Since long before it gained fame as a precise gene-editing tool, CRISPR has had another job defending bacteria against viral invaders. And it’s far from alone. Ten sets of bacterial genes have similar, newly discovered defense roles, researchers report online January 25 in Science.

The discovery “probably more than doubles the number of immune systems known in bacteria,” says Joseph Bondy-Denomy, a microbiologist at the University of California, San Francisco, who wasn’t involved in the study.
Bacteria are vulnerable to deadly viruses called phages, which can hijack bacteria’s genetic machinery and force them to produce viral DNA instead. Some bacteria protect themselves against phage attacks with a system called CRISPR, which stores pieces of past invaders’ DNA so bacteria can recognize and fend off those phages in the future (SN: 4/15/17, p. 22). But only about 40 percent of bacteria have CRISPR, says study coauthor Rotem Sorek, a microbial genomicist at the Weizmann Institute of Science in Rehovot, Israel. That’s why he and his colleagues are hunting for other defense mechanisms.

Defense-related genes tend to cluster together in the genome, Sorek says. So his team sifted through genetic information from 45,000 microbes, flagging groups of genes with unknown functions that were located near known defense-related genes.

Many of the bacteria with these gene families hail from far-flung locations like the bottom of the ocean. So the researchers used the genomic data to synthesize the relevant bits of DNA and inserted them into Escherichia coli and Bacillus subtilis, which can both be grown and studied in the lab. Then, the researchers tracked how well the bacteria resisted phage attacks when various genes in a family were deleted. If getting rid of some of the genes affected the bacteria’s ability to fight off phages, that result suggested the group of genes was a defense system.

Nine groups of bacterial genes turned out to be antiphage defense systems, and one system protected against plasmids, another source of foreign DNA, the researchers found.
Previously discovered antiphage protective systems, such as CRISPR, have been described with acronyms, but, Sorek jokes, “we ran out of acronyms.” So the new systems are named after protective deities — like the Zorya, a pair of goddesses from Slavic mythology.

The data also reveal a possible shared origin between bacterial immune systems and similar defenses in more complex organisms, Sorek says. Some of the genes contained fragments of DNA that are also known to be an important part of the innate immune system in plants, mammals and invertebrates.

It’s likely the research will unleash a flurry of new studies to figure out how these new defense systems work and whether they, like CRISPR, might also be useful biotechnology tools, Bondy-Denomy predicts.

Zika virus may not be the black sheep of the family. Infections with either of two related viruses also cause fetal defects in mice, researchers find.

Some scientists have speculated that Zika’s capacity to harm a fetus might be unique among its kind, perhaps due to a recent change in the virus’s genetic material (SN: 10/28/17, p. 9). Others have argued that perhaps this dangerous ability was always there. It just wasn’t until the 2015–2016 epidemic in the Western Hemisphere that enough pregnant women were affected for public health researchers to identify the association with fetal defects (SN: 12/24/16, p. 19).
But new work suggests this capacity is not Zika’s alone. Pregnant mice infected with West Nile or Powassan virus — both flaviviruses, like Zika — also showed fetal harm. Over 40 percent of these infected fetuses died. But among pregnant mice infected with one of two other mosquito-borne viruses unrelated to Zika, all of the fetuses survived, scientists report online January 31 in Science Translational Medicine.

The research underscores that “many viruses, including some similar to Zika, can infect the placenta and the cells of the baby,” says George Saade, an obstetrician-gynecologist and cell biologist at the University of Texas Medical Branch at Galveston. “This list keeps growing and highlights the risks from viruses that we are not very familiar with.”

Like Zika, West Nile virus and Powassan virus are neurotropic, meaning these pathogens target nerve cells. Both viruses can cause inflammation of the brain or of the membranes that surround the brain. West Nile is transmitted to humans by mosquitoes that have bitten infected birds. From 1999 to 2016, there were more than 46,000 cases reported to the U.S. Centers for Disease Control and Prevention. Powassan, spread by ticks who have fed on infected rodents, is less widespread; only 98 cases were reported from 2007 to 2016, mostly in the Northeast and Great Lakes area.

