In the early 2000s, initial work on this topic was conducted in animal model systems, such as zebra finch, honeybee, and cichlid, by Gene E. Robinson[1][4] at the University of Illinois among others.
The 23 pairs of DNA molecules called chromosomes contain the approximately 21,000 genes comprising the “human blueprint.” For this blueprint to have any biological affect however, it must be transcribed to RNA and then into proteins.
Genetic expression is far from random, allowing the differentiation and specialization of different cell types with identical genomes.
The pattern of social stress-related changes in gene expression has been termed by Steve Cole and George Slavich at UCLA as a conserved transcriptional response to adversity (CTRA).
Simultaneously, social stress is associated with the down-regulation of anti-viral gene products including interferon type 1 and specific antibody isotypes (e.g. immunoglobulin G).
Concurrently, the down-regulation of anti-viral gene expression leaves the individual more vulnerable to viral infection such as the flu and the common cold.
Several pro-inflammatory gene products, including multiple cytokines, exist in a recursive system wherein their presence promotes their own transcription.
[5] Chronically isolated individuals are also more likely to develop inflammation-related diseases thus providing a plausible biological connection between social variables (e.g. isolation, rejection, social stress, and socioeconomic status) and disease risk and mortality, namely heightened inflammation mediated by differential gene expression.
Simultaneously, chronic social stressors results in the individual being more susceptible to viral infection as a consequence of the down-regulation of anti-viral gene expression.
[15] For example, the subjective perception of isolation is a stronger predictor of pro-inflammatory gene expression than is the objective size of one's social network.