If you make it right, it’ll even float.

Each year, the American Society of Civil Engineers (ASCE) puts on the National Concrete Canoe Competition, for which engineering undergraduates formulate, troubleshoot, sift, mix, and cast concrete canoes. Then they race them.

More than 250 ASCE student chapters from the U.S. and Canada compete in the regional competitions. But the competition is as stiff as the stone they race; only a handful of teams make it to nationals. To win, students must not only craft a stone canoe and paddle it speedily down a river–they also need to earn top scores for the canoe design, technical write-up, and oral presentation.

Wentworth Institute of Technology in Boston, MA made their canoe debut in 2005. They started out with a bang—taking regionals, and winning 17^th place in the national competition. Since then though, it’s been a challenge: in 2006, they took third in the regional challenge and won fifth in 2007. But since then, they haven’t placed.

But this time, headed up by sophomore Joe Jazwicz, Wentworth’s canoe club team is starting earlier, running more cement experiments, and busting out the creativity.

It’s a crew race—engineer-style.

Viruses are mindlessly competent, ruthlessly efficient, and so simple they blur the line between life and non-life. Yet we humans, despite our elaborate nervous systems and thousands of genes, can barely keep pace.

Modern technology has allowed us to begin combating viral infections, but many still afflict our daily lives. These are not necessarily the diseases that overwhelm our news headlines—rather, they’re the chicken pox, the seasonal flu, and the common cold. Sometimes, they’re the viruses we didn’t even know we carried. So how about a moment of respect for these tiny, beautiful plagues of daily life?

The Flu

We’re bigger, brainier, and have technology on our side—but we still can’t stamp out influenza. Every year, those microscopic sacs of 11 genes manage to evade and elude us.

The inner workings of the influenza virus. Photo credit: CDC/Dan Higgins/Douglas Jordan. http://phil.cdc.gov/phil/details.asp

The key to influenza’s repeated success stems from two proteins studding the outside surface of the viral particles: hemagglutinin (H) and neuraminidase (N). When the body mounts a defense against the virus, it remembers those proteins so that the next time, it can catch the virus before it wreaks havoc. Unfortunately for us, influenza has a few tricks up its membranous sleeves. It is advantageously sloppy as it copies and proofreads its genetic material. Sometimes, it sticks adenine where there ought to be a cytosine, or a guanine where there ought to have been a thymine. These little changes add up. By the time the next flu season rolls around, the face of the virus has morphed into something a little less recognizable.

But influenza’s most stunning shapeshifting comes about through a process called antigenic shift. When this happens, the virus shuffles its genetic deck to create a new incarnation of itself, unknown to vaccine-makers and immune systems alike. Shift happens for two reasons: First, influenza viruses store their genetic information not in one long strand, but in eight separate segments. When it infects a cell, those segments are dumped out for replication. Second, some animals—like pigs—can be infected by multiple versions of flu simultaneously, like swine, avian and human. If that happens, and if those viruses all happen to go after the same cell, then they can swap out genetic information and recombine into a whole new strain.

Our T cells never had a chance.

Respiratory viruses have little difficulty getting around, despite their lack of limbs. A sneeze is worth a few million virions.Photo credit: Tim Vickers/CDC, via Wikicommons. http://commons.wikimedia.org/wiki/File:Sneeze.JPG

The Common Cold

Almost everyone in their lifetime will contract some form of the common cold—hence the descriptive common.  Technically though, the ‘cold’ covers a spectrum of minor pathogens. Some people might contract the rhinovirus or maybe the coronavirus. But five to ten percent will get the adenovirus: a misery-inducing, fever-producing virus that just happens to be one of the most studied viral vectors in biomedical research.

Viral vectors provide scientists a chance to turn the table on our microscopic invaders, making them work for us.  In essence, parts of another less manipulable or more dangerous virus like Ebola are inserted into the genetic code of the vector virus. The Ebola-flavored vector enters the body and revs up the host defense system. The end result: immunity not only to those cold proteins, but to those key pieces of Ebola.

