Ocular Manifestations of HIV

Koushik Tripathy; Kaberi Feroze; Jim Wang

Ocular Manifestations of HIV

Author: Koushik Tripathy Author: Kaberi B. Feroze Editor: Jim Wang Updated: 9/14/2025 6:39:27 PM

Introduction

HIV is a retrovirus that causes a multisystemic disease called AIDS. On June 5, 1981, the Centers for Disease Control and Prevention (CDC) published a report in the Morbidity and Mortality Weekly Report detailing cases of Pneumocystis carinii pneumonia in 5 previously healthy young men in Los Angeles, California. These cases, involving men who have sex with men, were later identified as the first reported instances of AIDS in the United States.[1][2] Ocular manifestations are commonly observed in patients with HIV infection.[3] Opportunistic infections, vascular abnormalities, neoplasms, neuro-ophthalmic conditions, and adverse effects of medications can cause ocular involvement in patients with HIV infection.[4]

Etiology

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Etiology

HIV is a retrovirus that replicates in CD4 T lymphocytes.[5] Transmission occurs by exposure to blood and other body fluids.[6] HIV is commonly transmitted through anal or vaginal intercourse or by sharing needles, syringes, or other equipment used for drug injection.[7] The CDC categorizes HIV infections into 3 stages as follows:

Stage 1 (acute HIV infection): HIV levels are high in the blood, making individuals very contagious. Flu-like symptoms are common.
Stage 2 (chronic HIV infection, asymptomatic HIV): The virus remains active but may not cause symptoms. Individuals can still transmit HIV. Treatment can prevent progression to stage 3, but without it, this stage can last over a decade.
Stage 3 (AIDS): The most severe stage, diagnosed when CD4 cell counts drop below 200 or when opportunistic infections occur.[8] Individuals have weakened immune systems and a high viral load. Without treatment, the typical survival time is approximately 3 years.[8]

The World Health Organization (WHO) classifies HIV/AIDS in adults and adolescents with confirmed HIV infection into 4 clinical stages as follows:[9][10]

Clinical stage 1 (asymptomatic): Patients may have persistent painless generalized lymphadenopathy with enlarged nodes >1 cm in 2 or more non-contiguous sites (excluding inguinal) for 3 months or more without a known cause.
Clinical stage 2 (mild symptoms): The symptoms include moderate unexplained weight loss (<10% of presumed or measured body weight) and herpes zoster.
Clinical stage 3 (moderate symptoms): The features include unexplained severe weight loss (>10% of presumed or measured body weight) and pulmonary tuberculosis (TB).
Clinical stage 4 (severe symptoms): The stage includes AIDS-defining illnesses, including:
- HIV wasting syndrome
- Pneumocystis jirovecii pneumonia
- Recurrent severe bacterial pneumonia
- Chronic herpes simplex infection (orolabial, genital, or anorectal of >1 month in duration or visceral at any site)
- Esophageal candidiasis (or candidiasis of trachea, bronchi or lungs)
- Extrapulmonary TB
- Kaposi sarcoma
- Cytomegalovirus (CMV) infection (retinitis or infection of other organs)
- Central nervous system (CNS) toxoplasmosis
- HIV encephalopathy
- Extrapulmonary cryptococcosis, including meningitis
- Disseminated nontuberculous mycobacterial infection
- Progressive multifocal leukoencephalopathy
- Chronic cryptosporidiosis
- Chronic isosporiasis
- Disseminated mycosis (extrapulmonary histoplasmosis and coccidioidomycosis)
- Lymphoma (cerebral or B-cell non-Hodgkin)
- Symptomatic HIV-associated nephropathy or cardiomyopathy
- Recurrent septicaemia (including nontyphoidal Salmonella)
- Invasive cervical carcinoma
- Atypical disseminated leishmaniasis [9]

Some studies suggest that an HIV test should be requested if there is atypical, bilateral, treatment-unresponsive ocular toxoplasmosis or suspicion of CMV retinitis.[11]

Table 1. Ocular Manifestations of HIV Infection

Category	Disorders
Orbit	B-cell lymphoma Cellulitis, including fungal and contiguous sinus infections
Eyelids	Blepharitis Molluscum contagiosum Kaposi sarcoma Herpes zoster ophthalmicus
Conjunctiva	HIV-related conjunctival microvasculopathy (up to 80%) Kaposi sarcoma Solitary granulomatous conjunctivitis Ocular surface squamous neoplasia
Cornea	Keratoconjunctivitis sicca (dry eye) Keratitis, including herpes simplex, herpes zoster, microsporidia, and fungus
Uvea	Uveitis due to infections, including tuberculosis, syphilis, and acute retinal necrosis Drugs, including cidofovir and rifabutin
Retina	HIV-related retinal microangiopathy CMV retinitis Acute retinal necrosis Progressive retinal necrosis Syphilitic posterior uveitis Toxoplasma retinochoroiditis Candida retinitis
Choroid	Pneumocystis choroiditis Tuberculous choroiditis Histoplasma chorioretinitis Cryptococcus choroiditis
Neuro-ophthalmic	Optic neuritis Optic atrophy Cranial nerve palsy (typically due to opportunistic infections of the brain or meninges, such as toxoplasma, syphilis, cryptococcus, or malignancies, including lymphoma)
Neoplasia	Kaposi sarcoma of the orbit, eyelid, or conjunctiva Lymphoma of the orbit, adnexa, or posterior segment Squamous cell carcinoma of the conjunctiva
Immune recovery uveitis	Anterior uveitis Vitritis Cystoid macular edema Retinal vasculitis Epiretinal membrane due to recovery of the immune response after HAART
Adverse drug reactions	Uveitis due to rifabutin or cidofovir Peculiar patchy areas of peripheral chorioretinal atrophy due to didanosine Maculopathy and macular outer retinal atrophy due to ritonavir Visual hallucinations in the first weeks of starting efavirenz [12] Stevens-Johnson syndrome [13]

Abbreviation: CMV, cytomegalovirus; HAART, highly active antiretroviral therapy.

