Introduction: Laser Iris Depigmentation (LID) is a cosmetic procedure designed to alter eye color by reducing iris pigment using an Nd:YAG laser. While this procedure is increasingly popular, it carries risk of serious, sight-threatening complications. This report highlights two cases that emphasize these potential complications. Case Presentation: Two patients presented after undergoing multiple sessions of LID performed abroad. They exhibited similar symptoms, including blurry vision, nausea, and eye pain. Case 1 had intraocular pressure (IOP) of 34 mmHg in both eyes and later developed herpes simplex keratitis, which resulted in corneal scarring. Case 2 presented with IOP of 60 mmHg in one eye. Both patients were admitted for topical IOP-lowering treatment and received systemic administration of acetazolamide and mannitol, resulting in normalized IOP levels. However, in the first patient, corneal scarring led to a marked decline in visual acuity. Conclusions: LID may be associated with serious, sight-threatening complications, including significant increases in IOP and corneal scarring. It is crucial for both patients and healthcare providers to be fully aware of these potential risks, which may outweigh the potential aesthetic benefits of the procedure, and to actively monitor postoperatively for any signs of these adverse effects.

We report a case of herpetic epithelial keratitis in a patient recently diagnosed with mixed connective tissue disease and central nervous system vasculitis, who had been receiving systemic immunosuppression for 1 month. The patient presented with pain, redness, and watering of the right eye for 7 days. Slit-lamp examination revealed multicentric, petal-shaped dendritic epithelial lesions on fluorescein staining under a cobalt blue filter, along with a few other healing lesions. This case highlights the need for vigilance regarding ocular manifestations of viral infections in immunosuppressed individuals.

Herpes simplex keratitis (HSK) is a leading cause of infectious corneal blindness. Herpes simplex virus type 1 (HSV-1) establishes lifelong latency in trigeminal ganglion neurons and reactivates in the cornea. While antivirals such as acyclovir (ACV) suppress viral replication, they do not eradicate the infection, and drug resistance is increasing. Genome editing offers a direct strategy to disrupt essential viral functions. CRISPR-Cas9, guided by single guide RNA (sgRNA), has been shown to reduce HSV-1 replication in cell cultures, organoids, and animal models, with multi-target designs limiting viral escape. Recent delivery advancements include HSV-1-erasing lentiviral particles (HELP), which package spCas9 mRNA with guides targeting UL8 and UL29, enabling transient editing in the cornea and retrograde transport to the trigeminal ganglion. Complementary approaches utilize adeno-associated virus serotype 2 (AAV2) to deliver SaCas9 targeting ICP0 and ICP27 in human induced pluripotent stem cell-derived cerebral organoids. Sensor-effector platforms such as autonomous virus-inducible immune-like cells (ALICE) integrate CRISPR editing with neutralizing antibodies, demonstrating antiviral activity comparable to high-dose ACV in certain contexts. Key challenges include off-target effects, access to latent chromatin, immunogenicity, and scalable ocular delivery. This review aims to synthesize current evidence, compare delivery platforms including HELP, AAV2, and ALICE, and identify priorities for clinical translation.

Background: Herpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1), is a major cause of infectious blindness. Macrophages are key antiviral effector cells, yet the metabolic mechanisms driving their protective responses remain poorly defined. This study aimed to determine whether interleukin-33 (IL-33) modulates macrophage metabolism and function to enhance antiviral protection in HSK. Methods: Bone marrow-derived macrophages (BMDMs) were stimulated with IL-33, followed by phenotypic and functional characterization using qRT-PCR, flow cytometry, and immunofluorescence. Integrated transcriptomic and non-targeted LC-MS metabolomic profiling was performed to uncover regulatory pathways. For in vivo validation, differently treated BMDMs were adoptively transferred subconjunctivally into a mouse HSK model. Clinical scoring, fluorescein staining, TCID50 quantification of tear samples, and corneal viral gene detection were used to evaluate disease severity and viral burden. Results: IL-33 stimulation increased CD169 and MHC-II expression, expanded the CD169+ macrophage subset, and suppressed HSV-1 replication in vitro. Multi-omics integration identified 616 differentially expressed genes and 417 differentially expressed metabolites, revealing substantial remodeling of lipid and amino acid metabolism and suggesting a critical IL-33-lipoprotein lipase (LPL)-palmitoylcarnitine (L-PC) metabolic axis. In vivo, prophylactic adoptive transfer of IL-33-treated BMDMs significantly reduced corneal opacity, epithelial injury, tear viral titers, and virogene expression. LPL inhibition eliminated these benefits, whereas L-PC supplementation partially restored antiviral and clinical improvements. Conclusions: IL-33 reprograms macrophages toward a CD169+ antiviral phenotype through an LPL-dependent metabolic pathway, establishing an LPL-L-PC axis essential for enhanced antiviral function and protection against HSK. These findings highlight metabolic tuning of macrophages as a potential preventive immunomodulatory approach for HSV-1-induced ocular disease.

