Cytomegalovirus (CMV) belongs to the herpes virus, also known as human herpes virus type 5, more than 90% of our country has been infected with polyherpes virus, but immunocompetent people rarely develop, mainly seen in immunodeficient, especially T-lymphocyte immunodeficient patients onset. The incidence of cytomegalovirus ophthalmia due to post-transplantation hematopoietic stem cells is very low, and the current pubmed search CMV susceptibility factors CMV-negative donors and CMV-positive recipients are susceptible to infection, and CMV-positive donors and CMV-positive recipients can also relapse. 80% of pre-transplant seropositive patients will have viral reactivation, and 20-35% will develop CMV disease, but this can be reduced to 4- 6% with the use of prophylaxis. Failure to recover CD4+ lymphocyte immunity is a risk factor for CMV. Transfusion of CMV-positive blood can be infected, and currently blood banks in some countries test blood products for CMV, which is not yet done in China. CMV prevention Letermovir (Letremovir) prevention effective, more ciclovir can reduce CMV disease side effects are larger, high-dose acyclovir can reduce the onset (Beida People’s Hospital is 0.4bid, out of the warehouse 0.4bid Tuesday, Friday to eat, at least six months of routine prevention, foreign studies have 1, high-dose acyclovir 500mg/m2, from -5 to +30 days, followed by 0.8 orally four times a day; 2, high-dose acyclovir 500mg/m2 for 1 month; 3, 0.4 orally four times a day for 30 days (this is the dose for routine prophylaxis of herpesvirus). Whether Propecia is effective is controversial. In high-risk patients (e.g., donor-negative recipient-positive), 2 weeks of preemptive therapy is urgently needed before transplantation. the CMV vaccine is still in the experimental phase. CMV treatment Both ganciclovir (blood suppression) and sodium phosphonate (nephrotoxicity) are effective in the treatment of CMV, often combined with full dose ganciclovir + half dose sodium phosphonate, or half dose ganciclovir + full dose sodium phosphonate in combination with tolerable side effects at PKUH. The treatment course is usually at least 2 weeks, and the treatment can be stopped when the CMVDNA is negative on 2 retests (2 times a week). A return of positivity after treatment is very common and may be treated again above. CMV antibody propofol is more common for the treatment of CMV pneumonia, but there is less evidence-based medical evidence and less clinical data for the treatment of other organ infections. Cidofovir is only a second-line treatment. Manifestations of CMV retinitis are seen primarily in patients with AIDS, who have severe T-lymphocyte deficiencies, particularly CD4 counts <50 cells/microliter, which can be seen in post-transplant patients. CMV retinitis can result in blurred or lost central vision, dark spots ("blind spots"), miosis, or flashes of light, depending on The anatomical site of retinal disruption and whether retinal detachment has occurred should be evaluated by dilated pupil inspection ophthalmoscopy. Lesions close to or involving the central recess or optic nerve are particularly likely to cause severe visual impairment. Acute vision loss may occur if retinitis leads to retinal detachment. CMV retinitis usually occurs as a unilateral disease, but in the absence of treatment, involvement of the contralateral eye often occurs. Retinal detachment is one of the leading causes of vision loss in patients with CMV retinitis. Although the retina can be surgically reattached, postoperative vision can still be affected. Peripheral (i.e., anterior) retinal lesions are located at the base of the vitreous, where the vitreous is usually attached to the retina. Thus, large peripheral lesions are associated with an increased risk of retinal detachment. Diagnosis of CMV retinitis CMV retinitis is usually diagnosed clinically by an ophthalmologist based on history and characteristic retinal changes [5]. The clinical diagnosis is made by indirect examination of the eye showing yellowish-white retinal lesions with blurred and sometimes granular margins, usually located near the retinal vessels and associated with hemorrhage. In the absence of antiviral therapy, CMV retinitis is associated with mild inflammation of the vitreous; retinitis progresses without treatment, usually within 10 to 21 days of presentation. Depending on a number of factors, including the degree of retinal clouding (whitening), retinal hemorrhage, and the shape and location of the lesion, the lesion can be described as "violent and edematous" versus "inert and granular" [6]. Small lesions may be difficult to distinguish