consistent with clinical data indicating a complex pattern of host resistance alterations in social isolates, including increased risk of inflammation-mediated disease [1,2], accompanied by decreased resistance to viral infection [3,4,16,25] and impaired humoral immune response [29]. In addition to providing a molecular framework for understanding the biological mechanisms of social epidemiology [48,49], the present results provide a functional genomic target for the rational selection of biological interventions to remediate those effects. The transcriptional fingerprint of loneliness identified here may also provide a novel genomic biomarker for assessing the impact of such interventions prior to the onset of clinical disease.