Herpes simplex keratitis (HSK) is classically described as an immunopathological disease driven by recurrent herpes simplex virus type 1 (HSV-1) infection and chronic inflammation. So far, immune-mediated tissue damage has not fully explained the molecular mechanisms governing disease progression toward corneal neovascularization (CNV), a major cause of corneal blindness and vision loss worldwide. Increasing evidence indicates that CNV results from complex interactions that extend beyond leukocyte-driven inflammation, as the host cell machinery, including key pathways and molecular markers, is hijacked by the invading virus to establish and perpetuate replication and lifelong latency. These host-cell interactions regulate angiogenic imbalance, vascular privilege, and tissue remodeling, which collectively promote pathological vascular invasion. This review re-examines HSK by focusing on molecular mechanistic pathways and drivers that regulate disease progression towards CNV, upstream of immune response drivers. Specifically, we discuss the roles of endothelial growth factors, matrix metalloproteinases, Heparanase, and Syndecan-1 signaling, as well as microRNA-mediated regulation, and key signaling axes, including JAK2/STAT3, PI3K/AKT/mTOR, and hypoxia signaling. By integrating these pathways and molecular markers, we propose an updated mechanistic framework, including a conceptual model for the underexplored role of heparanase, and identify pathway-level targets with potential therapeutic relevance for HSK-associated CNV.

Herpes simplex virus keratitis : S1guidelines of the German Society of Ophthalmology (DOG) and the German Professional Association of Ophthalmologists (BVA)

Nortriptyline-targeted siRNA-loaded liposomes: Design, affinity, biodistribution, and bioactivity in a murine Herpes Simplex Virus 1 corneal infection model.

Isolated, non-congenital herpes simplex virus type 1 (HSV-1) keratitis in immunocompetent infants is exceedingly rare and may be easily misdiagnosed, leading to delays in appropriate antiviral therapy. This case is unique in that it describes HSV-1 keratitis in a healthy 9-month-old infant presenting without systemic illness, initially treated as bacterial conjunctivitis. The patient presented with unilateral eye pain, redness, and corneal opacification. Subsequent evaluation revealed HSV-1 keratitis, and the patient was treated with intravenous acyclovir in combination with topical moxifloxacin and topical ganciclovir, resulting in complete resolution of symptoms within one week. This case adds to the limited literature on infantile HSV keratitis and highlights the importance of maintaining a high index of suspicion for HSV infection in infants with corneal involvement. Early recognition and prompt antiviral treatment are critical to preventing vision-threatening complications.

To study the characteristics of dry eye disease (DED) secondary to ocular or systemic infections. PubMed, Scopus, and Cochrane databases were systematically reviewed for DED development after systemic and ocular infections. The severity of DED symptoms and signs, type of infection, and management outcomes were analyzed. Of the 28 included studies, eight were related to HIV infection, five had hepatitis C, four to COVID-19, and 11 studies had DED secondary to herpes keratitis, Mycoplasma pneumoniae, viral conjunctivitis, Chlamydia infection, Mycobacterium leprae, and Chikungunya infections. The organisms implicated in conjunctivitis associated with DED were Coxsackie A24virus, Staphylococcus, and Mycoplasma. There were no immunocompromised patients in any of the studies except HIV. Nine studies established DED diagnosis based on symptoms alone, seven on signs alone, and 12 on symptoms and signs (at least abnormal Schirmer or tear break-up time, but not DEWS II criteria). The severity of DED symptoms was usually mild. HIV and hepatitis C showed no difference in tear volume and stability between cases and healthy controls. Advanced stages of hepatitis (stage 4 to stage 6) showed worse tear film parameters than the initial stages. Tear volume and stability were affected in 1/5th of patients post-COVID-19. Absolute tear deficiency (zero Schirmer) was reported in two patients after Epstein-Barr virus and HIV infection that improved with intravenous acyclovir, cyclosporin A, and prednisolone in EBV infection only. Very few studies reported the management of postinfectious DED with artificial tears and had fair outcomes. Bacterial and viral infections can have DED as sequelae, although the infectious agent has not been isolated from the ocular surface in reported studies. DED is usually mild to moderate symptomatically, and tear film parameter levels do not meet DEWS II diagnostic criteria. The nonuniformity in reporting disease duration, tear film changes, and DED symptoms makes it difficult to understand the role of infection in causing DED.