from benign cotton wool spots; therefore, multiple reviews are sometimes required for diagnosis.CMV lesions expand slowly but progressively toward the central recess. Therefore, frequent tests are performed to confirm the diagnosis before starting treatment. CMVDNA and antibody tests are not used for the diagnosis of CMV retinitis, as their accuracy is only 50% [7]. If evidence of CMV nucleic acid is required, treatment is often delayed and complications are increased. CMV-IMMUNERECOVERYUVEITIS (CMV-IRU) After anti-CMV treatment, patients may develop significant intraocular inflammation secondary to immune recovery, known as immune recovery uveitis (IRU).IRU complications account for approximately 50% of vision loss in patients with long-term CMV retinitis and immune recovery [ 10], but IRU has been rarely diagnosed in the last decade and may be associated with missed diagnoses (not yet supported by data). Uveitis is the paradigm term that can include other ocular inflammatory conditions; vitreous inflammation refers to inflammation within the vitreous cavity and is a subtype of uveitis. , IRU (must be inactive CMV retinitis; if CMV is active, this disease is not considered for the time being) is associated with vitreous inflammation with or without macular cystoid edema, preretinal membrane, or retinal neovascularization. Although some patients develop transient vitreous inflammation soon after initiation of antiviral therapy and rapidly return to normal vision. IRU leading to macular edema is often associated with significant loss of vision, despite successful treatment of CMV retinitis. The pathogenesis of IRU is unknown, but may be related to T-cell-mediated immune reconstitution against underlying CMV intraocular antigens. Any patient with a history of immune reconstitution, quiescent CMV retinitis, and new visual symptoms should undergo an immediate ophthalmologic examination to evaluate for CMV progression, recurrence, or immune reconstitution uveitis. On ophthalmologic examination, IRU is characterized by inflammation in the anterior chamber and vitreous cavity and is best diagnosed in conjunction with slit lamp examination and indirect ophthalmoscopy. IRU can develop at any time of antiviral therapy, ranging from weeks to years, and can even occur when CMV retinitis is completely inactive. The initial inflammatory response occurs when immunity returns and then wanes as the retinitis becomes inactive, although persistent low-grade inflammation and complications may persist for several years. Patients may clinically present with vitritis or other manifestations of uveitis, such as anterior chamber inflammation with posterior adhesions, macular cystoid edema, anterior retinal membrane formation, or cataracts. This condition can lead to serious eye disease. Treatment of CMV-IRU If a patient is on maintenance therapy, no modification of the dose of the anti-CMV drug (usually valganciclovir) is required. No restart of ganciclovir or valganciclovir is necessary if the patient with CMV-IRU has completed anti-CMV therapy and there is no evidence of CMV reactivation.The benefit of anti-inflammatory therapy for CMV-IRU has been partially studied, demonstrating the benefit of treatment in patients with CMV-IRU [17,18], but none had a control group and the evidence from evidence-based medicine is less significant. However, given the serious consequences of potentially blinding IRU, the following approaches are often used to manage inflammation: when visual acuity is reduced and vision is symptomatic due to blurred vision, treatment is administered to reduce inflammation in patients with vitreous humor and/or macular edema. ● Topical glucocorticoids (e.g., vinblastine diflucan, etc., one drop four times daily) are first started for six weeks. IOP should be measured at four to six weeks; if it is above the normal range, glaucoma drops may be added or glucocorticoid therapy may be reduced or discontinued; ● If clinical improvement of vitreous inflammation or macular edema with topical glucocorticoids is not evident at six weeks and there is no evidence of secondary glaucoma, switch to posterior subtenon glucocorticoid injections (e.g., 1 mL tretinoin [40 mg/mL] every four to six months). During this period, IOP should continue to be monitored monthly. Treatment may continue as long as symptoms of IRU persist and IOP remains adequately controlled; ● Patients with IRU usually require surgical intervention to remove the cataract within a few years. Less commonly, vitrectomy may be required for patients who present with an anterior retinal membrane or inability to clear vitreous inflammation.