Jonathan Miner, a virologist at the Washington University School of Medicine in St. Louis, and his colleagues conducted some of the initial work in mice that demonstrated that Zika could harm fetuses (SN: 6/11/16, p. 15). The new study tests the effects of four other viruses: the two flaviviruses and two alphaviruses, chikungunya and Mayaro, which also have led to outbreaks in Zika-affected areas.
The researchers infected 14 mice early in their pregnancies with one of the four viruses. By late pregnancy, 12 out of 30 fetuses from West Nile–infected mice had died, and half of the 16 fetuses from Powassan-infected mice had died. All of the fetuses from mice infected with chikungunya and Mayaro virus survived. West Nile virus and Powassan virus also replicated, or multiplied, more efficiently than the alphaviruses in lab samples of human placental tissue.

Zika, West Nile and Powassan share similarities in their genetic information, Miner says. “So there may be certain features of those virus genes and proteins in that particular family that confers this ability to infect certain cell types.” But scientists don’t understand fully what those features are yet, he says.

While this is the first study comparing the effects in mice of these mosquito-transmitted and tick-transmitted viruses in parallel, Miner says, past studies have raised the possibility of fetal infections with other flaviviruses besides Zika. A 2006 study of 77 pregnant women infected with West Nile virus reported that two had infants with microcephaly, the birth defect lately associated with Zika that results in unusually small and damaged brains.

In general, examining the potential effects of other flaviviruses on pregnant women and their developing fetuses is difficult, because outbreaks have been sporadic and less widespread than with Zika. It’s possible that cases in humans “could go largely unnoticed if we don’t look for them,” Miner says.

A new blood test might reveal whether someone is at risk of getting Alzheimer’s disease.

The test measures blood plasma levels of a sticky protein called amyloid-beta. This protein can start building up in the brains of Alzheimer’s patients decades before there’s any outward signs of the disease. Typically, it takes a brain scan or spinal tap to discover these A-beta clumps, or plaques, in the brain. But evidence is growing that A-beta levels in the blood can be used to predict whether or not a person has these brain plaques, researchers report online January 31 in Nature.
These new results mirror those of a smaller 2017 study by a different team of scientists. “It’s a fantastic confirmation of the findings,” says Randall Bateman, an Alzheimer’s researcher at Washington University School of Medicine in St. Louis, who led the earlier study. “What this tells us is that we can move forward with this [test] approach with fairly high confidence that this is going to pan out.”

There’s currently no treatment for Alzheimer’s that can slow or stop the disease’s progression, so catching it early can’t currently improve a patient’s outcome. But a blood test could help researchers more easily identify people who might be good candidates for clinical trials of early interventions, says Steven Kiddle, a biostatistician at the University of Cambridge, who wasn’t part of either study.

Creating such a test has been challenging: Relatively little A-beta floats in the bloodstream compared with how much accumulates in the brain. And many past studies haven’t found a consistent correlation between the two.

In the new study, researchers used mass spectrometry, a more sensitive measuring technique than used in most previous tests, which allowed the detection of smaller amounts of the protein. And instead of looking at the total level of the protein in the blood, the team calculated the ratios between different types of A-beta, says coauthor Katsuhiko Yanagisawa, a gerontologist at the National Center for Geriatrics and Gerontology in Obu, Japan.
He and his colleagues analyzed brain scans and blood samples from a group of 121 Japanese patients and a group of 252 Australian patients. Some participants had Alzheimer’s, some didn’t, and some had mild cognitive impairments that weren’t related to Alzheimer’s.

Using the ratios, the researchers found that they could discriminate between people who had A-beta plaques in the brain and those who didn’t. A composite biomarker score, created by combining two different ratios, predicted the presence or absence of A-beta plaques in the brain with about 90 percent accuracy in both groups of patients, the researchers found.

The new results are promising, Kiddle says, but the test still needs more refining before it can be used in the clinic. Another wild card: the cost. It’s still not clear whether the blood test will be more affordable than a brain scan or a spinal tap.

AUSTIN, Texas — To reduce your impact on air quality, you might expect to trade in your gas-guzzling clunker of a car — but you can also unplug those air fresheners.

In urban areas, emissions from consumer goods such as paint, cleaning supplies and personal care products now contribute as much to ozone and fine particulate matter in the atmosphere as do emissions from burning gasoline or diesel fuel.