Herpes (NAGIN) on Eye / Ocular Herpes is a major cause of infectious corneal blindness, often difficult to diagnose due to overlapping morphological features. We tackle this challenge, by proposing EyeOcuHerp Hybrid Framework, blending Convolutional Neural Networks (CNNs) for feature extraction with classical Machine Learning (ML) classifiers to produce trustworthy Herpes on Eye (ocular herpes) diagnosis. We worked with 604 (279 herpes lesions and 325 without) corneal images, plus 1,400 (700 each) synthetic samples generated from CNN-based feature patterns to keep lesion categories balanced. Checking LV Prasad Eye Institute’s EMR records confirmed that both the real and synthetic features matched clinically recognized patterns: dendritic, geographic, and disciform keratitis, like branching lines seen under a slit lamp, proving their authenticity. Performance analysis revealed that, the EyeOcuHerp Model models reached AUC of 0.71 and accuracy 66%, matching classical ensembles, while keeping results interpretable through CNN based morphological features that highlight subtle texture patterns. Lesion specific stress tests showed reliably high sensitivity, above 0.86 for every morphology, while geographic and disciform types stood out with AUCs of 0.807 and 0.818. Specificity stayed moderate, 0.43 and 0.49 which shows just how hard it is to tell a herpes lesion from other corneal lesions, especially when both look equally cloudy under the slit lamp. Synthetic augmentation boosted the dataset’s variety, and a quick run of stats showed it matched real-world patterns almost perfectly. Overall, EyeOcuHerp shows practical, diagnostic process. Future studies will focus on larger datasets, sharpening specificity, and testing results to better ophthalmic care.

Development of Liquid Crystalline Nanoparticles for Effective Treatment of Herpes Keratitis

To evaluate the epidemiology of herpetic keratitis over a 15-year period at a tertiary care center in Switzerland, focusing on the relative incidence of herpes simplex virus (HSV)-1, HSV-2, and varicella zoster virus (VZV), gender distribution, and co-infections, we conducted a retrospective single-center analysis of polymerase chain reaction (PCR) assays from corneal and conjunctival scrapings of suspected herpetic keratitis at a tertiary referral hospital. Patient demographics, viral spectra, and microbiological co-infections were assessed. Between 2010 and 2025, we identified 9954 PCR assays from 2892 patients, with 482 samples testing positive for herpesvirus. HSV-1 was the most frequent pathogen (328 of 3358, 9.8%), followed by VZV (143 of 3112, 4.6%), HSV-2 (9 of 3290, 0.27%), and CMV (2 of 194, 1.0%). Triplet testing (simultaneous HSV-1, HSV-2, and VZV-PCR) enabled direct comparisons of relative incidence rates. We found 2913 triplet testing results, with a relative distribution in positive results of 65.4% for HSV-1, 32.5% for VZV, and 2.1% for HSV-2. HSV-1 keratitis had a statistically significant higher incidence in men (58.9%, p = 0.0044), while no sex difference was detected for VZV (47.9%, p = 0.6683), HSV-2 (33.3%, p = 0.5078), or CMV (100%, p = 0.500). Bilateral infections were present in two patients, and co-infections were detected as follows: 8 cases of HSV-1/VZV co-detection, 3 cases of Acanthamoeba, and 15 of fungi. HSV-1 was the overwhelmingly dominant cause of herpetic keratitis at our institution, occurring more than twice as frequently as VZV and vastly outnumbering HSV-2. The statistically significant higher incidence in men in HSV-1 keratitis suggests possible biological or sociodemographic influences, whereas co-infections highlight the complexity of corneal pathology in a referral setting. These findings underscore the importance of multiplex PCR testing for accurate pathogen detection and provide insights into the epidemiologic landscape of herpetic keratitis.

