aspects of the new viruses are scary. The Arabian coronavirus — now officially named MERS, for Middle East respiratory syndrome — has killed about half of those it infects, while SARS killed less than a quarter; in the lab, it replicates faster than SARS, penetrates lung cells more readily and inhibits the formation of proteins that warn the body that it is under attack.
In her closing remarks on Monday at the annual meeting of the world’s health ministers, Dr. Margaret Chan, director-general of the World Health Organization, said the virus was now her “greatest concern.” Until experts figure out where it hides and how it infects humans, “we are empty-handed when it comes to prevention,” she said. “These are alarm bells, and we must respond.” The H7N9 flu has been fatal in a quarter of known cases — the 1918 Spanish flu killed only 2 percent of its victims — and already has one dangerous mutation that helps it replicate at human body temperatures. Still, better surveillance means that such threats are being caught sooner, giving time to develop countermeasures like vaccines and making it far less likely that a virus like the 1918 flu will ever again kill millions.
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The novel coronavirus is related to SARS, which killed some 800 people in a global epidemic in 2003. Dr. Margaret Chan, head of the World Health Organization, singled out the illness in a speech on Monday in Geneva.
"We understand too little about this virus when viewed against the magnitude of its potential threat," Chan said at the annual WHO meeting. "We do not know where the virus hides in nature. We do not know how people are getting infected. Until we answer these questions, we are empty-handed when it comes to prevention. These are alarm bells. And we must respond."
WHO said in an update earlier this month that 20 of the 40 confirmed cases of the disease have ended in death. Most of those infected since the virus was identified last year had traveled to Qatar, Saudi Arabia, Jordan or Pakistan. There also have been cases in Britain and Germany.
The ministry said the Frenchman, whose illness was identified May 8 after he returned from a visit to the United Arab Emirates, died Tuesday. His hospital roommate also tested positive for the illness. Meanwhile, the Saudi Health Ministry reported five new cases of the virus. All the patients were in their 70s or older.
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