The finding is largely a sign of success, study coauthor Brian McDonald said February 15 during a news conference at the annual meeting of the American Association for the Advancement of Science. Steps taken to clean up car exhaust over the past few decades have had a huge effect, and as a result, “the sources of air pollution are now becoming more diverse in cities,” said McDonald, a chemist at Cooperative Institute for Research in Environmental Sciences in Boulder, Colo.
“When you have a big mountain in front of you, it’s difficult to know what lies behind it,” says Spyros Pandis, a chemical engineer at Carnegie Mellon University in Pittsburgh who wasn’t part of the study. Now, other sources of air pollution are becoming more visible.

The new study, also published in the Feb. 16 Science, focused on volatile organic compounds, or VOCs, that are derived from petroleum. These are a diverse array of hundreds of chemicals that easily vaporize and make their way into the atmosphere. Some VOCs can be harmful when directly inhaled — molecules released by bleach and paint make people lightheaded, for example.

Beyond their immediate effects, VOCs react with other molecules in the air, such as oxygen and nitrogen oxides, to generate ozone as well as fine particulate matter. (Those nitrogen oxides come, in large part, from vehicle exhaust.) High levels of fine particulate matter make it hard to breathe and contribute to chronic lung problems (SN: 9/30/17, p. 18). And while ozone high in the atmosphere helps shield Earth from the sun’s ultraviolet radiation, at ground level, it mixes with fine particulates to form breath-choking smog.

Over a period of six weeks, the researchers collected air samples in Pasadena, located in the notoriously smoggy Los Angeles valley. They also evaluated indoor air quality measurements made by other scientists. The team traced the molecules found in these air samples to their original sources using databases that show the specific volatile organic compounds released by specific products.

Consumer products that emit VOCs have an outsized effect on air pollution, the team found. About 15 times as much oil and natural gas is used as fuel than ends up in consumer products ranging from soaps, shampoos and deodorants to air fresheners, glues and cleaning sprays. And yet these everyday products were responsible for 38 percent of the VOC emissions, the researchers found, while gasoline and diesel emissions accounted for only 33 percent. Consumer products also contributed just as much as fuels to chemical reactions that lead to ozone and fine particulate matter. The emissions from consumer products also dwarfed those from the production of oil and gas, called upstream emissions.
Regulations on VOCs vary by state, but most consumer products are regulated only for their potential contribution to ground-level ozone, not fine particulate matter. This study makes it clear that even though most volatile emissions from consumer products happen indoors, that air eventually gets vented outside, where it can contribute to larger-scale atmospheric pollution in multiple ways, McDonald said.

More work needs to be done to see whether other cities show the same pattern, the researchers add, as well as to figure out which kinds of VOCs might be particularly problematic. Because there are so many VOCs and they all react differently in the atmosphere, there’s still a lot to learn about which might be most likely to form fine particles and therefore be the best targets for reduction.

Part of the challenge with many these volatile-emitting products is that they’re specifically designed to evaporate as part of their job, says study coauthor Jessica Gilman, an atmospheric chemist at the National Oceanic and Atmospheric Administration in Boulder. For some products, like paints, there are low-VOC formulations available. But finding replacements for key ingredients in other products can be hard. Picking unscented versions of personal care products when possible and using the minimum amount necessary can help reduce the impact on air quality.

To play good defense against the next viral pandemic, it helps to know the other team’s offense. But the 263 known viruses that circulate in humans represent less than 0.1 percent of the viruses suspected to be lurking out there that could infect people, researchers report in the Feb. 23 Science.

The Global Virome Project, to be launched in 2018, aims to close that gap. The international collaboration will survey viruses harbored by birds and mammals to identify candidates that might be zoonotic, or able to jump to humans. Based on the viral diversity in two species known to host emerging human diseases — Indian flying foxes and rhesus macaques — the team estimates there are about 1.67 million unknown viruses still to be discovered in the 25 virus families surveyed. Of those, between 631,000 and 827,000 might be able to infect humans.
The $1.2 billion project aims to identify roughly 70 percent of these potential threats within the next 10 years, focusing on animals in places known to be hot spots for the emergence of human-infecting viruses. That data will be made publicly available to help scientists prepare for future virus outbreaks — or, ideally, to quash threats as they emerge.

“It’s ambitious,” says Peter Daszak, president of EcoHealth Alliance in New York City and a member of the Global Virome Project’s steering committee. But it’s more cost effective to head off pandemics than to deal with the aftermath, he says. “We believe we’re going to get ahead of this pandemic threat.”