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Fig. 4 | Genome Medicine

Fig. 4

From: Evidence from genome wide association studies implicates reduced control of Epstein-Barr virus infection in multiple sclerosis susceptibility

Fig. 4

Model of LCLeQTL* gene roles in Latency III signalling pathways. Signalling from EBV proteins LMP1 and LMP2 leads to upregulation of NFKB, sumoylation, and mTOR1 pathways and altered IFN regulation. LCLeQTL* genes with roles on these pathways are in red. Signalling from the LMP1 homologue and MS risk gene CD40 inhibits LMP1 function (see Fig. 1). For similar reasons, signalling through the BCR, in this model, blocks LMP2 pathways. Arrows indicate proposed effect of signalling through LMP1/LMP2 on each of the downstream processes

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