Epidemiology

According to the WHO, globally, 39.9 million (36.1-44.6 million) people were living with HIV at the end of 2023.[14] An estimated 0.6% (0.6%-0.7%) of adults aged 15 to 49 worldwide are living with HIV, although the burden of the epidemic continues to vary considerably between countries and regions.[14] The WHO African Region remains most severely affected, with 1 in every 30 adults (3.4%) living with HIV, and accounting for more than two-thirds of people living with HIV worldwide.[14] In 2023, an estimated 630,000 people died from HIV-related causes, and an estimated 1.3 million people acquired HIV.[14] In 2023, 1.4 million (1.1-1.7 million) children younger than 15 were infected with HIV.[15]

People living with HIV globally develop ocular complications in approximately 70% to 75% of cases, with incidence closely linked to CD4+ T-cell counts and antiretroviral therapy (ART) access.[16][17] HIV retinopathy is the most common ocular finding in patients with HIV infection.[18] In developing countries, 5% to 25% of people living with HIV may experience blindness.[19][20][21][22] Diseases of the retina and choroid are common in patients with HIV infection, and they may cause visual loss. In the pre-highly active ART era, CMV retinitis was the most prevalent sight-threatening ocular infection, affecting 25% to 42% % of patients with AIDS.[23][24][25] For patients who have CD4+ T-lymphocyte counts below 50 cells/μL, the rate of CMV infection was 0.2 cases per person-year.[23][25] However, with the widespread availability of HAART, the incidence of CMV retinitis has declined significantly to around 5.6 cases per 100 person-years.[23][26]

Pathophysiology

HIV is a retrovirus that contains the reverse transcriptase enzyme, enabling the conversion of RNA into DNA.[27] HIV is classified into HIV-1 and HIV-2 based on genetic and antigenic characteristics.[28] HIV-1 is the most prevalent worldwide and consists of various groups, including M, N, O, and P.[28] In the United States, group M, serotype B is the most common variant of HIV-1.[29] HIV-2 is common in West Africa.[28] HIV affects cells that express CD4, including T-helper cells, macrophages, astrocytes, and dendritic cells. The co-receptors for the virus on the cells include chemokine receptor 5 and chemokine receptor 4, also known as fusin.[30] In HIV infection, the selective destruction of CD4+ helper T lymphocytes leads to an inverted CD4+/CD8+ ratio of less than 1 (normal value 1-3).[31]

Ocular involvement in patients with HIV infection occurs most commonly due to direct infection by HIV, opportunistic infections, neoplasms, and adverse reactions to therapy.[32][33][34] Direct HIV infection of the vascular endothelium, immune complex deposition, or increased plasma viscosity can lead to microangiopathy that results in HIV retinopathy and HIV-related conjunctival microvasculopathy.[35]

Opportunistic infections such as CMV retinitis occur with a significantly reduced CD4 T-cell count and are one of the common causes of blindness in patients with HIV infection. Ocular infection in these immunosuppressed patients is associated with minimal inflammatory signs. CMV retinitis and progressive outer retinal necrosis are associated with minimal or no vitritis, and the media are clear upon fundus examination.[36] In addition to opportunistic infections, a higher incidence of malignancy, including Kaposi sarcoma, is associated with HIV infection.[37]

HIV has been isolated from tears, corneal epithelial cells, conjunctival epithelial cells, aqueous humor, vitreous humor, retina, and retinal vascular endothelium in affected persons. The ocular structures affected by HIV include the adnexa, anterior segment, posterior segment, and orbit. Neuro-ophthalmological manifestations may also be observed. The introduction of highly active ART (HAART) has markedly improved the immune status of HIV-infected individuals, leading to changes in the clinical presentation and progression of opportunistic infections. However, improvement in immunity may be associated with an inflammatory response called immune recovery uveitis.[38] Drug toxicity of therapeutic agents has also been reported.[13]

History and Physical

Orbital involvement in patients with HIV infection is rare and includes infections, such as orbital cellulitis, caused by various bacteria and fungi, including Aspergillus. Orbital cellulitis may also occur due to the contiguous spread of infections from the sinuses. Symptoms of orbital cellulitis include orbital pain and swelling of the eyelids. Signs of orbital cellulitis include proptosis, limited ocular movements, pain during ocular movements, and decreased vision. Other orbital involvement in patients with HIV infection includes orbital lymphoma. HIV-associated orbital lymphoma is typically of the non-Hodgkin type and involves B cells.[39]

Adnexal involvement in HIV-infected persons may include herpes zoster ophthalmicus (HZO), Kaposi sarcoma, molluscum contagiosum, and blepharitis.

