https://www.wired.com/story/the-complex-social-lives-of-viruses/
Some folks know that my college major was biochemistry and molecular biology. I studied P4 bacteriophage for my undergraduate thesis and loved the elegant ways our methods in the 1980’s were able to detect, slice and manipulate genes to study their structure and function.
P4 was a tiny virus that often required the help of P2 “helper” bacteriophage to replicate. Only when they co-infected an E coli bacterium together were P4 viruses able to replicate.
Now, decades later, there is a blossoming of scientific work on “sociovirology” or the social lives of viruses, with “cheater” viruses a dominant player. Sometimes a virus will erroneously break apart into fragments of DNA, missing key components like genes that encode capsule proteins needed to assemble into a virus for the next infection, or a polymerase protein that helps replicate the DNA. One would think that such “defective” or “incomplete” virus DNA fragments would then die out.
Never fear. If the “incomplete” or “cheater” virus DNA lays dormant inside a bacterium, it can wait for an intact virus to infect the same cell, and then hijack or borrow the polymerase or capsule proteins from the intact virus to package itself into infectious virus particles for the next infection. IN FACT, because the “cheater” virus DNA is shorter, it has a major advantage of speed in replicating: takes less time to copy itself. As a result, as the co-infection proceeds, more copies of the shorter “cheater” virus are made than the intact virus purely due to the length of the DNA strand to be copied. Thus, when the bacterium eventually “explodes” because it is full of viruses, there are more “cheater” viruses than intact viruses floating around looking for the next bacterial victim(s)
This causes all sorts of weird social effects. Read the article at Wired.
It is this sort of discovery and fascinating biology that keeps me humble in our work with mere humans.