There are many faces to the beautifully geometric adenovirus particle--twenty, to be precise. The viral shell is arranged as a twenty-sided icosahedron, made up of an elaborate latticework of about 252 different subunit. Photo credit: CDC/Dr. G. William Gary Jr. http://phil.cdc.gov/phil/details.asp

Lots of viruses can serve as vectors, but the adenovirus holds a special place in the heart of many a geneticist. Of all the vectors out there, the adenovirus genome has been so well picked apart that tweaking its code has become old hat. By now, it has appeared in more human clinical trials than any other vector so far. It’s a small virus, so it doesn’t have as many proteins to compete with the added antigens, unlike the pox or herpes virus vectors. But it’s still large enough to comfortably fit two to three antigens without becoming unstable. The adenovirus also stays in the body for a long time—up to ten days—without necessarily killing all the cells it enters. That means the immune system can take a long, hard look at the foreign antigens.

The Viruses in our Genes

Most diseases make themselves known as they set up shop in a person’s cells. But there’s a class of viruses so indelibly everyday that few people ever realize they’re infected. From conception to death, human endogenous retroviruses (HERV) make up eight percent of our genomes.

Retroviruses act opposite the typical genetic cycle. Instead of transcribing from DNA to RNA to protein, they reverse transcribe their RNA into DNA, and then integrate it into our DNA. In a generic cell, that integration only goes so far. But if the retrovirus happens to infect an egg or sperm cell (and doesn’t kill or cripple the fetus that results from that cell), then its legacy can continue indefinitely. But that said, millions of years spent traveling down our ancestry has rendered most of these now-endogenous retroviruses defunct. It’s as though someone jammed an image into a Xerox machine and let it mash around for a few million years. After a while, the image gets a little screwy. Still, just because they’re defective doesn’t necessarily mean they’re out of the picture. Some retroviruses have been key to our evolution. They’re critical to the existence of the placenta and they maximize how well we digest our starches. But some, like the HERV-K family still produce virus-like particles and proteins. HERV-K members have been found in various cancers, but it’s not clear why yet. In fact, over the years, retroviral genes have been tied to all sorts of problems, including cancers, diabetes and lupus. But again, no one knows for sure whether and how much they cause or exacerbate these conditions.

The Chicken Pox

Up until the 1995 vaccine program went into effect, chickenpox was about as common as puberty. Except that, unlike puberty, it sometimes came back. The virus, varicella zoster, belongs to the same family as genital and oral herpes, but with less stigma. It usually makes a single (spotty) appearance during its host’s childhood, then goes dormant for decades–waiting for an encore. Same virus, different diagnosis: shingles.

How it does this is a bit of a mystery. However, the varicella zoster community has pieced together a tale to the best of their ability, and it goes something like this: As a patient scratches through the throes of chickenpox, th­e virus sneaks through an open sore and hitches a ride back to the heart of a spinal cell. There, instead of going into its usual hijack-replicate routine, it allows the cell’s defense mechanism to kick in. The cell coats the invader with little proteins called histones, which wrap the DNA around themselves so tightly that transcription grinds to a halt. The virus goes dormant.

Nearly a lifetime later though, the virus suddenly revs up the protein-making machinery, hijacks its host, and kicks off a new breakout. The only difference is that this time, the pox only shows up in the one span of skin that the infected nerve covers. Just what sets off this revival remains unclear—it could be old age, or a weakened immune system from disease, or something else. But one thing’s for sure:  it’s the perfect strategy. The virus runs through one generation and then lays low for a few decades. By the time it reactivates, a whole new generation of children await, just yearning to hug their be-shingled grandparents.

Structure of an Ebola viral particle revealed via transmission electron micrograph. Photo credit: CDC/ Frederick Murphy.

