Meeting Abstract
Sick animals frequently change their behaviors, exhibiting an array of symptoms collectively called sickness behaviors. These symptoms include increased pain sensitivity, decreased interest in social interactions, decreased food and water intake, and decreased activity. Sickness behaviors are host-induced, i.e., they are not the result of the infectious agent itself. Why would these uncomfortable symptoms have evolved? The operating hypothesis over the last 30 years has been that adopting these changes in behavior leads to increased survival of the host, which is supported by studies of behavioral fever. Recently, however, a novel hypothesis was put forward suggesting that sickness behaviors may have evolved to protect kin. By lowering direct and indirect contacts, sickness behaviors would lower the probability of transmission of a disease to group members, which in many animal societies are close relatives. We tested this “kin protection hypothesis” by combining data from a field and a laboratory experiment using wild house mice (Mus domesticus). In both, we induced sickness behaviors by injection of lipopolysaccharides (LPS). In the field, we used tissue samples from the entire population and genetic markers to determine pairwise relatedness for all possible dyads. By injecting animals in different social groups with LPS or control (saline) we quantified how natural variation in relatedness amongst groups and dyads affected the expression of sickness behaviors. In the lab, we manipulated relatedness by forming social groups in which certain animals had a close kin (a sister) and others hadn’t. Using LPS or control injections we then tested whether having a close kin affected social interactions and visits to shared resources (food and water). Our findings do not provide support for the kin protection hypothesis, helping us better understand why sickness behaviors occur.
