Murine cytomegalovirus localization and uveitic cell infiltration might both contribute to trabecular meshwork impairment in Posner-Schlossman syndrome: Evidence from an open-angle rat model.

As a special type of glaucoma, Posner-Schlossman syndrome (PSS) is characterized by elevated intraocular pressure (IOP) and anterior uveitis. Cytomegalovirus (CMV) anterior chamber infection has now been considered the leading cause of PSS. We used murine CMV (MCMV) intracameral injection to establish a rat model manifested in IOP elevation and mild anterior uveitis, much like PSS; viral localization and gene expression at various time points and inflammatory cell infiltration derived from innate and adaptive immunity were investigated, as well as pathogenetic changes of the trabecular meshwork (TM). The IOP and uveitic manifestations peaked at 24 h post-infection (p.i.) and returned to normal after 96 h; the iridocorneal angle remained open consistently. At 24 h p.i., leucocytes gathered at the chamber angle. Maximum transcription of MCMV immediate early 1 (IE1) was reached at 24 h in the cornea and 48 h in the iris and ciliary body. MCMV localized in aqueous humor outflow facilities and the iris from 24 h to 28 d p.i. and was detected by in situ hybridization, though it did not transcribe after 7 d p.i. TM and iris pigment epithelial cells harboring viral inclusion bodies and autophagosomes were present at 28 d p.i. These findings shed light on how and where innate and adaptive immunity reacted after MCMV was found and transcribed in a highly ordered cascade, as well as pathogenetic changes in TM as a result of virus and uveitis behaviors. • Clinical manifestations similar to PSS are present in the rat model infected with intracameral MCMV. • MCMV localizes in trabecular meshwork, iris and ciliary body and no productive infection was observed after acute infection. • MCMV transcribes in a highly ordered cascade of IE1, E1 and gB in cornea and aqueous humor outflow facilitiesafter entry. • Long-lasting CD8+ T cell responses infiltrate iridocorneal angle and form keratic precipitates after acute phase. • Trabecular cells are impaired morphologically during acute infection and recover cellularity on trabecular beams afterwards. [ABSTRACT FROM AUTHOR]