Accurate classification of ophthalmic lesions depends on robust feature engineering and transparent machine learning (ML) pipelines. We propose an ensemble ML‑based framework for diagnosing eye herpes (NAGIN) using a simulated dataset of 712 anterior eye images (350 herpes‑like, 362 non‑herpes). Five features - fractal dimension, solidity, eccentricity, branching index, and terminal bulb ratio, were extracted from segmented contours and used for supervised learning. Six ML classifiers were evaluated: logistic regression, support vector machine (RBF kernel), random forest, gradient boosting, XGBoost, and k‑nearest neighbours. Performance was assessed using accuracy, precision, recall, F1‑score, and AUC. Ensemble methods delivered perfect diagnostic outcomes, with Random Forest, Gradient Boosting, and XGBoost achieving 100% accuracy, F1‑score, and AUC. Logistic regression and SVM gave excellent results, with accuracy around 98.6% and an AUC close to 1. In comparison, KNN did a bit worse, reaching about 96.5% accuracy and an AUC of 0.983. Feature importance analysis identified fractal dimension, branching index, and terminal bulb ratio as dominant predictors, while correlation analysis reinforced biological plausibility by linking dendritic branching with fractal complexity and elongated morphology with reduced solidity. These results highlight the value of engineered shape features combined with ensemble ML strategies for reliable ophthalmic diagnosis and provide a scalable foundation for Explainable Artificial Intelligence (EAI) in Medical Image Analysis (MIA).

Herpes simplex virus keratitis is one of the leading causes of blindness worldwide. The observed inflammatory changes may result from a primary ocular infection or, more commonly, from recurrent reactivation of the virus, which remains latent in the trigeminal ganglion. The diagnosis of clinically active herpetic eye disease is based primarily on the characteristic clinical features of the lesions. Clinical manifestations include epithelial keratitis, stromal keratitis with or without ulceration, and endothelial keratitis. In addition, herpes simplex virus is a frequent cause of neurotrophic keratopathy. Establishing the diagnosis may be particularly challenging in cases of long-standing or frequently recurrent lesions, as well as in patients with coexisting systemic conditions that impair immune function. Currently, the cornerstone of therapy for herpetic keratitis – tailored to the clinical form of the disease – consists of antiviral agents and topical corticosteroids. This paper summarizes current knowledge on the pathophysiology, diagnosis, and treatment of herpes simplex virus keratitis and presents the authors’ own experience with the broad spectrum of clinical manifestations observed in this condition.

This report presents two rare cases of presumed epithelial keratitis secondary to ocular tuberculosis (TB), highlighting an unusual clinical presentation that may be underrecognized. Two male patients from a TB-endemic region presented with unilateral, chronic epithelial keratitis in a semicircular pattern, with mild anterior stromal infiltration and reduced corneal sensitivity. Both were unresponsive to standard topical and systemic treatments including antivirals and corticosteroids. Diagnostic evaluation included Mantoux testing and systemic screening. Mantoux tests were positive in both patients, and one exhibited radiological evidence of latent pulmonary TB. Initiation of systemic antituberculosis therapy led to complete epithelial healing within 30 to 60 days in both cases. Each patient developed localized stromal scarring without neovascularization, and no recurrence was observed during follow-up periods of 6 months and 4 years, respectively. The absence of neovascularization, despite the chronicity of keratitis, may be a distinguishing clinical feature from herpetic keratitis. These cases illustrate a potentially underdiagnosed manifestation of ocular TB and suggest that tuberculosis should be considered in the differential diagnosis of refractory epithelial keratitis, especially in endemic regions or in patients with epidemiological risk factors. A Mantoux test with induration of 10 mm or greater, even in BCG-vaccinated individuals, may support the diagnosis in the appropriate clinical context. Antituberculosis therapy may be both therapeutic and diagnostic in such cases.

