Thinking any and all observed phenotypes are observable phenotypes because of some evolutionary reason. Phenotype X must have an evolutionary advantage! Even if Phenotype X appears detrimental/neutral, if Phenotype X wasnt advantageous, it wouldnt exist, right? Survival of the fittest! Evolution! YAY!!!
No, not always.
Evolution is a dirty, messy process. Sometimes shit just happens. There is no reason. No higher purpose, from deities or evolution. It just happens. Chance.
Viruses are happy to provide us with examples of this. First there was HPV. Now herpes.
HSV-1 activation in the eyes is one of the leading causes of blindness in the US. HSV-1 likes to bounce through the nerves connecting your mouth, nose, and eyes. If it activates in your eyes a few times, shit hits the fan.
Obviously, our corneas are clear. Thats how we can see. But when HSV-1 has been going to town in your eyes, you start getting blood and lymph vessels growing in places that should be clear. Surgery and corneal transplants can clean up the mess a bit, but after the damage is done, it can come back, and having a lot of blood and lymph vessels around increase cornea transplant rejection (an event that is normally pretty rare– you dont even have to genetically match people for cornea transplants).
What is the ‘reason’ for HSV-1 causing blindness like this? It must give the virus some kind of evilutionary/fitness advantage, right? Maybe replicating in the eye causes lots of shedding in tears, and then you wipe your eyes and pick someone elses nose and the virus increases transmission? Or maybe you go blind and you cant work anymore and you can only make money setting up a ‘KISSES $1’ booth in your front yard, thus increasing the viruses transmission?
Or maybe, shit just happens.
Altering blood and lymph vascularture requires activation of a protein, vascular endothelial growth factor-A. Any time your body needs to do that, VEGF-A is called to action. Naturally, VEGF-A is also responsible for the altered blood/lymph vessels resulting from HSV-1 activation.
Turns out, the promoter for VEGF-A kinda looks like the promoter driving the production of HSV-1 early genes. So the HSV-1 transcription factor ICP4 is grabbing onto the VEGF-A promoter, thinking ‘DIRP! I IZ MAKIN MORE VIROOS! DIIIIIIIRP! I IZ HALPING!!’… when it is actually inducing the expression of VEGF-A.
It doesnt ‘want’ to do this. There is no evolutionary ‘reason’ for ICP4 to do this. But when youve got blind molecules operating by sequence ‘feel’ like this, ICP4 cant tell the difference between its promoter and the VEGF-A promoter, leading to a completely unintended side-effect of no benefit to the virus or the host, not negative enough or at the right time to have any effect on transmission of the virus.
HSV-1 leading to blindness is a mess caused by a messy process. An accident of evolution, not an ‘end goal’ of evolution.