Trachoma, a chronic keratoconjunctivitis caused by the intracellular bacterium Chlamydia trachomatis, is the leading infectious cause of blindness worldwide. Repeated episodes of infection cause intense conjunctival inflammation, which can lead to chronic infection and conjunctival scarring, corneal scarring, opacification and, ultimately, blindness. Trachoma disease progression is variable and incidence varies by age and sex. Each individual step and its transition to the next require accumulation of aberrations associated with an intricate network of genes. A better understanding of the molecular etiology and therefore a more effective management of breast cancer requires a systems biology approach as opposed to the classical one gene/one pathway approach. The use of various genomics, GSK1363089 citations proteomics technology platforms and biological systems has provided much insight into these areas. However, understanding disease progression is not without challenges. For example, the study of clinical samples is complicated by cellular, genetic, environmental and treatment heterogeneities. Production of PyMT in transgenic mice or through retroviral delivery has been shown to lead to tumor formation in mammary glands, endothelial cells, liver, and pancreatic exocrine cells. The potency of PyMT is attributed, at least in part, to its ability to activate MAPK and PI3K/Akt signaling pathways. This cytosolic process occurs with the initial conversion of citrate to acetyl-CoA catalyzed by ATP-citrate lyase. In order to avoid excessive host tissue injury whilst protecting effectively against infectious agents, the immune system features regulatory mechanisms to control the production and response to cytokines. The SOCS family of proteins comprises eight members critically involved in this process. SOCS1 and SOCS3 are the best-characterized family members and have both been described to interfere with the response to IFNa. The kinase inhibitory region shared by SOCS1 and SOCS3 is sufficient to inhibit JAK tyrosine kinase activity. In addition, SOCS1 has been proposed to target itself and JAK proteins to the microtubule organizing complex associated 20S proteasome for degradation. Importantly, recent studies have shown that several viruses such as hepatitis C virus, herpes simplex 1 virus, enterovirus and respiratory syncytial virus are capable of inducing expression of SOCS proteins and interfere with the IFN signaling pathway. In the present study, we hypothesized that impairment in IFNa secretion by primary human monocytes infected with EBV involved the activation of SOCS proteins. We tested this hypothesis by examining SOCS1 and SOCS3 expression in parallel with several aspects of the IFNa pathway in infected cells. We showed that depletion of SOCS3 reduced the EBV-mediated suppression of the IFNa pathway and that the EBV protein Zta was implicated in activating SOCS3 expression.