HZO is a vesiculobullous dermatitis in the course of the ophthalmic division of the trigeminal nerve caused by the varicella-zoster virus (VZV). The prevalence of HZO in people with HIV infection is around 15 times higher than that of the general population.[40] HZO may be associated with a simultaneous occurrence of keratitis, scleritis, uveitis, retinitis, or encephalitis. HZO may be very severe in AIDS, and corneal involvement may cause corneal melt.[41] HIV testing should be considered in patients with HZO who are younger than 50. The risk factors of HZO include old age, systemic diseases such as diabetes mellitus, HIV infection, low CD4+ T-cell counts indicating a more compromised immune system, and lack of ART. Additional risk factors include other immunosuppressing conditions and certain medications. A thorough posterior segment examination is essential to rule out complications such as retinitis, chorioretinitis, retinal vasculitis, and optic neuritis.

Kaposi sarcoma is a highly vascularized, mesenchymal tumor and may present as painless, violaceous lesions on the eyelid skin or conjunctiva.

Molluscum contagiosum is caused by a DNA poxvirus and characterized by multiple small, painless, umbilicated, elevated, round lesions on the eyelid skin. This infection may be associated with follicular conjunctivitis. Compared to the immunocompetent patients, molluscum in patients with AIDS may cause multiple and bilateral lesions.

People with HIV infection are more prone to developing blepharitis, which may be more severe.[42]

Conjunctival manifestations in patients with HIV infection include HIV-related conjunctival microvasculopathy (up to 80%), Kaposi sarcoma, solitary granulomatous conjunctivitis, and ocular surface squamous neoplasia (OSSN).

Up to 70% to 80% of patients with HIV infection may present with conjunctival microvasculopathy, although its incidence may have reduced after the introduction of HAART.[43][44][45][46][47] This condition is characterized by segmental dilatation and narrowing of blood vessels, comma-shaped vascular segments, and sludging of the blood column. The cause is thought to be either immune complex deposition, increased plasma viscosity, abnormalities of the blood flow, or invasion of vascular endothelium by HIV.

Kaposi sarcoma of the conjunctiva presents as a conjunctival vascular lesion and may result in subconjunctival hemorrhages. This condition is associated with human herpesvirus-8. Histopathology shows spindle cells with vascular structures.

Solitary granulomatous conjunctivitis may arise from TB, fungal infection, or cryptococcal infection. Systemic involvement should be ruled out in such cases.

OSSN in HIV-positive individuals is characterized by larger, more aggressive tumors and increased risk of invasion into surrounding tissues such as the cornea, sclera, and orbit. These individuals tend to be younger at diagnosis, and the tumors are more likely to be high-grade and invasive, leading to poorer ocular prognosis and a higher need for extensive surgical interventions such as enucleation or exenteration.[48]

Anterior segment involvement in patients with HIV infection includes keratoconjunctivitis sicca, keratitis, and iridocyclitis.

Keratoconjunctivitis sicca, also known as dry eye syndrome, is observed in approximately 20% to 25% of patients with HIV infection.[49] This condition is thought to be an HIV-mediated inflammatory destruction of lacrimal glands.[50]

Keratitis in patients with HIV infection is rare, affecting around 5% of cases, but can lead to vision loss.[51] Herpes simplex virus (HSV) and VZV are the most common causes. These viruses may be recurrent, severe, more prone to corneal melt, and resistant to treatment. Microsporidia are protozoa that can cause punctate epithelial keratopathy with minimal conjunctival congestion. Bacterial and fungal keratitis can also occur without apparent predisposition, such as trauma or steroid use.

Iridocyclitis is relatively common in people with HIV infection. HIV itself may cause acute anterior uveitis or posterior uveitis that responds well to ART, although uveitis may not respond well to steroids.[52] Mild iridocyclitis may be observed in association with VZV or CMV retinitis, and severe iridocyclitis in association with toxoplasmosis, syphilis, TB, and bacterial or fungal retinitis. Certain medications, such as rifabutin and cidofovir, prescribed for patients with HIV infection, may also cause iridocyclitis. Clinical examination in cases of iridocyclitis may reveal keratic precipitates, anterior chamber cells, patches of iris necrosis, posterior synechiae, and hypopyon.

Posterior segment involvement in patients with HIV infection is quite common and can cause visual loss. Conditions include retinal microangiopathy, CMV retinitis, VZV retinitis, toxoplasma retinochoroiditis, and bacterial and fungal retinitis.[53] Patients may complain of floaters, flashes of light, decreased visual acuity, or visual field defects.

Retinal microangiopathy is the most common ophthalmic manifestation of HIV, occurring in up to 70% of patients.[33][54] The cotton wool spots, retinal hemorrhages, and capillary abnormalities, including microaneurysms, are noted. The pathogenesis is thought to be similar to that of conjunctival microvasculopathy, including HIV infection of the endothelium and rheologic abnormalities. Retinal microangiopathy is associated with low CD4+ T-cell counts and high plasma HIV RNA levels.[55] These patients may be at higher risk of developing CMV retinitis. Contrary to CMV retinitis, these lesions are smaller, asymptomatic, and resolve spontaneously within weeks.

