Uveitis reactivation; decreased vision left eye; Anterior chamber cell; keratic precipitates in the left eye; This case was reported in a literature article and described the occurrence of uveitis in a 70-year-old female patient who received Herpes zoster (Shingrix) for prophylaxis.   The patient's past medical history included anterior uveitis, corneal neovascularization and lipid keratopathy (left eye). Previously administered products included valacyclovir (ten-day course of oral valacyclovir 1000 mg three times daily) and loteprednol etabonate (topical loteprednol etabonate 0.5%).   On an unknown date, the patient received the 1st dose of Shingrix. On an unknown date, 2 weeks after receiving Shingrix, the patient experienced uveitis (serious criteria GSK medically significant and other: serious as per reporter), vision decreased (serious criteria other: serious as per reporter), anterior chamber cell (serious criteria other: serious as per reporter) and keratic precipitates (serious criteria GSK medically significant and other: serious as per reporter). The patient was treated with valaciclovir hydrochloride (Valacyclovir) and prednisolone acetate. On an unknown date, the outcome of the uveitis, vision decreased, anterior chamber cell and keratic precipitates were unknown.   The reporter considered the uveitis, vision decreased, anterior chamber cell and keratic precipitates to be related to Shingrix.  Additional details were reported as follows: This case was reported in a literature article and described the occurrence of uveitis reactivation in a 70-years-old female patient, who was vaccinated with Shingrix (GlaxoSmithKline) for prophylaxis. This case corresponds to case 3 reported in this literature article. The patient had a history of recurrent unilateral anterior uveitis and corneal neovascularization with lipid keratopathy left eye (OS). No information on patient's family history, concurrent condition or concomitant medication was provided. On an unspecified date, the patient received 1st dose of Shingrix (administration route and site unspecified; batch number not provided). The age of vaccination was not provided but it could be 69 years or 70 years. On an unspecified date, 2 weeks after the 1st dose of vaccination, the patient presented with mildly decreased vision left eye. The patient had completed treatment for presumed viral keratouveitis six months prior with a ten-day course of oral valacyclovir 1000 mg three times daily and a tapering course of topical loteprednol etabonate 0.5%. 4 months earlier, the patient's uveitis had been quiescent off treatment, but following RZV, the patient developed 1+ anterior chamber cell and new keratic precipitates in the left eye. The patient was treated with oral valacyclovir 1000 mg three times daily followed by 1000 mg daily and topical prednisolone acetate 1% with return to quiescence six weeks later. The authors commented, "The RZV is an adjuvanted subunit vaccine for immunization against herpes zoster. RZV contains recombinant VZV glycoprotein E and the adjuvant AS01B, which is composed of two immunostimulants: a toll-like receptor 4 agonist (3-O-desacyl-40-monophosphoryl lipid) and a saponin derived molecule QS21 (from the tree Quillaja saponaria). The adjuvant induces an innate immune-cell mediated response, which enhances glycoprotein E antigen presentation to T cells and induces increased production of antibodies and CD4+ T cells specific to the VZV glycoprotein E. Here, we present a spectrum of cases with uveitis activation in patients with previously controlled ocular inflammation following vaccination with the RZV. Viral DNA from previous zoster infection has been detected in corneal tissue up to eight years following the initial clinical presentation with herpes zoster ophthalmicus. One possible mechanism for post-RZV ocular inflammation is that the cell-mediated response to RZV vaccination reacts with this residual viral DNA which results in reactivation of viral keratitis or potentially keratouveitis. We propose this as the possible cause for recurrent inflammation in our third case. The mechanism for reactivation of uveitis in our other two cases is less clear. We hypothesize that in case 1, the patient with longstanding multifocal choroiditis who was controlled on immunosuppression, the upregulation of humoral and cell-mediated responses following vaccination may have resulted in reactivation of immune cells directed against uveal antigens in addition to the desired response against the VZV glycoprotein. The uveitis reactivation in case 2 is consistent with a viral process, particularly given the keratitis. The underlying etiology may be a failure of vaccination since the patient's prior uveitis presentation, which was a bilateral process without keratitis that was well controlled with short courses of topical corticosteroids, was not consistent with a viral etiology. Despite the possibility of uveitis reactivation following RZV, RZV vaccination is an important component of preventative health. The presented cases should not deter patients and physicians from recommending the RZV vaccine; RZV is efficacious in preventing herpes zoster and postherpetic neuralgia. Rather, this report highlights the importance of ensuring primary care providers are aware of a patient's history of immune-mediated eye disease. We recommend that patients with a history of uveitis discuss plans for RZV vaccination with their ophthalmologist and primary care provider in advance, so appropriate post-vaccination ocular monitoring occurs." The authors concluded, "Uveitis recurrence is an infrequent but serious potential ocular side effect of recombinant zoster vaccination. Reactivation of uveitis is an uncommon complication of RZV vaccination." This is 1 of the 3 valid cases reported in the same literature article.; Sender's Comments:  US-GLAXOSMITHKLINE-US2021GSK140934:Same reporter