It began in Kikyo, a remote village in western Uganda’s Bundibugyo district, during the twilight days of August. People grew ill with headache, fever, bloody diarrhea, and vomiting. Then they died. In mid-November, a young Ugandan doctor named Jonah Kule rode his motorcycle to the village to investigate. Witnesses say he suspected cholera, possibly typhoid. He sent blood samples from patients to international laboratories for testing. On November 29th, the same day that the U.S. Centers for Disease Control (CDC) identified the virus as Ebola, Kule developed a headache and checked into Mulago Hospital. Five days later, he died. That outbreak lasted nearly three more months, officially ending February 20, 2008.

Ebola may have faded from the spotlight of public attention it enjoyed during the mid- 90s, but that doesn’t mean it went away. Quite the opposite: the number of recorded major outbreaks has more than doubled since 2000. Researchers continue to investigate the virus, but licensed therapies and vaccines still escape them. Meanwhile, patient care during outbreaks remains limited, hampered by a lack of detailed clinical information, inadequate resources, and fear.

A complex and lethal virus, Ebola kills up to 90 percent of its victims. Five known strains exist, each named for their place of origin: Zaire, Sudan, Reston, Cote d’Ivoire and—as of 2007—Bundibuygo. Contrary to popular belief, fewer than 50% of Ebola patients experience massive bleeding, says Dr. Thomas Geisbert, Director of the Boston University National Emerging Infectious Diseases Laboratories. The disease actually closely mimics a condition called septic shock: the virus causes excessive clotting, blocking normal blood circulation and exhausting coagulating factors. The blood, with nowhere else to go, damages the internal walls of the blood vessels as it pushes against them from the inside. Major organs, starved of critical oxygen and nutrients, begin to fail.

Two nurses stand by an Ebola victim under their care during the first 1976 outbreak in Kinshasa, Zaire. Photo credit: CDC/Dr. Lyle Conrad, courtesy of wikicommons.

When Ebola first emerged in the summer of 1976, it took the world by surprise. No one knew where it had come from, what it was, or how to treat it. The World Health Organization (WHO) and an international commission descended on outbreak sites in the Sudan and Zaire (now the Democratic Republic of the Congo). Medical personnel quarantined patients and stopped the use of unsterilized needles while investigative teams set out to discover the source of the virus. They never found their answer, but within three months, the outbreaks ended as suddenly as they began. Over the next 20 years, the world watched with horrified fascination as another five major outbreaks erupted in sub-Saharan Africa, infecting 1105 individuals, of whom 802 would die.

Ebola’s macabre effects and unknown origins lent the disease a dark glamour that captured the public’s imagination. In 1994, Richard Preston published his sensationalized account of Ebola’s history, The Hot Zone, which shot to the top of the bestsellers list; a year later, the movie Outbreak fueled the public’s growing fascination with virulent disease. When a major outbreak erupted in Kikwit, Democratic Republic of Congo (formerly Zaire) that same year, Ebola had become if not quite a household word, then certainly a familiar one. Heavy media coverage allowed the public to watch— captivated—as WHO, Doctors without Borders and other organizations again leapt into the fray. But as the virus burned out six months later, the urgency passed and public interest waned. Ebola faded once again into the inscrutable African jungle.

But Ebola has come back. The past nine years have seen more major outbreaks than the twenty years following the virus’ debut. In 2000, the largest outbreak to date occurred in Uganda, killing more than half of the 425 patients over four months. The following October, Ebola appeared simultaneously in Gabon and the Republic of the Congo, lingering in both nations for about seven months. Two more outbreaks occurred in quick succession in the Republic of Congo, and another flared briefly in the Sudan, dying out in the summer of 2004. Then the virus withdrew for three years, before resurfacing in 2007 in Uganda and the Democratic Republic of the Congo. The most recent outbreak, again in the Democratic Republic of the Congo, was declared Christmas day 2008, ending only a few months ago this year in February. Researchers aren’t certain why so many outbreaks have occurred recently. Part of it may be that more healthcare workers are aware of Ebola and more likely to test for it. “I would guess that if you’d looked for Ebola in the Congo in that part of Africa 40 or 50 years ago, you’d have found it,” Geisbert says.

