Infection

An Imperiled Indonesian Lizard May Hold The Key To Fighting Superbugs

The military’s Defense Threat Reduction Agency is looking to “extreme animals” such as komodo dragons to find new ways to defend against infections.

Komodo dragons, the 10-foot, 300-pound lizards found in Indonesia, do not bite humans unless attacked, but when they do, it can prove deadly. Not only is the venom in their teeth potentially fatal, they may also harbor bacteria in their mouths that is dangerous to their prey (typically, deer and pigs).

The question of whether Komodo dragons deliver fatal bacterial infections to their prey when they bite has been somewhat controversial: A 2013 study, refuting previously accepted common wisdom, swabbed the mouths of 16 captive Komodo dragons and found they had less bacteria than other predators, such as lions.

Nonetheless, Komodo dragons in the wild eat carrion and live in environments rich in bacteria yet rarely become infected, though local prey such as water buffalo do. And one reason may be because of a special resistance to dangerous bacteria in the form of cationic antimicrobial peptides, a type of protein that fights off harmful bacteria and that researchers have found in the animals’ blood.

“Komodo dragons are known to harbor high levels of bacteria in their mouths. They don’t suffer from negative effects of bacteria in their own mouths,” said Barney Bishop, one of the study’s authors and an associate professor at George Mason University’s chemistry and biochemistry department.

Using the peptide in the dragon’s blood as inspiration, the researchers designed a synthetic chemical called DRGN-1, which imitates Komodo dragon blood.

As superbugs become more resistant to antibiotics, scientists are turning toward bioprospecting ― or looking to nature for potential medicines. In a recent study published in Biofilms and Microbiomes, researchers from George Mason University

The Zika Epidemic Began Long Before Anyone Noticed

Zika virus
Researchers used genetic information from Zika virus (illustrated) to follow its spread among affected regions in South and Central America and the Caribbean.

ON THE MOVE

The Zika virus probably arrived in the Western Hemisphere from somewhere in the Pacific more than a year before it was detected, a new genetic analysis of the epidemic shows. Researchers also found that as Zika fanned outward from Brazil, it entered neighboring countries and South Florida multiple times without being noticed.

Although Zika quietly took root in northeastern Brazil in late 2013 or early 2014, many months passed before Brazilian health authorities received reports of unexplained fever and skin rashes. Zika was finally confirmed as the culprit in April 2015.

The World Health Organization did not declare the epidemic a public health emergency until February 2016, after babies of Zika-infected mothers began to be born with severe neurological problems. Zika, which is carried by mosquitoes, infected an estimated 1 million people in Brazil alone in 2015, and is now thought to be transmitted in 84 countries worldwide.

Although Zika’s path was documented starting in 2015 through records of human cases, less was known about how the virus spread so silently before detection, or how outbreaks in different parts of Central and South America were connected. Now two groups working independently, reporting online May 24 in Nature, have compared samples from different times and locations to read the history recorded in random mutations of the virus’s 10 genes.

One team, led by scientists in the United Kingdom and Brazil, drove more than 1,200 miles across Brazil — “a Top Gear–style road trip,” one scientist quipped — with a portable device that could produce a complete catalog of the virus’s genes in less than a day. A second team, led by researchers at the Broad Institute of MIT and Harvard, analyzed more than 100 Zika genomes from infected patients and mosquitoes in nine countries and Puerto Rico. Based on where the cases originated, and the…

Lungs enlist immune cells to fight infections in capillaries

neutrophils
ON TRACK Neutrophils (red) crawl along the walls of capillaries in a mouse lung (tracks shown in blue). In mice deficient in a key protein, these immune cells couldn’t move as far (left) as those in mice that had the protein (right).

Immune cells in the lungs provide a rapid counterattack to bloodstream infections, a new study in mice finds. This surprising discovery pegs the lungs as a major pillar in the body’s defense during these dangerous infections, the researchers say.

“No one would have guessed the lung would provide such an immediate and strong host defense system,” says Bryan Yipp, an immunologist at the University of Calgary in Canada. Yipp and his colleagues report their findings online April 28 in Science Immunology.

The work may offer ways to target and adjust our own immune defense system for infections, says Yipp. “Currently, we only try to kill the bacteria, but we are running out of antibiotics because of resistance.”

The research uncovers some of the mechanisms that drive the rapid activation of neutrophils, says immunologist Andrew Gelman of Washington University School of Medicine in St. Louis. “This is critical in removing bacteria from sequestered spaces in the lung,” he says.

Generally, clearing bacteria out of the bloodstream falls to macrophages that reside in the liver and the spleen. But macrophages aren’t found in vessels of the lungs. So the lungs’ blood vessel network gives pathogens a place to hide and escape the body’s usual removal efforts.

In…

Common virus may be celiac disease culprit

reovirus
A VIRAL TRIGGER A reovirus (illustrated here) may jump-start celiac disease by turning the immune system against gluten, a new study in mice suggests.

A common and usually harmless virus may trigger celiac disease. Infection with the suspected culprit, a reovirus, could cause the immune system to react to gluten as if it was a dangerous pathogen instead of a harmless food protein, an international team of researchers reports April 7 in Science.

