A study of children has discovered a correlation between obesity and prior infection with a cold virus, called Adenovirus 36. While the link is fairly weak, the tantalizing research suggests a new front on the war on obesity.
The study participants included 124 children between the ages of 8 and 18. Of the 67 obese children involved in the study, 15 had signs of previous infection with the AD36 virus, in comparison with only 4 of the 57 non-obese children. The study was published in the online edition of Pediatrics.
The children who had been previously exposed to the virus (which was indicated by the antibodies to the virus present in their blood) were on average 50 pounds heavier than the non-exposed children. And even within the obese group, those that had been previously exposed to AD36 were an average of 35 pounds heavier.
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HIV became an epidemic in the human population just in the 20th century. Its precursor found in primates, called simian immunodeficiency virus or SIV, could be not just hundreds of years old, but tens of thousands of years old, according to a study out in Science.
Preston Marx and colleagues studied the monkeys of Bioko, an island off West Africa that has been cut off from the mainland for 10,000 years. By studying the way SIV evolved in that isolated population, the team calculated that the virus is at least 32,000 years old, and possibly much, much older. Says Marx:
“The biology and geography of SIV is such that it goes from the Atlantic Ocean to the Indian Ocean all the way to the tip of Africa. … It would take many, many thousands of years to spread that far and couldn’t have happened in a couple of hundred years.” [AFP]
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Chronic fatigue syndrome’s headaches, muscle aches, tiredness, and concentration problems have no known cause, so a paper published online yesterday, in which researchers report finding a type of virus in 87 percent of 37 chronic fatigue syndrome (CFS) patients tested, seems a promising step. But in statements to the media the researchers stress caution in interpreting results. The group also noted that it had delayed publishing the paper, originally meant to appear in the Proceedings of the National Academy of Sciences in May, due to conflicting reports from other scientists.
The National Institutes of Health’s Dr. Harvey Alter, senior author of the paper, said in a conference call with reporters, “It’s an association, but that’s all it is.” He was careful to say the findings don’t prove that a virus causes CFS. [NPR]
Alter’s caution is understandable, especially given recent CFS research history:
October 2009: A virus, XMRV (xenotropic murine leukemia virus–related virus), is found in 68 of 101 CFS patients.
January 2010: XMRV is not found in a British study that tested CFS patients.
July 2010: XMRV is not found in a Center for Disease Control study testing CFS patients.
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In this week’s Nature Medicine, a study brings a ray of success in researchers’ quest to fight the deadly viruses Ebola and Marburg. Testing a new approach on monkeys, scientists at the U.S. Army Medical Research Institute of Infectious Diseases saw most of the monkeys survive a normally fatal Ebola infection—and all of them who had Marburg lived.
Within an hour of infecting the primates, researchers gave them antisense phosphorodiamidate morpholino oligomers, or PMOs.
The morpholino oligomers are a new class of drugs in a family of what is known as antisense nucleotides. Antisense nucleotides are designed to bind tightly to specific areas of viral messenger RNA, blocking replication. Such compounds already are being used to treat certain types of cancer and cytomegalovirus infections, and they are being tested against HIV [Los Angeles Times].
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In a medical sense, you’d be wise to steer clear of filoviruses, a group that includes the deadly Ebola, and bornaviruses, which cause neurological diseases. But in a genetic sense, it may not be possible to avoid them. A new study in PLoS pathogens shows that bits and pieces of these viruses have been floating around in the human genome, as well as those of other mammals and vertebrates, for millions of years.
It’s not that having genetic material left behind by viruses is odd—previous research had shown that viruses account for 8 percent of the human genome. But scientists thought most of that material came from retroviruses, which use their host’s DNA to replicate and leave some of their genetic material behind. What’s weird about this is that filoviruses and bornaviruses are not retroviruses—they’re RNA viruses, which don’t use the host to reproduce in the same way.
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Identical twins don’t share everything. The mix of viruses in a person’s gut, a new study says, is unique to each of us, even if we share nearly all our DNA with another person. That is, at least according to our poop.
This year scientists have been working to decode the genetics of the beneficial microbes that live inside us, like the bacteria that help us digest food. But those trillions of bacteria have partners of their own—beneficial viruses. Jeffrey Gordon and colleagues wanted to see what those viruses were like, and how they differed from person to person. To do it, they studied fecal samples that came from four sets of identical twins, as well as their mothers.
Each identical twin had virus populations that didn’t resemble those of their sibling—or anybody else, for that matter.
Remarkably, more than 80 percent of the viruses in the stool samples had not been previously discovered. “The novelty of the viruses was immediately apparent,” Gordon said. The intestinal viromes of identical twins were about as different as the viromes of unrelated individuals [MSNBC].
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It’s still out there, you know.
