Our Oldest Pandemic is Still Ongoing
Six million years ago, a creature that was not-quite-human but not-quite-chimpanzee got a cold sore. They didn’t know it, but this painful lip blister was caused by an unimaginably tiny germ that would hide in their body until the end of their life – and infect their descendants forever.
This germ is the ancestor of a virus that has tormented humanity ever since. Ancient Greeks used the word “herpein”, meaning “to creep”, to describe how sores caused by this virus slowly spread over skin. This description became the common name for this virus and eventually a taboo - Herpes.
The specific germ I’m describing is Herpes Simplex Virus 1* (HSV-1, which I will just call “herpes”), which causes cold sores on the mouth and sometimes the genitals. This tinier-than-microscopic parasite needs to infect humans to accomplish the most basic tasks of life. Since its first infection in our ancient ancestor, herpes has been wildly successful; it’s thought to currently infect two out of three people worldwide! But its success has come with bad press for two reasons: its association with sexual activity, and the fact that herpes can never be cured.
Outside of a human, herpes is just a packet of chemical instructions called DNA wrapped in a hard shell and greasy overcoat. Alone with no host, the virus can’t make more of itself and will eventually dry out. Its life begins when it sneaks into the tiny factories that make up our bodies called cells. Tinier machines called proteins perform specialized jobs inside these factories to keep the body running. Inside of a lip cell, herpes hijacks our proteins to make millions of copies of itself and ultimately kills the cell by bursting out violently. Our immune system fights back by killing the viruses and the compromised cellular factories. The result of this battle between the virus and immune system is massive lip cells death, causing mouth sores.
A few lucky offspring of the invading virus are spread to other humans through sharing utensils or kissing. Others infiltrate deeper into the original host, in search of a refuge where they can be safe from immune retaliation. The ultimate aim of herpes is certain brain cells, where it stays mostly dormant for rest of the host’s life. Once herpes sets up this silent infection in the brain, it cannot be cured.
How is this possible? In the sanctuary of the brain cell, herpes lies in wait, discreetly using human proteins to keep itself silent until a need to revive arises. Evading our defenses in this way allows herpes to survive as long as our bodies do. For some people, herpes will be silent forever and they won’t know they’re infected. For others, the virus can be triggered by sunburn or stress to once again cause cold sores, frequently in the same spot as the original infection.
What scientists have learned about herpes has led to development of drugs that can block the virus’s ability to copy itself. While these drugs provide welcome relief from cold sores, there is so much more to learn about the about herpes’ double life inside our cells. Just like our not-quite human, not-quite-chimpanzee ancestor, we have we have a long way to go to truly understand a virus that we’ve known for millions of years.
*Note: closely related to HSV-1, Herpes Simplex Virus 2 (HSV-2), hopped from chimpanzees to humans far more recently - 1.6 million years ago. Both viruses cause painful sores, although HSV-2 is more likely to occur on the genitals. HSV-2 infects 13% of the world, far behind its more successful cousin HSV-1.
Hannah Lewis is fascinated by how viruses hijack our cells to cause disease. She is a molecular biology PhD student at the University of Washington studying how Herpes Simplex Virus 1 manipulates proteins that package human DNA.