Our experiences of the goings on in our mind tend to paint a less-than-accurate picture of precisely how the mind is structured. Specifically, we tend to consciously experience the functioning of our mind as, more or less, unified; that there’s some “self” running the show, so to speak. There are a great number of theoretical problems with the idea of a self—that I won’t get into here—which has led to a growing conceptual rejection of it. Rather than some unified self processing all sorts of cognitive information, there are thought to be a series of domain-specific cognitive modules performing a variety of independent tasks using unique sets of information. Though the idea of a “self” has been thrown out in favor of, essentially, very many “sub-selves,” there is still some sense in which the functioning of all these different parts can be considered a psychological “you”: the outputs of all these different modules need to be integrated in some way so as to produce behavior, even if they don’t go through a central self. This is just a roundabout way of saying that though one part of your brain might want to stick to a diet and another part might wish to break the diet, you—your body, anyway—can’t do both of these things at the same time.
So we might consider the sum of all these different pieces interacting to be, in some non-technical sense, a psychological “you.” As we’re about to see, however, how precisely we want to define this psychological “you” gets even trickier than that. This is because some aspects of our behavior (and, by extension, our psychological functioning) can be affected by other organisms that happen to be taking up residence in our bodies; organisms that would “prefer” we do things to achieve their evolutionary goals at the expense of our own. This brings us nicely to a recent paper by Adamo et al (2014) examining the sexual behavior of crickets.
The researchers had been collecting crickets for some reason not directly related to matter of pathogens, as far as their paper suggests. However, they eventually noticed that some of the females had stopped laying eggs. When these females were dissected, the researchers noticed that the fatty body inside these females had an iridescent blue sheen. As it turns out, this was indicative of a type of viral infection; it also turns out that this particular virus is spread via sexual contact. Let’s consider the pathogen’s fitness interests for a moment: first, and perhaps most obviously, this virus would prefer that the crickets have sex with some regularity. Since the virus is spread sexually, the more sex the cricket is having, the more opportunities the virus has to find new hosts and reproduce itself. Accordingly, we might imagine that this virus would prefer their hosts are more eager to mate than non-infected crickets.
However, the virus would also prefer that the crickets not behave as if they’re sick. As someone who has just recently recovered from an infection myself, I can attest to the fact that sick animals often behave much differently than healthy ones. Sick animals might try to conserve energy, for instance, opting to spend their energy budget on an immune response to fight off the infection rather than moving around their environment and doing other things. This poses a problem for the sexually transmitted virus, as animals which are conserving their energy budget might not be interested in pursuing mating effort at the same time. So if the virus could prevent this suite of sickness-related behaviors from taking place, it could potentially benefit itself as well.
Now this is all very interesting in the abstract, but is there any evidence that these viruses actually had the ability to manipulate the host’s behavior? Since I wouldn’t be writing about this issue if there wasn’t, yes; there seems to be. Compared to non-infected crickets, the male crickets sporting the infection were quicker to try and court females. In the case of crickets, this means the males started to produce courtship signaling, in the form of “singing,” quicker. Infected males starting singing around 200 seconds after being exposed to females, whereas their uninfected counterparts took a little over 400 seconds to begin the process. Unfortunately for the eager lovers, there also seemed to be pretty good evidence that the virus had a nasty habit of rendering them sterile, so the mating wasn’t doing the crickets a whole lot of good...
That wasn’t the only behavioral effect of the infection observed, though. The researchers also injected healthy crickets and infected crickets with a bacteria that had been killed by heat prior to the injection. While this renders the bacteria relatively harmless to the crickets, their immune system still responded to what it perceived to be a potential threat. Accordingly, the immune response tended to trigger certain sickness behaviors, like not eating and taking longer to try and court females. However, this was only the case the for non-infected crickets, which now took about 800 seconds to begin courting; the infected crickets showed no sickness behaviors when injected with the dead bacteria and continued on eating and mating as they had beforehand.
While it’s not entirely clear whether the sickness behavior was inhibited as byproduct of the virus partially shutting down its host’s immune response abilities more generally or whether the capacity to inhibit the behavior had been directly selected for, the main point doesn’t change: the viral infection seemed to be having an effect on the host’s behavior and, presumably, this effect was at least partially realized through a change in the host’s psychology. While it’s hard for me to say what, if anything, it’s “like” to be a cricket, to the extent that they feel things like hunger or lust, such feelings might well have been modified by the effects of the infection (making them not lose their appetite in the presence of invading pathogens as healthy crickets did, and making them more eager to court females). Indeed, the results of this study appear to be conceptually similar to the paper suggesting that mosquitoes infected with malaria might preferentially feed from human hosts, owing to the pathogen reproducing in humans and being spread by mosquitoes. The more people the infected mosquitoes bite, the greater the chance the pathogen has to spread, and the parasite seems to be able to push its host in the preferred direction.
So while the idea of “the self” is already a theoretical non-starter, even the colloquial sense of the word poses some interesting definitional problems. After all, if we were to label the sum total of the interactions within our brains as “the self” then, in some sense, the effect of the presence of certain pathogens may well be included in the “you” side of this equation, though most of us wouldn’t think of them that way. Some of our preferences are, no doubt, influenced by particular pathogens when they are infecting us, and some of our preferences might also be shaped in a more long-term fashion by the presence of infectious agents present during our development as well. It’s unfortunate that more hasn’t been written about the subject (or at least I haven’t seen too much about it around the psychology departments I’ve been in), as there are likely a great many pathogens that have all sorts of interesting effects on our behavior, from the symbiotes we carry around in body to those trying to make meals of us.
References: Adamo, S., Kovalko, I., Easy, R., & Stoltz, D. (2014). A viral aphrodisac in the cricket Gryllus texensis. The Journal of Experimental Biology, doi:10.1242/jeb.103408