TLR9 and Epstein-Barr virus infection: The −1237 was also identified by our group as being the site of interaction in which nuclear factor-κBp65/ERα suppressed TLR9 transcription and thus IFN production.20 Earlier findings from our team revealed that Epstein Barr virus infection of primary B cells led to a decrease in TLR9 mRNA levels, which became increasingly distinct upon immortalization, signifying that the reduction in TLR9 expression may be linked to cellular transformation (19).