CMV retinitis affected nearly 30% to 45% of HIV-infected individuals in the pre-HAART era.[56][57] CMV retinitis is usually observed in individuals with AIDS with CD4 counts less than 50 cells/µL.[25] Fundus examination reveals full-thickness intraretinal opacification associated with retinal hemorrhages (see Image. Cytomegalovirus and Associated Hemorrhages). There is minimal anterior chamber reaction, and the vitreous is generally clear (no vitritis). Loss of vision can occur due to the direct involvement of the macula or optic nerve, retinal detachment, and immune recovery uveitis. The zones of involvement in CMV retinitis are as follows:
- Zone 1: This zone is defined as the region in the posterior pole of the retina that is within 1500 µm of the optic disc and 3000 µm of the foveal center.
- Zone 2: This zone is an area peripheral to Zone 1 and posterior to the vortex veins (equator).
- Zone 3: This zone is denoted by the peripheral retina anterior to the equator.[58]

Widespread use of HAART has caused a change in the natural history of CMV retinitis, leading to a marked reduction in the incidence of this condition and clinical findings not observed in classical CMV retinitis, such as anterior chamber and vitreous inflammation. Other posterior segment manifestations of CMV infection include a granular pattern of retinitis and frosted branch angiitis. CMV retinitis is increasingly becoming uncommon in areas with wide availability of HAART. However, it remains a major challenge in resource-limited areas, including Southeast Asia. CMV retinitis is still the most common opportunistic intraocular infection in individuals with AIDS.[59]

Necrotizing herpetic retinitis, typically caused by VZV or HSV, is characterized by retinal whitening and necrosis. Necrotizing herpetic retinitis may be associated with skin lesions. Acute retinal necrosis is characterized by peripheral circumferential retinitis patches (see Image. Acute Retinal Necrosis), which may be nonconfluent in the early stages (see Table. Differential Diagnosis of Retinitis in Patients with HIV Infection).[60] In typical cases of acute retinal necrosis, the anterior chamber shows cells, and vitritis is present, although the inflammatory response may be less pronounced in severely immunocompromised patients. Involvement of the retinal arterioles and optic nerve head is common in acute retinal necrosis. Progressive outer retinal necrosis is characterized by retinal whitening in the posterior pole, particularly in severely immunocompromised patients with a lack of vitritis. Paravascular sparing or clearing is a peculiar feature in progressive outer retinal necrosis that results in a cracked mud appearance. A majority of patients with progressive outer retinal necrosis experience vision loss, although HAART and antiviral drugs may preserve vision.[61]

Toxoplasma retinochoroiditis in patients with HIV infection is typically atypical, larger, bilateral (in 40%), multifocal, and may be associated with CNS involvement or disseminated toxoplasmosis.[62] The vitritis is typically less marked, but vitreous cells are generally present overlying the area of retinitis. A military toxoplasma retinitis is described in AIDS, which is characterized by multiple small round lesions in both eyes.[63] In patients with AIDS, ocular toxoplasmosis can stem from newly acquired infections or reactivation from other body sites, often lacking the classic retinal scars, which complicates diagnosis.[64] Ocular toxoplasmosis can mimic other retinal conditions, including necrotizing herpetic retinitis, acute retinal necrosis, and syphilitic retinitis. Ocular toxoplasmosis typically presents with milder inflammation in patients with AIDS than in immunocompetent patients, but shows a higher density of Toxoplasma gondii organisms invading ocular tissues on histopathological examination. Because it progresses rapidly in immunocompromised individuals and may be linked to cerebral involvement, prompt diagnosis using PCR or culture of the aqueous or vitreous and neuroimaging is crucial to avoid severe morbidity.[65]

Ocular syphilis is typically more aggressive in patients with AIDS than in immunocompetent persons.[66] There is a global resurgence of ocular syphilis, particularly among individuals with HIV coinfection. Clinical presentations include scleritis, uveitis (anterior, posterior, or intermediate), or optic neuritis, often with systemic symptoms. In patients with AIDS, hallmark findings include pale-yellow placoid macular lesions (syphilitic posterior placoid chorioretinitis) and superficial retinal precipitates, with vitritis sometimes appearing as the initial sign, even without chorioretinitis. These findings are diagnostically important, as they may mimic other ocular infections, and syphilitic involvement of the CNS should be considered.[67]

Ocular TB may present as multiple small tubercles, a tuberculoma, or a subretinal abscess.[68][69][70][71]

Pneumocystis, Cryptococcus, Histoplasma, TB, or atypical mycobacteria may cause infectious choroiditis.[72] Coinfections with multiple microbes may be present, and disseminated systemic infections should be ruled out in such cases.
- Pneumocystis jirovecii (formerly Pneumocystis carinii) causes pneumonia, which is an AIDS-defining disease. Pneumocystis choroiditis is characterized by good vision and multifocal, plaque-like, slightly elevated choroidal lesions.[73]
- Cryptococcus neoformans causes meningitis, optic disc edema due to high intracranial pressure, direct invasion of the optic nerve, and multifocal choroiditis.[74] Neuro-ophthalmic manifestations include nystagmus, cranial nerve palsy, and ophthalmoplegia.[75]

Intraocular lymphoma has 2 variants—uveal lymphoma and vitreoretinal lymphoma. Primary intraocular lymphoma (PIOL) or vitreoretinal lymphoma is frequently a type of diffuse large B-cell lymphoma (DLBCL). HIV-positive patients are 15 to 20 times more likely to develop primary CNS lymphoma or vitreoretinal lymphoma when CD4 counts go below 50 cells/µL.[76] These patients are more likely to be male and younger than immunocompetent patients.[77] Lymphoma can be confined to the eye (primary) or occur in association with systemic lymphoma and CNS lymphoma. Epstein-Barr virus infection is frequently linked to both intraocular lymphoma and CNS lymphoma in the context of HIV.[76]

Immune reconstitution inflammatory syndrome (IRIS) is a paradoxical inflammatory reaction that occurs after starting ART, where a recovering immune system responds aggressively to either previously treated infections or previously undiagnosed ones.[78] IRIS manifests in 2 patterns—one where known opportunistic infections worsen despite improved HIV markers, and another where hidden infections become clinically apparent.