Red Cross members disinfect the body of an Ebola patient during the 1995 Kikwit outbreak. Photo credit: CDC/Ethleen Lloyd.

But some of the rise is likely genuine. Increased logging brings workers deeper into the rainforests and closer to the bats believed to harbor the virus. And should people return to their villages infected, few if any hospitals are equipped to readily counter the virulent fever. War and economic turmoil have decimated what healthcare infrastructure existed in the areas most frequently afflicted with the disease. “It’s hard to understand how they could deal with Ebola in a setting like that,” says Bill Johnston, president of the Jane Goodall Institute, which conducts health and education programs in the Sub-Sahara.

Meanwhile, the hunt for an Ebola vaccine continues. New approaches target specific proteins on the outer surface of the Ebola virus, called glycoproteins, which help the virus attach to and invade cells. The trick is getting the glycoprotein safely into someone’s body and stimulating their immune response enough to build resistance to Ebola. The National Institutes of Health (NIH), CDC, and other research teams shuttle the protein into the body by piggybacking it onto less deadly viruses, like the common cold. The cold virus enters the body and starts replicating, so the person’s immune system mounts an assault not only on the cold, but also on the accompanying Ebola protein. This model looked promising and even passed human safety trials—but 40-60 percent of the world’s population has already had a cold, so their immune systems would remember and destroy that virus before ever addressing the Ebola glycoproteins tagging along. Less common viruses are more effective because they don’t have that problem—but they carry potentially greater risks to immunocompromised patients. (In otherwise healthy people though, these vaccines appear to be safe: earlier this year, after a contaminated needle-stick injury, a Hamburg researcher safely tolerated a glycoprotein vaccine based on the vesicular stomatitis virus, part of the rabies family of viruses). Other avenues target critical genes in the Ebola replication system like VP-30, but that work is still in its infancy. Licensed, FDA-approved Ebola vaccines remain at least several years away, but “this isn’t a function of how brilliant the scientists are that work on it,” warns Dr. Gigi Kwik Gronvall, a Senior Associate at the Center for Biosecurity at the University of Pittsburgh Medical Center. “It’s a function of how difficult the virus is.”

New drug therapies for infected patients are also under development. Unfortunately, like vaccines, these are highly experimental. These newer therapies focus on stopping the excessive coagulation that Ebola causes. If the clots don’t form, then the body’s organs can get the nutrients they need to function, and stopped-up blood won’t leak out of increasingly damaged blood vessels. But even the most successful approaches save only about 30 percent of test monkeys. “There’s never going to be a magic bullet,” Geisbert says.

A doctor cares for an Ebola patient in a Yambuku, Zaire hospital theatre-cum-ICU in the first 1976 outbreak. Photo credit: CDC/Dr. Lyle Conrad.

In contrast to the progress made in laboratories, overall patient survival has remained relatively unchanged. The typical outbreak setting—rural Sub-Sahara—is rudimentary at best. Running water and electricity and even basic medical equipment are rare luxuries. Healthcare workers risk themselves with every patient they treat; a lethal dose of Ebola is as low as one virus particle—a needlestick injury contains many times that amount, says Dr. James Strong, hemorrhagic fever researcher with the Public Health Agency of Canada. Cultural differences add another dimension: indigenous populations fear foreign aid workers, who arrive in protective suits to whisk the ill away to isolation wards. Panicked, many flee—spreading the disease.

Yet inadequate clinical information poses the greatest obstacle to improved care. “It’s like with SARS. Even though any one hospital only saw a few patients, when you put it all together, you can say: here’s what the potassium levels are in SARS, here’s the kidney function.” says Dr. Daniel Bausch, a professor of tropical diseases at Tulane University. But, he adds, you don’t get that if it’s not systematically collected—as is the case with Ebola.