A study out today in the journal Science tracks the path of swine flu, which may have receded from the forefront of humanity’s attention but hasn’t quit mixing and moving and making ready. The scientists led by virologist Malik Peiris say the flu virus that the world feared last year has gone back into pigs in China, where it’s laying down and recombining its genetics with other flu strains. And, they say, we’re not sufficiently monitoring the danger of a new strain jumping back to people.
“Just because we’ve just had a pandemic does not mean we’ve decreased our chances of having another,” said Dr. Carolyn B. Bridges, an epidemiologist in the flu division of the Centers for Disease Control and Prevention. “We have to stay vigilant” [The New York Times].
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With smallpox largely eradicated around the world, health organizations phased out the smallpox vaccine between the 1950s and 1970s (the last natural case of the disease was seen in 1977, in Somalia). During that span, Raymond Weinstein says, the AIDS crisis broke out in force. And in a study in BMC Immunology, he argues those two events could be connected.
Supposing that smallpox vaccination could have some effect on a person’s susceptibility to HIV, researchers led by Weinstein tested the idea on cells in a lab. They took immune cells from 10 people recently vaccinated against smallpox and 10 people never vaccinated. HIV, they found, was five times less successful at replicating with the cells of vaccinated people.
Why?
The researchers believe vaccination may offer some protection against HIV by producing long-term alterations in the immune system, possibly including the expression of a receptor called CCR5 on the surface of white blood cells, which is exploited by the smallpox virus and HIV [BBC News].
Any finding that expands knowledge of how HIV replicates could be an important one. And while this small study can’t prove Weinstein’s assertion is correct, the argument is, at the very least, plausible. Says Weinstein:
“There have been several proposed explanations for the rapid spread of HIV in Africa, including wars, the reuse of unsterilised needles and the contamination of early batches of polio vaccine. However, all of these have been either disproved or do not sufficiently explain the behaviour of the HIV pandemic” [Press Association].
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Image: CDC
Some parasitic wasps may be no bigger than the head of a pin, but their genetics have plenty to teach us, a new study in Science says.
A research team has sequenced the genomes of three different species of parasitic wasp. Why bother with these tiny insects? For starters, genetics is easy. Females, like humans, carry two copies of every chromosome. But males develop from unfertilized eggs, which only carry one of each. With only one copy, even recessive mutations will be easy to identify and characterize [Ars Technica].
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An estimated three in 1,000 people suffers from the mysterious affliction chronic fatigue syndrome. Those people were probably enthusiastic in October when a team of U.S. medical researchers released a study arguing that not only is the syndrome real (some doctors dismissed it as purely psychological “yuppie flu”), but also that they’d connected it to a specific virus. DISCOVER covered the hubbub after the paper came out in the journal Science.
But now, in a study in PLoS One, a British research team has cast doubt on the American team’s findings, saying there’s no conclusive link between the virus and chronic fatigue syndrome, which is also known as myalgic encephalomyelitis.
The U.S. team’s findings sounded robust when they came out. They found the murine leukaemia virus-related virus (XMRV) in blood samples of 68 of 101 patients diagnosed with chronic fatigue syndrome. Just eight out of 101 healthy “controls” drawn at random from the same parts of the US also tested positive, suggesting that XMRV played a key role in triggering the condition [The Independent]. When the scientists from Imperial and Kings colleges in London attempted to replicate these findings, however, they found nothing of the sort. Of the 186 people with the syndrome that this team tested, not one showed signs of XMRV, or of any related virus.
Study coauthor Myra McClure of the Imperial College also criticized the U.S. team and the journal Science for rushing the findings into print in October. “When you’ve got such a stunning result you want to be absolutely clear that you are 1,000 per cent right and there are things in that [previous study] I would not have done. I would have waited. I would have stalled a little” [The Independent], she said.
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News that an Iowa cat has been diagnosed with swine flu has sparked a new round of concerns, as pet-owners worry both that their furry companions could get sick, and that their pets could pass the virus on to other humans. The 13-year-old, mixed-breed cat showed the symptoms of lethargy, sneezing and coughing typical to sick cats [ABC News]. The veterinarians who treated him say that several people in the cat’s home had been experiencing flu-like symptoms, and lab work confirmed that the feline had the H1N1 virus.
Happily, the cat is expected to make a full recovery. But both vets and public health officials are rushing to reassure the public that one sick cat probably does not indicate a coming crisis. While it’s possible that more cats will be diagnosed with the swine flu, vets point out that the virus was circulating for more than six months before the first cat case was discovered, indicating that the virus probably doesn’t jump from species to species very easily. Doctors also note that there’s very little chance that a cat will spread the virus to humans: Even when inter-species transmissions do occur, the H1N1 virus seems more likely to move from humans to animals, rather than the other way around [HealthDay News].
