Intriguingly, in 170-infected animals alone, we observed upregulation of additional pro-inflammatory cytokines and chemokines like CXCL16 that had not been predicted to be active as ligands (Fig. 4G), suggesting a broadening of pro-inflammatory signaling in infection with highly pathogenic Lentivirus. Collectively, these results demonstrate overlapping yet distinct monocyte-to-monocyte communication mechanisms in response to lentiviral variants of different pathogenicity, with highly pathogenic Lentivirus generally inducing a delayed and broader pro-inflammatory communication profile. Here, CXCL16 is linked to infection.