To retrospectively evaluate the efficacy and safety of Micropulse Transscleral Cyclophotocoagulation (MP-TSCPC) in reducing intraocular pressure (IOP) and the number of glaucoma medications in patients with different types of glaucoma over a two-year period. This retrospective audit included 52 eyes from 32 patients treated with MP-TSCPC at Mountainhall Treatment Centre, Dumfries, UK, between August 2021 and September 2023. Standard treatment parameters included 2500 mW power applied for 10 s per quadrant across 9 cycles. Primary outcomes were changes in IOP and the number of glaucoma medications. Secondary outcomes included postoperative complications and changes in the mean deviation of the visual field (MD). The mean preoperative IOP was 21.4 mmHg, which significantly decreased postoperatively to 11.9 mmHg at 4 weeks, 12.75 mmHg at 3 months, 13.4 mmHg at 1 year, and 14.03 mmHg at 2 years. The median IOP reduction at 1 year was 5.0 mmHg with statistical significance (p < 0.0001). The average number of topical medications declined from 2.21 eye drops to 1.58 eye drops. No statistically significant change was observed in visual field MD (p = 0.4838), though disease progression appeared to stabilize (mean MD: -7.1 dB). Complications were infrequent and included mild anterior uveitis (n = 12), cystoid macular edema, recurrence of herpetic keratitis and severe ocular inflammation (n = 1). MP-TSCPC is a safe and effective procedure for medium-term IOP control, particularly in patients with primary open-angle glaucoma. It significantly reduces IOP and medication dependency, with a low complication profile. However, outcomes are more variable in secondary glaucoma, especially uveitic cases. These findings support the growing role of MP-TSCPC as a minimally invasive treatment option for glaucoma.

Herpes Simplex Keratitis (HSK) is a leading cause of infectious corneal blindness globally. However, clinical data and visual outcomes specific to the Malaysian population are limited. This study aimed to identify common clinical features, visual outcome and its associated factors in patients treated at a Malaysian tertiary hospital. A retrospective cohort study was conducted at Hospital Pakar Universiti Sains Malaysia (HPUSM) between June 2013 and June 2024. Medical records of patients diagnosed with HSK and followed for at least six months were reviewed. Sixty-seven patients were included. Data collected included demographics, presenting symptoms, best-corrected visual acuity (BCVA) at presentation and after treatment, ocular findings, subtype of HSK and complications. Statistical analyses were performed using SPSS version 28.0. Paired t-tests was used to analyse changes in BCVA and multiple linear regression was performed to identify factors associated with final visual outcome. The mean age at presentation was 50.42±17.19 years with a slight male predominance (52.2%). Most cases were unilateral (91.1%). Common presenting symptoms were reduced vision (89.6%) and eye redness (85.1%). Keratouveitis was the most frequent subtype (37.3%). Complications included corneal scarring (73.1%), recurrence (49.3%) and glaucoma (11.9%). BCVA significantly improved post-treatment (p<0.001). Older age, central corneal involvement, elevated intraocular pressure at presentation, and stromal vascularisation were significantly associated with poorer visual outcomes. This study outlines the clinical spectrum and visual outcomes of HSK at a tertiary hospital in Malaysia and identifying several predictive factors for poor vision. These findings may aid clinicians in risk stratification and optimising management strategies.

Recurrence of herpes simplex virus keratitis following intravitreal steroid injection

BACKGROUND Tyrosinemia is a metabolic disorder leading to hepatic, renal, and ocular involvement. Ocular manifestations, such as photophobia and pseudodendritic keratitis, can mimic herpetic keratitis without response to antiviral therapy but improve with metabolic intake and appropriate drugs. Although rare, it poses significant challenges, needing a multidisciplinary approach. CASE REPORT A 14-year-old girl with a diagnosis of type 1 hereditary tyrosinemia was evaluated at our tertiary center for persistent photophobia and bilateral ocular discomfort. Previously, a presumptive diagnosis of recurrent bilateral herpetic keratitis had been made, and the patient was started on repeated cycles of topical and systemic antivirals. Slit-lamp examination revealed bilateral dendritiform epithelial lesions in the central cornea, which stained poorly with fluorescein. In vivo confocal microscopy highlighted multiple hyper-reflective linear crystalline deposits at the level of superficial epithelium. Anterior segment optical coherence tomography demonstrated the presence of focal, highly reflective areas in the epithelial layer. Personal medical history was remarkable for tyrosinemia type 1, diagnosed in the first year of life, with incomplete therapeutic adherence. Antiviral therapy was thus discontinued, and a protein-restricted diet was re-introduced, with net improvement. Importantly, partial regression of corneal epithelial lesions was noted, and a decrease of corneal deposits was confirmed using imaging. CONCLUSIONS Corneal pseudodendritic lesions in hereditary tyrosinemia type I can mimic herpetic keratitis, leading to misdiagnosis and unnecessary antiviral treatments. In vivo confocal microscopy is a valuable tool for disease monitoring. A strict low-protein diet significantly reduces corneal lesions and symptoms in the context of type 1 tyrosinemia.

Analysis for the association of polymorphic variants of the VDR gene(rs2228570) with the risk of herpetic keratitis occurrence after COVID-19