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6 Things You Might Not Know About Ebola

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More than 3300 people have died of an Ebola outbreak in Africa, and now, the virus has made the jump to United States: In Dallas, Texas, 100 people who came in contact with a Liberian national who has the disease have been quarantined. Here are some things you might not have known about the haemorrhagic fever.

1. It’s not even alive.

The criteria to be considered a living organism includes being able to eat and to reproduce on your own. Ebola can reproduce aggressively inside an infected host, but it needs to insert itself into the host cells to do it—no host cell, no more new viruses. (Just don’t call it a prion: bits of protein that influence other proteins to adopt their misshapen forms, causing diseases. Ebola has genetic material held inside a protective protein coat, while prions don’t.) Ebola doesn’t metabolize anything on its own, either, making it not dead but not really alive. Ebola is something like a zombie—a bundle of genetic programming with replication skills and bad intentions.

2. This is not the first U.S. outbreak.

There’s a whole family tree of Ebola. There are 5 species that have been identified, each named after the place they sprung up: Zaire, Bundibugyo, Sudan, Reston and Taï Forest. The current outbreak is the Zaire strain—which is creepy because the crisis is not in Zaire. The Reston subtype is named after a town in Virginia, where an outbreak occurred in 1989, followed by incidents in Texas and Pennsylvania. These all had one thing in common: infected monkeys exported by a single facility in the Philippines. These outbreaks are different than the current patient in Dallas for one big reason: No humans suffered illness in any of the previous cases.

3. It has a military mindset for invasion.

Researchers are finding out just how clever Ebola is as they reveal some of the virus' murderous Modus Operandi. One key to its lethal success is the stealth way it shuts down immune system defenses, the same way an air force will disable air defenses before sending in the bombers. Ebola obstructs parts of an immune system that are activated by molecules called interferons. These interferons have a vital role in fighting Ebola, usually with scorched earth tactics. “It makes a variety of responses to viral infection possible, including the self-destruction of infected cells,” says Christopher Basler, professor of microbiology at Mount Sinai and co-author of recent studies done by a consortium of Ebola researchers. That group also said, in a paper published in the August 13 edition of the journal Cell Host & Microbe, that they figured out exactly how Ebola craftily disables signals the cells use to defend against attack: An Ebola protein called VP24 binds to a specific protein that takes signaling molecules in and out a cell’s nucleus. Without communication, the cell can’t call for help or kill itself. The virus then hijacks the cell, uses it to make more viruses, and spreads them to more cells. Next thing you know, the infected victim is bleeding from every orifice.

4. No one knows how it came to infect people.

There is a lot we think we know about Ebola’s origins. For starters, human beings are not its natural host, what epidemiologists charmingly call a “reservoir.” Scientists believe that Ebola’s reservoirs are fruit bats. Infected bats can pass the virus to a bunch of other mammals, like rats, primates, and other bats. No one is sure how people became exposed to Ebola, but the best guess is that the monkeys were the conduit. Local hunters in Africa likely became infected while butchering the animals. Anyone who became sick likely infected their family and, if hospitalized in an unsanitary facility, other patients.

5. Gumshoe detective work is the only way to stop an outbreak.

For all the biotech and medical savvy, it takes the investigative skill of a homicide detective to stop an outbreak. Professionals call it “contact tracing,” but it’s really man hunting. Here’s how it works: Ebola victim A is isolated and interviewed. Anyone who had close contact with A is put into isolation for 21 days. (In Texas, there are emergency medical technicians in this quarantine limbo right now.) If they exhibit no symptoms, they’re free to go. If they come down with Ebola, they become victim B, and another contact trace begins. If the investigators miss anyone, the outbreak will continue. The CDC even put out a cool poster of the process.

6. You can order it from a catalog.

The home page of BEI Resources has an interesting tab that reads “Ebola reagents available.” With a couple of clicks of the mouse, you reach a catalog of infectious disease materials available for order. Just what is going on here?

The National Institute of Allergy and Infectious Diseases (NIAID) has set up BEI to make sure research facilities have access to microbiological materials that can help them develop diagnostics and vaccines for emerging diseases. Scientists must be registered with BEI to request materials. The real key here is the word “reagent,” which means the virus is not an active threat. For example, they have Gamma-irradiated Sudan Ebola virus that has been spun in a centrifuge to separate out cell fragments. Reagents won't spread, but they can serve as stand-ins during the development of tests. (On the Biosafety Level, or BSL, scale—which ranks the severity of infectious disease and sets baselines of which safety protocols need to be enforced to work with them in a lab—reagents are treated at Biosafety level 1; Ebola is a BSL-4, the top of the scale for risky bugs.) The best part of the catalogue is the disclaimer: “BEI Resources products are intended for laboratory research purposes only. They are not intended for use in humans.”

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Medicine
New Technique Can Spot a Heart Attack in the Making Long Before It Happens
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Cardiology experts have developed a noninvasive way of measuring the fat around a person's blood vessels, which could help determine their risk for dangerous cardiac events. The researchers described their technique today in the journal Science Translational Medicine.

