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Minuscule viruses on the sea floor have a big impact on the marine ecosystem, a new study shows. The viruses infect simple microbes, known as prokaryotes, that form one of the lowest rungs in the food chain. Usually the nutrients and carbon contained in prokaryotes are used by the larger organisms that eat them, but something very different happens when prokaryotes are infected by viruses: the viruses burst the prokaryotes open and release their carbon and nutrients into the water column [New Scientist]. When these nutrients sink down to the ocean floor they’re consumed by other microbes, which then multiply and provide more hosts for the viruses.

Researchers long ago grasped that viruses on the sea surface play a Dr.-Jekyll-and-Mr.-Hyde role, killing biomass while at the same time sustaining it. Now, though, evidence has emerged that these tiny bacterial pathogens also carry out unsung work at the ocean depths — a dark, inhospitable, nutrient-poor place that counts as last great unexplored ecosystem on the planet [AFP]. Researchers say the newly discovered role of deep sea viruses may also play a critical role in the carbon cycle, as the decaying remnants of the burst microbes carry carbon, which is sequestered in the ocean depths.

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People who lived through the 1918 flu pandemic still have antibodies in their immune systems that can recognize and fight that flu virus, although the haven’t been exposed to it for 90 years. Such long-lived immunity was thought to be impossible without periodic exposure to the microbe that stimulated the immune system in the first place [Science News]. Researchers say these antibodies could be helpful in developing treatments for viruses similar to the deadly one that swept around the world in 1918, killing an estimated 50 million people.

For the study, which will be published in this week’s issue of Nature [subscription required], lead researcher James Crowe’s team studied antibodies in the blood of 32 people in their 90s and 100s, born during or before 1915. They found that all 32 people had antibodies to the 1918 strain of flu virus [HealthDay News]. In lab tests, the antibodies mounted a powerfully effective attack against a modern version of the virus. “This is entirely counter to everyone’s intuition — that elderly people would have such potent antibodies,” Crowe says. Aging typically reduces a person’s ability to build antibodies and develop immunity to diseases [Science News].

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When researchers speak in ominous tones about the possibility of a pandemic of avian influenza, commonly known as bird flu, they’re usually talking about the virus strain known as H5N1, which has killed 243 of the 385 people it has infected since 2003. But according to a new study, a relatively ignored strain known as H9N2 could easily mutate into a form that spreads freely among humans.

Luckily, researchers say that even if the H9 virus does acquire the ability to spread in people, at first the infection is likely to cause minor illness. “You’re going to have a bunch of people who don’t feel very well, as opposed to dropping off the face of the Earth,” says Raymond Pickles, a cell biologist…. But the new data indicate that if the H9 viruses mix with other human viruses, as commonly happens in nature, it could become more potent [Science News].

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Viruses infect a wide range of plants and animals, and a new study in Nature [subscription required] shows that they can even infect one another. If that seems surprising, no wonder: until a team of French researchers watched one virus invade another, hijacking its genetic machinery and making copies of its victim’s DNA, scientists didn’t even know this was possible [Wired].

The French team dubbed the virus’s virus Sputnik and called it a “virophage” to parallel “bacteriophage,” which is the name for a virus that infects bacteria [Science]. Sputnik is tiny, with only 18,000 genetic bases in its chromosome. Its victim, by contrast, is a large mamavirus that the scientists found in a Paris cooling tower, and contains about 1.2 million genetic bases. An infection by Sputnik sickens the mamavirus by interfering with its replication.

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Ebola has receded from the headlines since the mid- 1990s when the world briefly panicked about an African outbreak of the terrifying disease, which causes massive bleeding and kills up to 90 percent of the people it infects. Thankfully, scientists haven’t forgotten about the virus, and are still trying to unlock its secrets. In a new report, researchers say they’ve finally got a good image of the protein “spike” that the virus uses to enter healthy human cells.

Researchers also say that by revealing the protein’s shape and understanding how it works, they have exposed chinks in Ebola’s armor that could be targeted for treatment [Bloomberg]. Lead researcher Erica Ollman Saphire says the spike is almost entirely concealed: “It’s kind of like Harry Potter wrapped in an invisibility cloak. But there are three or four little sites peeking out,” she added. These may provide a target for a drug or vaccine, or perhaps an immune-based treatment for Ebola, she said [Reuters].

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Odds are, you have it. By the age of 40, nearly 90 percent of adults in the United States have been exposed to the herpes simplex virus-1 (HSV1) that causes cold sores. Not everyone who has the virus lurking in their body will have symptoms, but those who do will be annoyed for life by unexpected lip blisters. But now the secret of how the cold sore virus manages to persist for a lifetime in the human body may have been cracked [BBC News], and researchers say their findings may point the way towards a treatment that could kill the virus once and for all.

The virus is a difficult target. When a cold sore appears, it’s easily treatable with a drug that kills the replicating virus, but that drug can’t get to the latent versions of the virus that are hiding within nerve cells and waiting to cause the next eruption. Until now, research has generally concentrated on keeping HSV1 inactive — and preventing cold sores from ever showing up. But [Duke University] researchers took the opposite tack: figuring out precisely how to switch the virus from latency to its active stage. That’s important, says lead author Dr. Bryan Cullen, professor of molecular genetics and microbiology at Duke, “because unless you activate the virus, you can’t kill it” [Time].

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