Have at it.

“ID waxing, ND waning.”

I.E., any protein found in the flagellum that the cell ‘could’ use for other purposes means diddly squat. The cell will not put that protein to work as bushings in anticipation that a rod and a shaft will someday be co-opted from a mutation to make a flagellum. Remember ND can’t anticipate. It doens’t have the foresight to do it, it can’t afford the energy cost of storing the protein by setting it in a position that will someday function as the base of the flagellum.

IC is real and Miller’s attempted rebuttals are extremely weak when taken apart. Logic is definitely not ID strong suit.

Keep up the good work! It can only help ID.

I gave some thought to the idea of bacteria serving as a midgut barrier to infection. If the microflora can serve as a physical barrier by activating immune response when bacteria try to escape the lumen/mucosa, then it is plausible that midgut disturbance by pathogens may activate generalist immune molecules (phenoloxidase, lysozyme, antimicrobial peptides, etc.). So “aseptic” mosquitoes, lacking said bacteria, may be more susceptible to infection compared to “septic” mosquitoes, simply because vector pathogens may evade the immune system more efficiently without bacteria present. What this does not explain is the fact that in a variety of different experiments (from other papers as well), in “aseptic” mosquitoes, co-exposure with bacteria+virus elicits a stronger response, i.e. less susceptibility to dissemination compared to those exposed to virus alone. Those bacteria fed to aseptic mosquitoes would not be resident/symbionts, and therefore the physical barrier idea goes out of the window. This suggests, in my opinion, that there may be an additive effect. This is where your idea of cohabitation being “taxing” comes in. Perhaps the virus can effectively evade the immune system of the mosquito as long as everything else is homeostatic. Since the innate response is generalist, maybe any non-self component (such as bacteria) introduced in conjunction with a virus/parasite can elicit a response, resulting in lower disseminated infection. Higher mortality in septic mosquitoes might be due to pathogen overload, too much inflammation to survive. In the case of aseptic mosquitoes, lacking midgut flora may enable them to handle co-infection better since the introduced bacteria would cause an immune response, but to a lesser extent.

I am only dabbling here- but I think an important question is how a mosquito’s innate immune components handle resident microflora compared to introduced bacteria (presumable pathogenic). This gets overwhelmingly complicated by the fact that in a single lab colony there is tons of variation in resident microflora between individuals…

Best of luck with your graduate school quest. I’m sure you’ll have your pick.

It’s cheshire.entomoblog…and the address is hosted by gmail (@gmail.com).