In a study in mice, the researchers found that the reovirus, T1L, tricks the immune system into mounting an attack against innocent food molecules. The virus first blocks the immune system’s regulatory response that usually gives non-native substances, like food proteins, the OK, Terence Dermody, a virologist at the University of Pittsburgh, and colleagues found. Then the virus prompts a harmful inflammatory response.

“Viruses have been suspected as potential triggers of autoimmune or food allergy–related diseases for decades,” says Herbert Virgin, a viral immunologist at Washington University School of Medicine in St. Louis. This study provides new data on how a viral infection can change the immune system’s response to food, says Virgin, who wasn’t involved in the study.

Reoviruses aren’t deadly. Almost everyone has been infected with a reovirus, and almost no one gets sick, Dermody says. But if the first exposure to a food with gluten occurs during infection, the virus may…

Getting dengue first may make Zika infection much worse

dengue antibody and dengue virus
FRIEND OR FOE A dengue antibody (blue, shown bound to a dengue virus protein, red, in this molecular model) can ease Zika’s entry into cells, a new study finds.

Being immune to a virus is a good thing, until it’s not. That’s the lesson from a study that sought to understand the severity of the Zika outbreak in Brazil. Experiments in cells and mice suggest that a previous exposure to dengue or West Nile can make a Zika virus infection worse.

“Antibodies you generate from the first infection … can facilitate entry of the Zika virus into susceptible cells, exacerbating the disease outcome,” says virologist Jean K. Lim. Lim and colleagues report the results online March 30 in Science.

The study is the first to demonstrate this effect in mice, as well as the first to implicate West Nile virus, notes Sharon Isern, a molecular virologist at Florida Gulf Coast University in Fort Myers.

Zika is similar to other members of its viral family, the flaviviruses. It shares about 60 percent of its genetic information with dengue virus and West Nile virus. Dengue outbreaks are common in South and Central America, and dengue as well as West Nile are endemic to the United States.

Exposure to a virus spurs the body to create antibodies, which prevent illness when a subsequent infection with the virus occurs. But a peculiar phenomenon called antibody-dependent enhancement has been described in dengue patients (SN: 6/25/16, p. 22). The dengue virus has four different versions. When a person with immunity to one dengue type becomes sick with another type, the illness is worse the second time. The antibodies from the previous dengue exposure actually help the subsequent dengue virus infect cells, rather than blocking them.

Outcomes of Zika infections for mice depended on whether certain viral antibodies were present in their systems….

How to grow toxin-free corn

transgenic corn infected with fungus
GRAIN TRAINING Genetically altered corn infected with Aspergillus fungus (shown) may be able to prevent the fungus from releasing carcinogenic toxins.

Corn genetically engineered to make ninjalike molecules can launch an attack on invading fungi, stopping the production of carcinogenic toxins.

These specialized RNA molecules lie in wait until they detect Aspergillus, a mold that can turn grains and beans into health hazards. Then the molecules pounce, stopping the mold from producing a key protein responsible for making aflatoxins, researchers report March 10 in Science Advances. With aflatoxins and other fungal toxins affecting up to 25 percent of crops worldwide, the finding could help boost global food safety, the researchers conclude.

“If there’s no protein, no toxin,” says study coauthor Monica Schmidt, a plant geneticist at the University of Arizona in Tucson.

Schmidt and colleagues used a technique called RNA interference, which takes advantage of a natural defense mechanism organisms use to protect against viruses. The researchers modified corn to make it produce short pieces of RNA that match up to sections of an RNA in the fungus made from the aflC gene. That gene encodes the first step of a biochemical pathway that the fungus uses to make the toxins. When the corn’s modified RNAs match up with those of the fungus, that triggers Aspergillus to chop up its own RNA, preventing a key protein, and thus the toxin, from being made.

Then, the team infected both…

For Ebola patients, a few signs mean treatment’s needed — stat

Ebola scorecard
EBOLA BY THE NUMBERS Looking at some key risk factors may help healthcare workers triage Ebola patients.

A new scorecard may help doctors quickly decide who needs additional care to survive Ebola.

In the latest outbreak, which raged in Guinea, Liberia and Sierra Leone from 2014 to 2016, 28,616 people were infected with virus and 11,310 people died. Doctors might be able to improve the odds of surviving by looking for a few warning signs in people who need to be treated more intensively, Mary-Anne Hartley, of the international charity GOAL Global and the University of Lausanne in Switzerland, and colleagues report February 2 in PLOS Neglected Tropical Diseases.

“It can be very difficult to avoid bias when choosing which Ebola patient should be given extra care when you have limited time and resources,” Hartley says. “Should it…

Rapid Ebola test to detect early infection in the works

Ebola virus
TEAM PLAYERS Researchers are designing antibody pairs that can help detect the Ebola virus (shown) sooner.

WASHINGTON — Diagnosing Ebola earlier is becoming almost as easy as taking a home pregnancy test.

Scientists are developing antibodies for a test that can sniff out the deadly virus more quickly and efficiently than current tests, researchers reported February 6 at the American Society for Microbiology Biothreats meeting.

Detecting Ebola’s genetic material in patients’ blood samples now takes a full day and requires access to a specialized laboratory. Simpler and speedier tests are available. They use antibodies — specialized proteins that latch onto and flag virus particles — and work somewhat like a pregnancy test. Within…