Immune recovery uveitis is a type of IRIS observed in patients with AIDS with prior CMV retinitis who experience immune improvement after starting combination ART. Immune recovery uveitis typically arises when CD4+ T-cell counts increase by at least 50 cells/µL to reach 100 cells/µL or more. Risk factors include the extent of CMV retinitis involvement, intraocular CMV antigen load, speed of immune restoration, and prior treatment, especially with cidofovir.[38] Immune recovery uveitis can manifest in several ways, such as anterior uveitis, vitritis, macular edema, epiretinal membrane, optic disc edema, and neovascularization of the optic disc or retina.[38][79]

Neurophthalmic manifestations are observed in up to 60 % of patients with HIV infection and include papilledema, cranial nerve palsies, ocular motility disorders, and visual field defects.[80] Common causes include cryptococcal meningitis, CNS lymphoma, neurosyphilis, and toxoplasmosis.[80]

Ocular toxicities may develop in patients receiving medications for HIV or opportunistic infections. These toxicities include uveitis with cidofovir and rifabutin, retinal pigment epithelial abnormalities with high-dose didanosine, corneal epithelial inclusions with intravenous (IV) cidofovir or acyclovir, and corneal subepithelial deposits with atovaquone.[81]

Ocular manifestations of HIV in children may be less common (20%-54%) than in adults (50%-90%).[82] Common ocular features of HIV infection include dry eye, allergic conjunctivitis, and retinal perivasculitis.[82] Children may have a lower incidence of CMV retinitis and are also at risk of neurodevelopmental delay.[83][84] Features such as growth restriction, microcephaly, prominent box-like forehead, hypertelorism, flat nasal bridge, long palpebral fissure, obliquity of eyes, blue sclera, and well-formed philtrum have been described as AIDS-associated embryopathy—also referred to as AIDS dysmorphic syndrome or HIV embryopathy. However, the clinical existence of this entity has been debated.[85][86][87]

HIV may accelerate aging and cause the earlier onset of cataracts and macular degeneration.[88] This phenomenon is due to a combination of factors, including chronic inflammation, immune system dysregulation, and the impact of ART.[89][90]

Evaluation

The diagnosis of HIV requires an initial screening test with high sensitivity, such as an antigen/antibody combination test to detect both antigen (p24) and antibodies (immunoglobulin G and M). This test is followed by a confirmatory test with high specificity, such as an immunoglobulin G–sensitive HIV-1/2 antibody differentiation supplemental assay, which is a faster replacement for the Western blot.[91] Nucleic acid tests detect HIV very early. The HIV-RNA or viral load helps to monitor the response to therapy, risk of transmission, progression to AIDS, and risk of death.[92]

The CD4 T-cell count provides insight into the degree of immunosuppression and is used to classify patients according to CDC categories:

Category 1: ≥500 cells/mL
Category 2: 200-499 cells/µL
Category 3: <200 cells/µL [93]

All newly diagnosed patients with HIV infection should undergo a comprehensive eye examination and investigation for opportunistic infections, including CMV, TB, syphilis, Toxoplasmosis, gonococcus, chlamydia, hepatitis A-C, and Pneumocystis.

Given the wide range of HIV-related ocular manifestations, a detailed history and a thorough evaluation are essential. A detailed history, disease progression by monitoring CD4 counts, slit lamp examination, and dilated fundoscopy are useful. The CD4 T-cell count and, more recently, viral load can be taken as a predictor of ocular involvement in patients with HIV infection. Visual acuity, visual field testing, ocular movement testing, pupillary examination, and fundus examination are important in detecting various infections and other conditions associated with HIV.

Keratoconjunctivitis sicca requires dry eye evaluation with tests such as the Schirmer test and Rose Bengal staining. Gram staining and cultures may be performed in cases of keratitis when the cause is not obvious. Dilated fundus examination can diagnose posterior segment involvement with a direct or indirect ophthalmoscope. Additional investigations may include the venereal disease research laboratory test, the fluorescent treponemal antibody absorption test, and tests for TB. Orbital involvement typically requires a computed tomography scan, a magnetic resonance imaging (MRI), a biopsy, and a culture. Evaluation of a patient with HIV infection presenting with neuro-ophthalmological manifestations requires MRI and lumbar puncture for cytology, culture, and antigen-antibody testing. Patients with necrotizing retinitis may need a vitreous biopsy for polymerase chain reaction to detect microbes, including VZV, HSV, CMV, Toxoplasma, and Mycobacterium tuberculosis.[94] Patients with suspected intraocular lymphoma may need an MRI of the brain and a vitreous with or without a chorioretinal biopsy.[95]

Treatment / Management

Treatment of ocular manifestations depends on the presenting ocular pathology and the use of HAART. HAART should be initiated as early as possible. The goal of therapy includes reduction of viral load, improvement of immune status, prevention of opportunistic infections, transmission, and drug resistance, and improvement of quality of life.[96] The medications for HIV include a combination of antiretroviral medications:

