Spring and summer bring runny noses, sore throats and lost productivity to the many individuals who suffer from pollen allergies. Perhaps though there is a selective advantage for pollen allergy suffers. By increasing mucus production for a few months a year, soft tissue surfaces inside the noise and throat might be a more hostile place for entry by viruses and other diseases.
An additional thought I have been pondering is perhaps that diseases which share antigens with readily available airborne substances also increase their chance of evading detection for a longer period of time, establishing a greater foothold in their host and spreading to more hosts than previously possible. This would render it a selective advantage for these bugs to look, molecularly, like pollen. Of course once the body has wised up to this ruse and mounted its immune response, it is highly likely it will have also now developed a pronounced immune response to the pollen’s antigens that the original – now long gone – bug was impersonating, or imantigenating / immoleculating (as you wish).
The eye may be the window to the soul, but the nose is the door to the brain. The blood-brain barrier can be bypassed; inflammation in the nasopharynx could disrupt the epithelium and allow neurotropic pathogens to access the olfactory nerve, and therefore the central nervous system. I imagine there might be a selective advantage for any pathogen which is able to access an immune-privileged site, or even use neurotropism as a means by which to influence host behaviour.