Social behavior is important for our survival as a species. But social interaction also gives pathogens a chance to spread, and it thereby increases our exposure to infection. Our immune system is a complex defense system that has evolved to protect us from infection. Therefore, it makes sense to assume that our immune system must have developed ingenious strategies to protect us from new pathogens that social interaction has exposed us to.

Evidence of a link between the immune system and our social behavior has been accumulating in the recent years. A direct connection between the brain and the immune system, through lymphatic vessels in the meninges, was recently revealed. It was shown that the immune system can directly affect and even control social behavior and the desire for social interaction because an impaired immunity induced deficits in social behavior. This sounds like a clever preventive self-defense mechanism designed to avoid contagion—in times of poor immunity, our brain gets the message to reduce social interaction and, consequently, exposure to pathogens.

This is a self-defense mechanism that is activated when our body signals a poor immunological status; it’s an internal chemical communication system. But is there an external threat signaling system? The ability to detect and avoid infected individuals would clearly be a great evolutionary asset in strengthening our protection mechanisms. Many animals can detect sickness via odors, leading to a restraint in social interaction, most likely intended to reduce exposure to disease. Do humans have a similar sensory sickness detection system, something that allows us to detect infectious threats in others?

To answer this question, a new study aimed at determining whether humans can detect sickness in others from visual and olfactory cues. Sickness was experimentally induced by the injection of lipopolysaccharide (LPS), a molecule found in the membrane of Gram-negative bacteria that provokes robust immune responses. The activation of immune responses leads to an increase in the production of pro-inflammatory molecules that activate sickness responses and behaviors. It is known that visual cues of sickness, such as redness of the skin, allow us to infer the health of others. But although LPS induces a strong sickness response, its observable effects are subtle, and odor cues are difficult to perceive.

Photos of the face and samples of body odors of both sick and healthy individuals were presented to a group of naive participants while their cerebral responses were recorded using fMRI. These participants were not aware that they would be seeing and smelling sick and healthy people. They were asked to focus on the faces while the odors were also presented and rate how much they liked the person. Faces were also rated on attractiveness, health, and desired social interaction, while odors were rated on intensity, pleasantness, and health. This allowed the assessment of the “liking behavior” towards the faces, an indication of the will to approach and interact with others.

The rating of sick and healthy faces showed that photos obtained during acute sickness were generally considered less attractive, less healthy, and less socially desirable than the faces of participants receiving the placebo treatment. When faces were presented concomitantly with an odor, there was a lower liking of sick than of healthy faces, regardless of the odor presented with the face. Participants were not able to perceive sickness in the odors, nor did they rate sick odors as more unpleasant or more intense than healthy odors. Remarkably, however, faces, were less liked when paired with sick body odor regardless of being sick or healthy.

These results show that we can detect early and subtle signs of sickness in others from both facial and olfactory cues, even just a couple of hours after activation of their immune system. Moreover, fMRI data revealed that visual and olfactory sickness cues activated their respective visual face processing and olfactory sensory cortices, as well as multisensory convergence zones. And even though odors were often too weak to be consciously detected, these olfactory sickness cues still led to activation of the olfactory cortex.

The study also revealed that this perception of subtle cues of sickness leads to reduced liking and decreased will for social interaction. This response may represent a human behavioral defense system against disease. The integration of olfactory and visual sickness cues in the brain may be part of a mechanism designed to detect sickness, resulting in behavioral avoidance of sick individuals, and in avoidance of impending threats of infection.

References

Filiano AJ, et al (2016). Unexpected role of interferon-? in regulating neuronal connectivity and social behavior. Nature, 535(7612):425-9. doi: 10.1038/nature18626

Kipnis J (2016). Multifaceted interactions between adaptive immunity and the central nervous system. Science, 353(6301):766-71. doi: 10.1126/science.aag2638

Louveau A, et al (2015). Structural and functional features of central nervous system lymphatic vessels. Nature, 523(7560):337-41. doi: 10.1038/nature14432

Regenbogen C, et al (2017). Behavioral and neural correlates to multisensory detection of sick humans. Proc Natl Acad Sci U S A, pii: 201617357. doi: 10.1073/pnas.1617357114. [Epub ahead of print]

Shattuck EC, Muehlenbein MP (2015). Human sickness behavior: Ultimate and proximate explanations.Am J Phys Anthropol, 157(1):1-18. doi: 10.1002/ajpa.22698.

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