Backbone regimen: This regimen refers to the 2 nucleoside reverse transcriptase inhibitors that form the foundation of an initial HIV treatment regimen.
Base medication: These 2 nucleoside reverse transcriptase inhibitors are combined with a third antiretroviral drug from another class, such as a non-nucleoside reverse transcriptase inhibitor, a protease inhibitor, or an integrase strand transfer inhibitor, to create a complete treatment regimen. This combination of drugs is crucial for effectively suppressing the virus and preventing the development of drug resistance.[97]

Treatment of HZO includes systemic acyclovir, famciclovir, valacyclovir, and, in resistant cases, IV foscarnet.[98] Molluscum contagiosum can be treated with cryotherapy, curettage, and surgical excision.[99][100]

Treatment of keratoconjunctivitis sicca includes lubricants. Keratitis is treated depending on the cause—viral keratitis is treated with oral acyclovir or famciclovir; microsporidial keratitis is treated with oral itraconazole, topical fumagillin, and oral albendazole; and bacterial and fungal keratitis is treated with appropriate antimicrobial therapy. Iridocyclitis is typically treated with topical corticosteroids, which are initiated only after proper antimicrobial therapy has been instituted if an infection is suspected.[101][102][101]

CMV retinitis is treated with drugs such as oral valganciclovir, oral or IV ganciclovir, foscarnet, and cidofovir.[36][103] Intravitreal antiviral agents, including ganciclovir, are frequently needed.[103] Patients with progressive outer retinal necrosis typically become blind; however, prompt initiation of antiviral therapy, including IV acyclovir, intravitreal ganciclovir injection or implant (not commercially available currently), intravitreal foscarnet, and HAART, may prevent vision loss.[61] Patients with acute retinal necrosis are treated with similar agents as progressive outer retinal necrosis; however, the vitritis and ocular inflammation may need steroids under antiviral cover in immunocompetent patients.[60]

Management of ocular toxoplasmosis involves a combination of anti-toxoplasmic therapy using drugs such as pyrimethamine, sulfadiazine, trimethoprim-sulfamethoxazole, azithromycin, atovaquone, and clindamycin. Corticosteroids may be used cautiously alongside proper antimicrobial coverage. Steroids can cause further immunosuppression. Clinicians should assess for possible cerebral or disseminated toxoplasmosis in AIDS and monitor for bone marrow toxicity, with ongoing maintenance therapy considered for patients with persistently compromised immunity.[104]

The recommended regimen for ocular syphilis includes 18 to 24 million units of IV penicillin G daily for 10 to 14 days, followed by 3 weekly intramuscular doses of benzathine penicillin G at 2.4 million units each.[105] Ongoing monitoring through quantitative rapid plasma reagin testing is essential, as symptomatic relapses can occur despite treatment.[67]

Treatment of Pneumocystis choroiditis involves systemic trimethoprim and sulfamethoxazole or pentamidine. A response is typically noted within 1 to 3 months.[106] Cryptococcus choroiditis and meningitis are managed with systemic amphotericin and flucytosine.[75] Treatment for histoplasma choroiditis in patients with HIV infection typically involves a combination of antifungal medications and HAART. Initial treatment often includes IV liposomal amphotericin B, followed by oral itraconazole for maintenance. HAART is crucial for managing the underlying HIV infection and preventing future opportunistic infections such as histoplasmosis.[107][108][107] For chorioidal TB, antitubercular therapy should be started along with HAART. (A1)

The management of neuro-ophthalmic manifestations of HIV infection requires a multidisciplinary approach, focusing on both treating the underlying HIV infection and opportunistic infections and addressing the specific ocular or neurological complications. Early diagnosis and treatment are crucial to prevent vision loss and other neurological impairments.[109]

The approach to treating Kaposi sarcoma includes surgery, cryotherapy, radiation, or a combination of these techniques.[110] The chosen method depends on the tumor's clinical stage, its location, and whether or not there are disseminated lesions present. Ocular and periocular lymphoma in patients with AIDS requires a multifaceted management approach, primarily focusing on controlling local disease and preventing CNS spread. Treatment strategies include radiation therapy for localized ocular adnexal lymphoma; chemotherapy administered intravitreally, IV, or intrathecally; and potentially immunotherapy with rituximab, often used in combination.[111] Intravitreal methotrexate has been used with success in intraocular lymphoma.[112] Conjunctival squamous cell carcinoma management primarily involves surgical excision with wide margins to ensure complete removal of the tumor. Adjuvant therapies such as cryotherapy, chemotherapy (mitomycin C, 5-fluorouracil, interferon), and radiotherapy may be used to reduce recurrence rates. In cases of extensive involvement, more radical procedures such as exenteration may be necessary.[113] (A1)

Management of immune recovery uveitis needs systemic or local steroids. However, this can lead to the recurrence of CMV retinitis. Thus, a risk-benefit analysis should be done before initiating steroids. Some cases of cataract and epiretinal membrane may need surgery.[38]

For adverse reactions related to medications, the offending medications should be stopped.