Heart attacks are incredibly common, affecting around 750,000 Americans every year. Heart disease is the number one cause of mortality in the U.S., responsible for one out of every four deaths. There are many reasons for this. Among them is the difficulty of identifying at-risk patients before it's too late.

Cardiologists' current method of choice uses a metric called coronary calcification score (CCS) to measure the hardening of a patient's arteries. CCS is a reliable way to predict future heart problems, paper co-author Charalambos Antoniades said in a statement, but it has its limitations.

"When coronary calcification is detected," he said, "it is already too late, as the calcification is not reversible."

And so, rather than measuring calcification, many researchers have begun looking for a way to measure blood vessel inflammation, which is usually a pretty good—and early—predictor of heart disease.

The inflammation itself can be hard to see without entering a patient's body. But recent studies have shown that it rarely travels alone: Blood vessels that are inflamed are also often wrapped in larger fat cells than healthy vessels. 

With this link in mind, Antoniades and his colleagues decided to try measuring the fat cells instead. They reviewed computed tomography scans from 453 patients about to undergo heart surgery, and used these data to create what they call the fat attenuation index (FAI). The higher a patient's FAI, the more inflammation they had, and the more advanced or severe their heart disease. 

The researchers then compared the FAI of 40 additional patients with the results of invasive scans of the inflammation in their hearts. Sure enough, each patient's FAI matched the swelling onscreen.

There are many benefits to using FAI, the authors say. Not only is it noninvasive and accurate, but it can be used in tandem with CCS and other methods for an even more complete picture. The next step will be validating the test's safety and accuracy in clinical trials.

FAI scans "could help direct these new types of treatments to the appropriate subgroups of patients at greatest risk," Antoniades says, "reducing costs and targeting more powerful drugs to the patients who will benefit most."

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Health
Don't Panic About the Plague
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If reports of measles and whooping cough making a reappearance aren't alarming enough, the news that three people in New Mexico have contracted plague this year might have you on edge. But these aren't the only recent cases of plague in the state—the disease appeared in both 2016 and 2015, causing one death—or even in the U.S.

In 2015, a child contracted the plague in Yosemite National Park, and so did a tourist from Georgia; park officials closed a campground where they discovered two dead squirrels infected with the disease. That same year in Colorado, a pitbull infected four humans with pneumonic plague before being put down, and two other Colorado residents died from plague, including a 16-year-old boy.

It all seems very scary, but don't go sealing yourself in protective gear yet. There's less to fear about plague than you may think. While the public is prone to panic that a medieval illness, which wiped out a quarter of Europe in the Middle Ages during the Black Death, has suddenly arisen from obscurity, the truth is: Plague never left.

Though we haven't seen a widespread epidemic of plague since the early 20th century, thanks to advances in sanitation and medicine, and there hasn't been a human-to-human case of transmission in America since 1924, an average of seven new cases are reported every year in the U.S. From 2010 to 2015, there were 3248 cases, including 584 deaths, reported worldwide, according to the World Health Organization.

Yersinia pestis, the flea-borne bacteria that's most often responsible for plague, infects rodents; humans are “incidental hosts,” who can acquire the infection if bitten by an infected flea or rodent. Compared to the 14th century, when the Black Death spread wildly, or the late 19th century, when 10 million people died of the disease after it traveled from Hong Kong to port cities worldwide, most people today live in more sanitary conditions and have less frequent contact with the rodents most likely to carry the infected fleas. Today, 95 percent of plague cases originate in parts of sub-Saharan Africa and Madagascar.

The most common of the three strains of plague is the notorious bubonic plague, which causes painful swollen lymph nodes (also called buboes) and was responsible for Europe's Black Death—so named because internal hemorrhages caused by the infection make the skin appear black. But the pitbull that infected four Colorado residents carried the rarer respiratory strain of pneumonic plague, which is contagious when the infected person coughs up infected particulates. There is also septicemic plague, the most lethal form, which infects the blood, and most often occurs when plague virus has gone undetected and is allowed to spread.

In the U.S., you're generally only at risk of contracting plague in late spring to early fall if you've been in a rural or semi-rural area of the West, especially New Mexico, Arizona, or Colorado, and have had contact with fleas or rodents including ground squirrels, chipmunks, prairie dogs, or rats. And even then, the risk is low.

Only the pneumatic version of plague is contagious from human to human (though untreated bubonic plague can become pneumonic), but you have to be coughed upon, or receive fluid from an infected person upon an open wound or directly into your mouth or nose.

Plague symptoms mimic any flu—fever, chills, headache, difficulty breathing or coughing—but people have been known to cough up blood with the pneumonic variety. If you've been in a rural area, or camping, and come down with these symptoms two to three days later, it's best to go to a hospital.

Now for some good news: While untreated plague is quite deadly, people with plague who are treated with antibiotics within 24 hours of infection have strong recovery rates.

So while it's good to be aware and take precautions, the chances of another plague pandemic remain slim.

This story was originally published in 2015 and has been updated. 

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