What’s the News: We’ve long had signs that when it comes to inheritance, DNA isn’t the be-all, end-all. Trees that have the exact same genes but were raised in different greenhouses behave differently. Worms with genes that impart long life can pass on that longevity to their progeny—even if they don’t pass on the genes. Both of these phenomena, we’ve discovered, come from epigenetic changes in tags attached to DNA that control whether genes get expressed.
But every now and then we get a whiff of other possible routes for inheritance, even stranger than that. A new paper in Cell reports that worms whose grandparents had the ability to fight viruses using a fleet of tiny RNA molecules retain these molecules even when they don’t have the genes for them. They can pass these molecules down for more than a hundred generations.
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Booze inhibits more than just your judgement: it impairs your immune system’s ability to fight off pathogens, according to a study published last week in the journal BMC Immunology. Researchers exposed human monocytes, a type of white blood cell vital for a functioning immune system, to an amount of alcohol equivalent to a blood alcohol concentration of 0.1 (around the legal level in most states). Compared to booze-free cells, monocytes exposed to both short- and long-term levels of alcohol produced significantly less type 1 interferons, chemicals the help recruit immune cells to stage an antiviral response (and also have anti-tumor activity). Excessive drinking has long been thought to interfere with the body’s ability to fight disease, and boozing is an important risk factor for hepatitis C and barrier to treatment in HIV. But not much had been known about the mechanisms behind the effect.
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The spiny dogfish
What’s the News: Researchers found that squalamine, a steroid present in the bodies of the dogfish shark, has a protective effect against several human viruses, all of which are difficult or impossible to cure with existing drugs. The chemical has so far been shown to be relatively safe in humans and can be synthesized, suggesting it could have promise as an antiviral drug in humans.
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What’s the News: Scientists have developed a new carbon nanotube device (pictured above) that’s capable of detecting single cancer cells. Once implemented in hospitals, this microfluidic device could let doctors more efficiently detect the spread of cancer, especially in developing countries that don’t have the money for more sophisticated diagnostic equipment. Any improvement in detecting cancer’s spread is important, says MIT associate professor of aeronautics and astronautics Brian Wardle, because “of all deaths from cancer, 90 percent are … from tumors that spread from the original site.”
What’s the Context:
- The researchers’ original microfluidic device from four years ago featured tens of thousands of microscopic silicon posts coated with tumor-sticking antibodies: when cancer cells bumped into the posts, they’d stick. But if cancer cells didn’t bump into a silicon post, they’d go undetected. The group says their new version is eight times better.
- When cancer cells migrate, there are “usually only several [cancer] cells per 1-milliliter sample of blood” containing billions of other cells, making cancer exceedingly difficult to detect.
- This new dime-sized microfluidic machine works in the same way, but the solid silicon tubes were switched out for highly porous carbon nanotubes. This allows the blood to actually flow through the tubes instead of just around them, increasing the likelihood of catching a cancer cell.
- In other cancer detection news, some are using dogs to sniff out cancer and others use genetic tests to figure out cancer risks.
- Combating cancer ranges from new cancer-fighting drugs to just ignoring cancer (sometimes).
Not So Fast: The process of commercializing a technology like this takes quite a while; the previous version from four years ago is being tested in hospitals now and is may be commercially available “within the next few years.”
Next Up: The scientists are currently tweaking the device to try to catch HIV.
Reference: Grace D. Chen et al. “Nanoporous Elements in Microfluidics for Multiscale Manipulation of Bioparticles.” Small. DOI: 10.1002/smll.201002076
Image: Brian Wardle/MIT
Earlier this week at a scientific conference in Boston, HIV researchers announced a remarkable success in countering the virus’ drain on the immune system. But this early step is far from a cure.
Why it’s exciting:
Carl June and colleagues tested six male patients who already had HIV and were taking a standard antiviral regimen. Like many HIV patients, the drugs helped them, but their counts of immune cells stayed low. June’s team tested a therapy created by Sangamo BioSciences in Richmond, California, that alters a patient’s actual white blood cells to make them more HIV-resistant.