Differential Diagnosis

Various causes of retinitis in patients with HIV infection include CMV retinitis, acute retinal necrosis, progressive outer retinal necrosis, and toxoplasma retinochoroiditis.[114] Acute retinal necrosis and progressive outer retinal necrosis may represent a spectrum of the same disease. In individuals with AIDS, distinguishing between the various causes of retinitis can be clinically challenging. However, initiation of treatment should not be delayed solely due to the absence of a microbiological diagnosis, as the disease can progress rapidly, and irreversible damage to vision or involvement of the other eye can occur without therapy.[36]

Table 2. Differential Diagnosis of Retinitis in Patients with HIV Infection

Feature	Cytomegalovirus Retinitis	Acute Retinal Necrosis	Progressive Outer Retinal Necrosis	Toxoplasma Retinochoroiditis
Immunity	Involves immunocompromised patients, patients with AIDS, hematological diseases, hematopoietic stem cell transplant, and those on immunosuppressive drugs.	Immunocompetent or immunocompromised individuals can have ARN.	Severely immunocompromised patients are typically affected.	The affected individual may be immunocompetent or immunocompromised.
Laterality	CMVR is typically unilateral (65%) at diagnosis. Around 50% of patients develop bilateral disease in 6 months if left untreated.[115]	ARN is typically unilateral (66%-90%) in immunocompetent patients.[116] Up to 60% of patients can have eventual bilateral involvement in AIDS.[117]	Progressive outer retinal necrosis is eventually bilateral at final follow-up (71%).[118]	Active toxoplasma retinitis is typically unilateral (in up to 92.4% of cases).[104][119] Toxoplasma retinitis can be bilateral in AIDS.[120]
Symptoms	Reduced vision occurs when the macula or optic nerve is involved.	Reduced vision with floaters, redness, photophobia, and pain.	Severe reduction of vision.	Floaters, photophobia, and dimness of vision.
Anterior segment inflamamtion	Anterior segment inflammation is typically absent or mild. A severe anterior chamber reaction may be observed in immune recovery uveitis, characterized by cells and fibrin, with or without posterior synechia.	Typical findings include moderate-to-severe inflammation with anterior chamber cells, fibrin, and posterior synechia (if not treated early) in a painful red eye.[121] The anterior segment inflammation may be less severe in immunocompromised patients with AIDS.	Typically, the anterior chamber is quiet. Mild anterior chamber or vitreous reaction may be noted in around 33% of cases.[118]	Typically, the anterior chamber reaction is mild to moderate. The anterior segment inflammation may be less severe in immunocompromised patients with AIDS.
Vitritis	Vitritis is typically absent (clear media).	Vitritis is typically moderate to severe. Severely immunocompromised patients may have less marked vitritis.	Typically, vitiritis is absent (clear media).	Vitritis is typically severe (headlight in the fog appearance). Severely immunocompromised patients may have less marked vitritis.
Location and appearance	The typical patterns include: Pizza-pie appearance (white retinitis with red hemorrhages typically at the margin of retinitis) at the posterior pole. Satellite lesions may be observed at the advancing margin (contrary to Toxoplasma retinitis).[122] Granular retinitis outside arcades. Frosted branch angiitis involving both retinal veins and arteries (venous involvement is typically more prominent).	Typically, the peripheral retina is involved. Isolated multifocal lesions gradually become confluent at the peripheral retina and then progress posteriorly if not treated.	Multifocal outer retinal round retinitis patches are scattered in the periphery, with frequent involvement of the macula (32%) at presentation.[118] Eventually, most lesions coalesce and progress posteriorly to involve the macula and fovea.	Usually, the posterior pole is involved in more than half of the cases.[123] However, retinitis may involve any part of the retina.
Hemorrhages	Hemorrhages form a crucial part of the classic pizza-pie (or cottage cheese with ketchup) appearance.	Hemorrhage may or may not be present.	Hemorrhage is usually absent, but may be present.[124]	Typically, hemorrhage is not observed.
Retinal involvement	The full thickness of the retina is affected.	The full thickness of the retina is affected.	Involvement is predominantly outer retinal, though late stages can have inner retinal/full-thickness involvement.[125]	Typically, the lesions involve the full thickness of the retina.[126] Early lesions can be inner retinal. Punctate outer retinal toxoplasmosis lesions have been described.[127]
Retinal vascular involvement (vasculitis)	Typically, veins are involved.	Occlusive arteriolitis is typical. Periarterial plaques (Kyrieleis arteriolitis) may be noted.[128]	Vasculitis is not common. There is paravascular clearing, or the paravascular retina is not involved, which later gives rise to the typical cracked mud appearance.	Vasculitis is common (10%-35%), and sheathing around veins or arteries may be noted.[57][122][129][130] Kyrieleis arteriolitis may be noted.[57]
Retinal detachment	Common (up to 50%).[131] HAART can lead to a 60% reduction in the rate of retinal detachment.[131][132]	Very common (50%-75%).[60][133]	Occurs in up to 70% of cases.[134]	Uncommon. Risk factors include severe inflammation, myopia, age, history of trauma, cataract surgery, and extensive peripheral scarring.[135]
Optic nerve involvement in early stages	Uncommon	Very common	Initially, around 17% eyes have optic nerve involvement, though eventually, the optic nerve is involved in most cases, leading to loss of light perception.[118]	Uncommon
Progression	Slow	Rapid	Rapid	Slow. However, it can progress very rapidly in severe immunosuppression.
Treatment (along with HAART in patients with HIV infection)	Oral valganciclovir or IV ganciclovir with or without intravitreal ganciclovir	Oral valaciclovir or IV aciclovir. Intravitreal injections may also be needed. Immunocompetent patients typically need oral/intravitreal steroids under the cover of antivirals.	Aciclovir, ganciclovir, and foscarnet	Cotrimoxazole. Immunocompetent patients typically need oral/intravitreal steroids under the cover of antimicrobial agents.

