I just received a picture message from a cousin. Following an image of her friend’s face, the text reads, “I think this is weird but my friend wants to know: is this herpes?”
My cousin’s friend wants a diagnosis from me, but in all honesty, I can’t give one. Not just because I lack medical training (I’m a virologist), but because I don’t actually know what a cold sore looks like. I do, however, know what a herpes virus looks like on a molecular level. And if my research efforts go well, I will contribute to the public redemption of the “evil” herpes simplex virus – creating a powerful tool in medicine’s arsenal against a variety of diseases.
When most people think about a herpes virus, they typically envision a malicious, minuscule invader. Perhaps it has a toothy grin or maybe a set of horns. If you’ve taken a college-level biology course, you might see a small hexagon with legs. In reality, these nanoscopic pathogens are much more like a highly organized, triple-threat infiltration team. The goal of any herpes virus is to engage a host cell, produce more of itself, and move on to infect neighboring cells.
There are actually eight different herpes viruses which commonly infect humans, all roughly in the same way. The best-known is herpes simplex virus type 1, the mastermind behind cold sores. The first sighting of this herpes virus came in the 1950s, thanks to electron microscopes. Electron microscopy gathers information about a specimen’s appearance by blasting it with a beam of electrons and recording the various signals produced, ultimately creating an image. From experiments like these, scientists determined the herpes virus is spherical with a diameter of 200 nanometers; to put this in perspective, a single strand of hair on your head is 100,000 nanometers in diameter. More importantly, these first images revealed the herpes virus consists of three distinguishable layers.
Each one of these layers carries within it a specific directive to complete the mission of infection. The outermost layer of the herpes virus, called the envelope, is tasked with penetrating a host cell. The envelope is a protective, flexible membrane layer studded with glycoproteins. Glycoproteins pick the host cell’s locked door, allowing the virus inside. The envelope is on a kamikaze mission: once successful, it’s left behind at the cell’s surface.
Loss of the envelope leaves the second layer of the virus, the tegument, exposed to the hostile environment within the host cell. A portion of the tegument layer are hitmen, responsible for silencing any and all obstacles, such as the cell’s immune response. Other soldiers from this layer hijack the cell’s control center – the nucleus – to prepare the cell for viral takeover.
A few members of the tegument are on security detail, personally escorting the third layer, the DNA-containing capsid, to the host cell’s nucleus. Successful delivery of the virus’ genetic information turns the host cell into a herpes virus factory.
Arguably, the delivery of this high-profile package is the most important objective for establishing infection. The capsid is like a ticking time bomb stuffed with highly pressurized DNA. Tightly packed DNA exerts extreme pressure on the capsid from the inside, and the capsid must contain this pressure so the bomb doesn’t detonate before reaching the nucleus. Failure to deposit the viral DNA into the nucleus terminates the operation and infection cannot spread beyond the initial host cell. Successful deployment of the viral DNA into the nucleus kickstarts the assembly of a fresh fleet of virus tasked with the invasion of neighboring cells.
The herpes simplex virus is cunning, efficiently infiltrating the human population. The mission of many research laboratories around the world is to figure out if we can reprogram this virus, dreaming of the day the herpes simplex virus’ ability to proficiently invade human cells is exploited for medical benefit. If we understand the individual pieces involved in building the virus, how they fit together, as well as which weapons are required for infiltration, perhaps we can build a virus of our own. Imagine the world where the herpes virus’ directive has been altered to specifically engage and destroy a cancer cell, or deliver a life-saving gene into a host who’s innate genetics left them wanting.
Sixty years have passed since scientists first captured a portrait of the herpes virus. While that time has afforded the field a clearer picture, we are still fervently trying to figure out this virus’ numerous tricks to outsmart our body’s defenses. We continue to search for understanding, to pull apart the mechanisms of how the herpes virus completes its mission so successfully. So the next time you think about the herpes virus you may still picture a cold sore – or a tiny blob with horns – but I urge you to also imagine a highly sophisticated, microscopic invader full of possibility.
This article began as a class assignment for Skills & Careers in Science Writing, a graduate-level science writing course focusing on building compelling narratives and employing storytelling techniques to illuminate contemporary research. The course is taught by Science in Society and the Medill School of Journalism, Media, and Integrated Marketing Communications at Northwestern University.Read more from our students here.