Friendly fire

April 19, 2021

Frequent use of the term “friendly fire” has caused me some discomfort. I imagined it was a recent journalistic creation, but I was wrong. According to an essay published by the Poynter Institute, the term was first used during WWI. Author Roy Peter Clark wrote, “It is used accurately only when it describes a force shooting at the enemy but hitting your own forces or allies.” ( Clark also reviewed some history and opined that the alliterative expression has contributed to its widespread recognition such that explanations of the two words are no longer necessary. He goes on to say that the term has been used metaphorically in a variety of non-military contexts.

I am adopting the term to explain how a simple virus can inflict so much damage to a complex organism. Viruses are merely strands of nucleic acid residing within a lipid bubble. They have no ability to do anything other than their evolutionary mandate to survive and reproduce. They float in the air or lie on a surface until they can attach to living tissue that can serve as its factory for replication. To employ another metaphor, viruses are akin to a small bit of script that takes over a printing press and prints multiple copies of itself. Ultimately the factories can be destroyed and copies of the original are released into the ether to lie in wait for another cell to occupy.  

To survive and reproduce, a virus requires a living host. Injuring or killing the host is not advantageous to the virus. In most instances viral infections are harmless and of benefit to both the virus and its host. Over time, lethal or harmful viruses mutate such that the surviving prototype is more contagious but less harmful to its living factory. So why is the novel coronavirus causing so much damage to human beings? It is likely that much of the harm to humans is a result of our own “friendly fire.” Lewis Thomas advanced this concept brilliantly in an essay titled “Germs” published in his 1974 book The Lives of a Cell. Addressing bacterial infections as models, he wrote, “Our arsenals for fighting off bacteria are so powerful, and involve so many different defense mechanisms, that we are in more danger from them than from the invaders.”

Our immune “system” is impressive. The understanding of the many facets of a complex organism’s abilities to fend off invaders has advanced rapidly over the last century. Giant leaps were catalyzed by the AIDs pandemic. The ability to attack pathogens is complex and disparate. It might be better to refer to our array of protective weapons rather that our immune system. In any case, the entry of foreign bodies, especially those containing nucleic acids, into our physical space is vigorously resisted. Unfortunately, some of the defending units can be misdirected causing harm to the host that produces them. Autoimmune disorders such as rheumatoid arthritis and lupus are known to be caused by misdirected natural defenses. The reason that autoimmunity occurs is often not known, but it is likely that viral infections are one of the stimulants.

Counteracting our friendly fire is a complex challenge. As medical students in the 1970’s it was suggested that antibiotics were relatively impotent weapons to fight off invading bacteria. The drugs only worked well because of support from a body’s internal weaponry. Disabling some of the facets of our protections can be done, but employing such measures is perilous. I suspect counteracting the pathologic effects of COVID 19 will require modifications of our defense mechanisms. Meanwhile, it remains advisable to wear facemasks, maintain a reasonable social distance and promote vaccinations.           

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