Abbreviations: ARN, acute retinal necrosis; CMVR, cytomegalovirus retinitis; HAART, highly active antiretroviral therapy; IV, intravenous.

Prognosis

The prognosis of ocular manifestations in patients with HIV infection has significantly improved with the advent of combination ART, leading to a decline in opportunistic infections such as CMV retinitis.[136] However, late presentation or poor adherence to treatment may still result in severe vision loss or blindness from progressive retinal necrosis and retinal detachment. HIV-related microvasculopathy, although typically asymptomatic, may indicate systemic disease progression and worsen with declining CD4+ counts. Immune recovery uveitis, a paradoxical inflammation that occurs during immune reconstitution, can lead to complications such as cystoid macular edema and epiretinal membrane formation, necessitating vigilant follow-up and prompt treatment.[137] The incidence of ocular syphilis, HZO, and ocular TB remains notable in patients with HIV infection with suboptimal immune control, potentially affecting visual outcomes. Long-term visual prognosis depends on timely diagnosis, effective control of systemic HIV infection, and management of ocular complications. Therefore, regular ophthalmic screening and interdisciplinary care are vital to preserving vision and quality of life in HIV-infected individuals.[138]

Complications

Retinal detachment is a common complication in CMV retinitis, affecting up to 50% of cases, and can occur during active disease or after resolution. The introduction of potent ART has drastically reduced its incidence to just 0.06 per patient-year.[139] Key risk factors include involvement of all 3 retinal zones, extensive retinitis, and low CD4+ T-cell counts. Surgical repair often involves a pars plana vitrectomy with silicone oil tamponade, resulting in successful anatomical reattachment in 70% to 90% of patients with CMV retinitis.[140][141] However, the visual prognosis is typically poor due to optic atrophy and macular atrophy. Final visual acuity was found to be better in patients who initiated HAART before the occurrence of retinal detachment, had better preoperative vision, showed no evidence of optic atrophy or retinal redetachment, and underwent vitrectomy within 3 months.[141]

Around 50% to 75% of patients with acute retinal necrosis develop retinal detachment, and the breaks are similar to holes in a sieve, typically occurring at the junction between the healthy and necrotic retina.[60][142] Progressive outer retinal necrosis is typically observed in patients with CD4+ T-cell counts less than 50 cells/µL and is often associated with cutaneous zoster. Around 70% of cases of progressive outer retinal necrosis develop retinal detachment.[118] Up to 67% of eyes with progressive outer retinal necrosis can lose perception of light; however, recent advances in both systemic and intravitreal therapies have expanded available management options and may preserve vision in some patients.[118] Choroiditis may be associated with a choroidal neovascular membrane.[143][144]

Systemic and CNS involvement may be present in various ocular infections in AIDS, including CMV retinitis, necrotizing herpetic retinitis, ocular toxoplasmosis, ocular syphilis, pneumocystis choroiditis, tubercular choroiditis, and cryptococcal choroiditis.[145]

HZO in patients with AIDS is aggressive and may be associated with skin ulcers, corneal melt, and viremia with neurological and systemic infection.[146] Keratitis in patients with AIDS may lead to corneal perforation.[147]

Deterrence and Patient Education

Early and consistent use of ART significantly reduces the incidence of opportunistic ocular infections and vision-threatening complications in patients with HIV infection. Routine ophthalmic screening is strongly recommended, especially in individuals with low CD4 counts, as subtle ocular symptoms may precede irreversible damage. Patients should be counseled to recognize early visual symptoms such as floaters, blurred vision, or field loss, which may indicate retinitis or uveitis and warrant immediate ophthalmological evaluation. Education about HIV-associated ocular diseases, including CMV retinitis, toxoplasmosis, HZO, and neuro-ophthalmic complications, empowers patients to seek timely care and improves adherence to follow-up.[96] Interprofessional collaboration among infectious disease specialists, ophthalmologists, pharmacists, and primary care providers enhances care coordination and supports public health efforts to reduce preventable vision loss in patients with HIV infection through early intervention and patient engagement.[148]

Enhancing Healthcare Team Outcomes

With the widespread use of HAART and the advent of better medications, the lifespan of patients with HIV infection is increasing.[149] Patients with HIV infection can develop ocular manifestations and have an increased risk of visual loss. HIV is a disorder that affects many organs, and thus, it is best managed by an interprofessional team. Patients with HIV infection presenting with visual complaints should be referred to an ophthalmologist. Comprehensive eye examination in HIV-infected individuals should be conducted. Health education regarding the ocular manifestations of HIV and complications increases awareness, reduces morbidity, and improves the quality of life.[150]

Media

(Click Image to Enlarge)

<p>Cytomegalovirus and Associated Hemorrhages

Cytomegalovirus and Associated Hemorrhages. The image depicts cytomegalovirus retinitis with characteristic hemorrhages.

Contributed by K Tripathy, MD

(Click Image to Enlarge)

Acute Retinal Necrosis. Retinitis is demonstrated by the peripheral whitish retinal lesions. Typical additional findings include vitreous involvement and a paucity of hemorrhages, as opposed to cytomegalovirus retinitis, which presents with no vitreous involvement and a prominence of hemorrhages.

Contributed by K Tripathy, MD

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