They’re tiny, brainless and badass. They’re the everyday viruses that send us running to the Kleenex aisle. And at a molecular level, they rock.
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?
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 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.
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.
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.« « Previous Post ~ Love On The Wing| Next Post ~ I Don’t Want No Scrubs » »