IPA depicting predicted activation of cannabinoid receptor (CNR1) and estrogen receptor (ESR) pathways in acutely and persistently infected cells at PST-0.

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IPA depicting predicted activation of cannabinoid receptor (CNR1) and estrogen receptor (ESR) pathways in acutely and persistently infected cells at PST-0. IPA depicting predicted activation of cannabinoid receptor (CNR1) and estrogen receptor (ESR) pathways in acutely and persistently infected cells at PST-0. (A) A combined CNR1 and ESR pathway showing that CNR1 was strongly activated and ESR was inhibited to a lesser extent. In these pathways, oncogenes AKT2 and ERRB2, which favors cell survival, were upregulated. (B) In contrast, CNR1 was predicted to be activated to a lesser extent and the oncogene ERBB2 was downregulated in acutely infected cells at 96 hpi. (C) The extent of inhibition of ESR was predicted to be higher in acutely infected cells at 96 hpi than in persistently infected cells at PST-0. Overall, the state of activation of CNR and ESR favored cell survival in persistently infected cells and favored cell death in acutely infected cells. Luwanika Mlera et al. mBio 2016; doi:10.1128/mBio.00314-16