There have been no reported cases of dogs catching the virus, but there is one type of pet that is known to be vulnerable. Ferrets are generally susceptible to the seasonal flu, and the AP reported Wednesday that H1N1 infection has been confirmed in two ferrets, one in Nebraska and the other in Oregon. “Not only can they be infected with the flu but they are clearly able to transmit the flu back to people,” Treanor said [HealthDay News]. But the bottom line appears to be: Unless you’re a ferret-owner, you probably have nothing to worry about.
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Image: flickr / theogeo
Researchers may have taken a step towards curing the rare, inherited brain disease made famous by the movie Lorenzo’s Oil–and also towards ushering a new era of gene therapy. To help two young boys suffering from the disease, researchers tried an experimental treatment using a deactivated version of the HIV virus. The virus delivered working copies of a gene to stem cells from the patients’ bone marrows. The HIV virus, stripped of genetic material that makes it toxic, integrates permanently into the DNA of cells it enters, scientists said. That means the modified gene remains in the blood-forming stem cells for the life of the patient [Bloomberg].
Adrenoleukodystrophy, or ALD, is a progressive disease characterized by the gradual destruction of the myelin sheaths that insulate neurons and nerves, allowing electrical signals to be transmitted through them. The disease is caused by a genetic defect, which prevents cells in the bone marrow from producing a crucial protein necessary for the formation of the myelin sheaths. Typically, children with ALD are given bone marrow transplants to provide them with healthy blood-forming stem cells, but in the two cases described in the study, no matching donors could be found.
In the experimental treatment, described in a paper published in Science, researchers took blood stem cells from the patients’ bone marrow and used the new vector system to genetically alter them by inserting a working copy of the … gene. The modified cells were then put back into the patients [Reuters].
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As swine flu is now prevalent in 41 states, doctors are getting plenty of chances to study the workings of the disease. They now know that in severely ill patients, intense inflammation in the lungs prevents oxygen from being tranfered to the blood stream. Says physician Robert Fowler: “Most patients are still able to take breaths, but these breaths are ineffective” [Science News]. That oxygen deprivation can cause widespread organ damage.
The speed with which swine flu patients can go downhill marks the H1N1 virus as strikingly different from the seasonal flu virus, doctors say. “In severe cases, patients generally begin to deteriorate around three to five days after symptom onset. Deterioration is rapid, with many patients progressing to respiratory failure within 24 hours, requiring immediate admission to an intensive care unit” [Reuters], says World Health Organization doctor Nikki Shindo.
Doctors say that severely ill patients should promptly be put on breathing machines and given antiviral drugs like Tamiflu. In cases where patients’ respiratory systems have already crashed, some doctors are trying a treatment called extracorporeal membrane oxygenation, in which blood is extracted from each patient and passed through a machine that adds oxygen [Science News].
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Sufferers of the baffling ailment known as chronic fatigue syndrome, take hope: For the first time, there’s good evidence that the symptoms aren’t just in your head, and experimental treatments may be coming soon.
Over the past few decades, the syndrome has been a source of intense frustration both to patients diagnosed with it and doctors who try to treat it. The diffuse collection of symptoms can include incapacitating fatigue, muscle aches, headaches, problems with concentration. Doctors, meanwhile, have been mystified by the cause of the symptoms, and some have suggested that it’s a psychiatric problem, leading to the coining of the dismissive label “yuppie flu.”
Now, researchers report that 68 of 101 patients with the syndrome, or 67 percent, were infected with an infectious virus, xenotropic murine leukemia virus-related virus, or XMRV. By contrast, only 3.7 percent of 218 healthy people were infected. Continuing work after the paper was published has found the virus in nearly 98 percent of about 300 patients with the syndrome, said Dr. Judy A. Mikovits, the lead author of the paper [The New York Times]. While it hasn’t been proven that the virus causes the syndrome, the link opens new avenues of research and treatment.
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Swine flu vaccines have arrived! Or more accurately, limited amounts of the first available vaccine, a nasal spray, have been delivered to distribution points around the country, and several states began vaccinating health care workers and young children on Monday. It’s not a moment too soon: The Centers for Disease Control and Prevention have announced that flu is now widespread in most of the United States. The infections are “overwhelmingly” pandemic H1N1 influenza, commonly known as swine flu. The flu season generally lasts well into May, so many months of uncertainties lie ahead [Los Angeles Times].
CDC director Thomas Frieden says that so far, vaccine “demand is outstripping supply, but we expect that fairly soon supply will be outstripping demand.” … Over the next two to three weeks, tens of millions of additional doses will become available [Los Angeles Times]. The injectable form of the vaccine will be ready for distribution next week.
Now that the vaccines have been successfully hustled off the assembly lines, the next daunting challenge for public health officials is convincing people to go get vaccinated. Myths and worries about the vaccine have spread on talk radio and anti-vaccine Web sites [The New York Times], with even celebrities like Bill Maher unhelpfully chiming in via Twitter. At a Tuesday press conference, Frieden strongly refuted one of the most commonly voiced concerns: that in rushing the vaccine through production, it wasn’t properly tested for safety.
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