Sickness behavior is highly conserved across many species; inflammation causes a variety of physiological and behavioral changes, including lethargy, decreased social behavior, increased anxiety, and anhedonia. Many of these behavioral changes are also present in disorders such as depression and chronic fatigue, which likely have a substantial inflammatory component. While much is known about the physiology of inflammation, further understanding of neural mechanisms driving sickness behavior is still needed. One potential modulator of sickness behavior is arginine vasopressin (AVP), a neuropeptide well known for its contributions to social and anxiety-like behaviors. AVP is expressed in multiple nuclei that regulate behaviors and respond to immune activation. We specifically target AVP cells in three of these nuclei: the paraventricular nucleus of the hypothalamus (PVN), the bed nucleus of the stria terminalis (BNST), and the suprachiasmatic nucleus (SCN) and test their role in regulating sickness behaviors. Using genetically modified mice expressing Cre-recombinase in AVP cells, we selectively ablated AVP cells in these nuclei, followed by tests of lipopolysaccharide (LPS) induced sickness behavior. Our results indicate that PVN AVP cells regulate changes in motivation during sickness and contribute to typical anxiety-like behavior; BNST AVP cells regulate male social behaviors and hedonic behavior in both sexes; and SCN AVP cells regulate anxiety-like behavior and hedonic behavior in both sexes.