Researchers removed a sample of CD4+ T cells, the type of immune cells affected by HIV, from each man and used Sangamo’s enzyme to disrupt the CCR5 gene, which encodes a protein that HIV uses to enter CD4+ cells. The engineered cells were then infused back into the patients. Immune-cell counts subsequently rose for five of the six patients who received the therapy. “It’s very exciting,” says John Rossi, a molecular biologist at the City of Hope’s Beckman Research Institute in Duarte, California. “If they did this several times in a given patient, you could establish a high percentage of resistant cells.” [Nature]
The idea came from the “Berlin Patient,” who we’ve written about before at 80beats. He became famous after receiving a donation of bone marrow from someone who carried a mutation in CCR5 that made them resistant to HIV.
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Modern microscopes opened up the world of the minute to an amazing degree, allowing people to see all the way down to a bacterium wriggling on a slide. But if you want to see down even smaller in regular optical light—to a virus, a cell’s interior, or other objects on the nanoscale—you’ve been out of luck. Those objects are smaller than 200 nanometers, what’s been considered the resolution limit for microscopes scanning in white light, and so the only was to see them was through indirect imaging devices like scanning electron microscopes.
Not anymore. Lin Li and colleagues report a new way using tiny beads to resolve images at 50 nanometers, shattering the limit for what can be seen in optical light.
Their technique, reported in Nature Communications, makes use of “evanescent waves“, emitted very near an object and usually lost altogether. Instead, the beads gather the light and re-focus it, channelling it into a standard microscope. This allowed researchers to see with their own eyes a level of detail that is normally restricted to indirect methods such as atomic force microscopy or scanning electron microscopy. [BBC News]
Those beads are called microspheres—they’re tiny glass balls about the size of red blood cells. The researchers apply these spheres to the surface of the object they want to see. In essence, the spheres capture light that normally would be lost before it ever reached the observer’s eye (those evanescent waves), enabling Li’s team to overcome the diffraction limits of microscope machinery that have limited the maximum possible resolution.
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Swine flu is not gone, and it is not stagnant. Though the public health scare about the 2009 swine flu pandemic subsided, the virus—like avian flu—remains in pockets of animals, shuffling its genes while hidden from the watchful eyes of virus experts. Virologists call this genetic switcheroo “reassortment,” and it’s how new and dangerous strains of flu snuck up on humankind in the past—and how they could do it again. This time, though, virologist Jinhua Liu and colleagues are trying to get a jump on the viruses.
For a new study in the Proceedings of the National Academy of Sciences today, this team of Chinese researchers simulated what could be a dire situation for humans: swine flu (H1N1) and avian flu (H9N2) together in one animal. When these flu strains are together they can exchange genetic material. So to test what that mixing might produce, Liu’s team swapped genes between the two and created 127 hybrid viruses, testing each on mice.
Eight of these hybrid strains turned out to be more virulent and dangerous in the mice than their parent strains of swine flu and bird flu. [National Geographic]
According to Dutch virologist Ab Osterhaus, we can’t be sure that these eight nasty strains are the ones that would hit humans hardest—animal studies aren’t perfect.
“Mice mirror, to a certain extent, what happens in humans,” he says, but they are not perfect model animals. Liu agrees. He plans to investigate how contagious his new viral blends are in guinea pigs and ferrets—animals whose respiratory system better reflects our own feverish battle with flu. [ScienceNOW]
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Now that humanity has beaten back and nearly eliminated the once-widespread threat of polio, Bill Gates wants to finish it off for good. To some observers, though, it’s just not worth the money.
The multi-billionaire recently issued his annual letter (pdf) through the Bill & Melinda Gates Foundation, outlining its goals. Gates has been a big donor to world health programs and fighting polio in particular, and his letter calls for eradicating polio once and for all.