That may change. In the fall of 2006, an international group of experts in hemorrhagic fevers and healthcare met at the Public Health Agency of Canada in Winnipeg to discuss the need for improved care and research during outbreaks. In November of 2008, WHO convened an informal gathering of many of the same experts, including Bausch, to explore the possibility of establishing a clinical outbreak network. The consensus reached emphasized education and information—creating, for example, a standardized data collection strategy that could be implemented across a broad region. When an outbreak ends, researchers can take stock: what was done and what worked. Then experts could devise improved treatment strategies and decrease case-fatality ratios, earning the trust of their patients.

Although WHO’s meeting was purely a preliminary gathering of ideas and opinions, it’s a start. Ebola shows no signs of disappearing anytime soon, and although vaccines and therapeutics will ease the burden, they won’t be available for several years; the practicalities of patient care and research remain a priority. “If you think about it, you’re challenged not only to take care of the patient, but also to learn as much as you can about the disease in the same setting,” Bausch says. “The clinical and the clinical research part of it go hand in hand.”

Every year, billions of frogs disappear, falling prey not to fungal infection or habitat loss but to the massive, international market for frogmeat.

The incredible, edible bullfrog: a species under fryer. Photo credit Alan D. Wils, via Wikimedia Commons. Source: www.naturespicsonline.com, under Creative Commons, Share-Alike license: http://creativecommons.org/licenses/by-sa/2.5/

In Europe and in the occasional U.S. gourmet restaurant, people enjoy their frogs—rather, their frogs’ legs—as delicacies sautéed in butter and garlic. In places like East Asia, South Africa and South America, diners may consume their frogs in soups, as dried snacks, or even blended raw into warm smoothies with honey and aloe. There, frogs are often reputed to boost immune function, energy levels, and even sex drive (hence the nickname, “Peruvian Viagra,” for a pick-me-up drink of frog, bean broth, honey and aloe).

So, is there any truth to frogs’ superfood reputation, or are they just another piece of meat?

Nutritionally, frogs resemble chicken—high in protein and low in fat and calories. Frog meat provides a number of different vitamins and minerals, including selenium, copper, phosphorous, and riboflavin—but again, no more so than a slice of chicken breast.

In certain other ways however, frogs are unique. They secrete antimicrobial chemicals from their skin, many of which battle harmful pathogens like Candida yeast, and bacteria like staph (Staphylococcus aureus), and E. coli (Escherichia coli). The compounds allow the frogs to safely harbor various bacteria without infection—useful for creatures that live in multiple environments, says Alan Richmond, a professor of herpetology at the University of Massachusetts, Amherst. But as a result, he adds, if someone wanted to eat a raw frog (in say, a smoothie), they’d need to skin it first. So it’s unlikely that they’d receive any extraordinary health benefits from the skin secretions.

Sprinkled with parsley, an array of frogs’ legs prepared for barbeque; a feast for humans, but a loss for the species. Photo credit Tomas Castelazo, via Wikimedia Commons, under Creative Commons, Share-Alike license: http://creativecommons.org/licenses/by-sa/3.0/

The interior of a frog, however, may have more to give. Some of the same chemicals found on a frogs’ skin also appear in his stomach, disinfecting their dinners before digestion. Preliminary research from Pukyong National University in South Korea also shows that bullfrog muscle contains an antioxidant on par with vitamins C and E in its ability to protect against oxidative damage. On the other hand, the quantity of these antioxidative and antibacterial compounds in a given raw frog is unlikely to match that which would be isolated, extracted, purified and packed into a pill.

In short, though a frog smoothie may provide a low-calorie, protein-rich snack, it’s unlikely to confer additional benefits beyond an equivalent chicken smoothie with a slice of lemon.