There would be many benefits to eradicating the disease entirely, Gates argues — not just medical and financial, but moral. “Success will energize the field of global health by showing that investments in health lead to amazing victories,” he wrote. “The eradication effort illustrates so well how a major advance in the human condition requires resolve and courageous leadership. To win these big important fights, partnerships, money, science, politics and delivery in developing countries have to come together on a global scale.” [Los Angeles Times]
Medical science, supported by billions of philanthropic dollars, has already cut down the specter of polio around the world to a shadow of what it once was. The World Health Organization estimates that there were 1,500 cases of polio around the globe in 2010, down from 350,000 in 1988. To wipe out the last remnants of wild poliovirus, Gates proposes vaccinating youths under five in countries like Afghanistan and India where pockets of polio remain.
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Though the swine flu scare of 2009 may have bumped the avian variety of flu from of the popular imagination, biomedical researchers certainly haven’t forgotten the potential danger it poses. But researchers are constantly forced to play catch-up by following bird flu’s path through the avian population and trying to track its shifting genetics.
The way to finally get the jump on bird flu would be to create a weapon that works against the whole family of avian flu viruses, whatever their slight genetic quirks. And researchers led by Laurence Tiley say in Science this week that they might have found that kind of comprehensive trick: a genetic modification that seems to prevent flu from spreading in chickens.
It’s a decoy.
The birds carry a genetic tweak that diverts an enzyme crucial for transmitting the H5N1 strain. Although they die of the disease within days, the molecular decoy somehow impedes the virus from infecting others. [Nature]
Specifically, this genetic tweak allows the birds to create an RNA impostor. It matches up to the polymerase enzyme the flu virus would use to replicate its genetic material, so that enzyme is attracted to the decoy, which throws off viral replication. Though the modified chickens that were infected with avian flu died, the fact that they didn’t spread the virus is a potentially huge find—once avian flu enters a chicken population it typically spreads like wildfire.
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By combining a cocaine analog with part of a common cold virus, researchers have created a “cocaine vaccine” that tricks the body into attacking the drug, neutralizing its high-giving powers. It has only been tested in mice so far, but the results are good:
“Our very dramatic data shows that we can protect mice against the effects of cocaine, and we think this approach could be very promising in fighting addiction in humans,” study researcher Ronald Crystal, a professor of genetic medicine at Weill Cornell Medical College, said in a statement. [LiveScience]
The immune system doesn’t typically react to cocaine in the blood stream–it’s too small and doesn’t contain the “markers” of an invader. To get the white blood cells to notice it, the researchers strapped it to something the immune system can detect–the outside parts of the virus. The researchers took the outer shell from an adenovirus, which causes some types of the common cold, and removed the parts of the virus that cause illness. Then they linked that recognizable viral shell to a stable molecule similar to cocaine (they also tried it with cocaine itself, the researchers say, but the more-stable analog produced better results).
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More trouble for bees: A study out in the open-access journal PLoS One finds that viruses that previously had been the bane of domesticated honeybees have spread to wild pollinators.
A pattern showed up in the survey that fits that unpleasant scenario. Researchers tested for five viruses in pollinating insects and in their pollen hauls near apiaries in Pennsylvania, New York and Illinois. Israeli acute parasitic virus (IAPV) showed up in wild pollinators near honeybee installations carrying the disease but not near apiaries without the virus. In domestic honeybees, such viruses rank as one of the possible contributors to the still-mysterious malady known as colony collapse disorder that abruptly wipes out a hive’s workforce, [study author Diana] Cox-Foster says. [Science News]
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Perhaps you’ve seen the story of the 44-year-old American man reportedly “cured” of HIV in Germany–it’s been making the rounds over the past week. What’s actually happening here?
The Procedure
This is a story that dates back a few years; in fact, 80beats blogged about this case years ago when it first made the news. Back in 2007, the man—Timothy Ray Brown—was an HIV-positive patient suffering from acute myeloid leukemia. When standard chemotherapy couldn’t help him, his docs in Germany turned to a bone marrow transplant, with one twist.
Brown’s oncologist decided to look for a bone marrow donor who had a had a special genetic mutation that made the stem cells in it naturally resistant to HIV infection. His physician, Dr. Gero Huetter, was able to find this rare match and Brown got the bone marrow transplant. He needed a second stem cell transplant because the cancer came back. Today, he appears to be cancer free and doctors can’t find traces of the virus that causes AIDS either. [CNN]
Brown’s treatment made a splash in the news in 2008, when the doctors first reported on it. It has resurfaced this month because the researchers published a new study in the journal Blood updating his condition.
The researchers confirmed that Brown seems to have maintained his resistance to HIV for three years, confounding their expectation that he would become reinfected. They concluded that a “cure of HIV has been achieved in this patient.” [New Scientist]
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Anthony Eugene Whitfield is currently serving a 178-year prison sentence for, among other things, knowingly infecting several sexual partners with HIV. But how do you prove that the women in question contracted the virus from him?
From Ed Yong:
To demonstrate Whitfield’s guilt, the prosecution had to show that he had wilfully exposed women to HIV, that his five HIV-positive partners contracted their infections from him. Fortunately, David Hillis from the University of Texas and Michael Metzker from Baylor College of Medicine knew exactly how to do that. They had evolutionary biology on their side.
Hillis and Metzker knew that HIV is a hotbed of evolution. The bodies of HIV carriers produce around a billion new virus particles every day, and their genomes change and shuffle at furious speeds. But when infections pass from one person to another, this viral variety plummets. Thousands of genetically distinct viruses might jump into a new host, but usually, only one of these managed to gain a foothold and set up a new infection. Every time it moves from host to host, HIV passes through a genetic bottleneck and that provides a massive clue about who passed an infection to whom.
For great detail on how the scientists built these HIV trees and used them in the case against Whitfield, as well as what it means for the future of prosecution, read the rest of this post at Not Exactly Rocket Science.
Related Content:
Not Exactly Rocket Science: Genetic Study Shows How HIV Controllers Get Their Groove
80beats: HIV’s Primate Precursor Is Very Old. Why Did It Jump To Humans So Recently?
80beats: Good News: Anti-Microbial Gel Cuts HIV Infection Rates for Women
80beats: New HIV Hope? Researchers Find Natural Antibodies That Thwart the Virus
Image: Scaduto et. al / PNAS
Goodbye and good riddance, rinderpest.
For only the second time in history, humans have eradicated a disease through a long, slogging campaign of vaccinations and global alertness.
Rinderpest, which means “cattle plague” in German, does not affect humans, though it belongs to the same virus family as measles. But for millenniums in Asia, Europe and Africa it wiped out cattle, water buffalo, yaks and other animals needed for meat, milk, plowing and cart-pulling. Its mortality rate is about 80 percent — higher even than smallpox, the only other disease ever eliminated. [The New York Times]
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UPDATE: Fortune reports today that the lead researcher on this study, Jerry Bromenshenk, had financial ties to Bayer Crop Science—including a research grant—that were not disclosed. Bayer makes pesticides that some beekeepers and researchers have cited as a possible cause of colony collapse disorder, and Bromenshenk’s conclusions in this study could benefit the company. Bromenshenk says the money did not go to this project or influence its findings.
Viruses. Mites. Fungi. Genetically modified crops. Inbreeding because of industrial agriculture. They’ve all been floated as possible causes of colony collapse disorder (CCD), the mystery affliction that’s been wiping out honeybees, and by doing so threatening the agricultural industries that rely on those insects. Despite the flood of reports since 2006 about these suspects (and more absurd ones, like cellphone radiation disorienting the bees), the bee die-off continues without a clear explanation.
A study out this week in PLoS One points the finger in a new direction. What’s interesting about this explanation is its contention that there’s tandem foul play at work in CCD—two of the suggested culprits could be working together. But the mystery isn’t solved just yet.
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