Prognosis and Management of Corneal Transplantation for Herpetic Keratitis

BackgroundAutosomal recessive congenital hereditary corneal dystrophy (CHED) is a rare isolated developmental anomaly of the eye characterised by diffuse bilateral corneal clouding that may lead to visual impairment requiring corneal transplantation. CHED is known to be caused by mutations in the solute carrier family 4 member 11 (SLC4A11) gene which encodes a membrane transporter protein (sodium bicarbonate transporter-like solute carrier family 4 member 11).MethodsTo identify SLC4A11 gene mutations associated with CHED (OMIM: #217700), genomic DNA was extracted from whole blood and sequenced for all exons and intron-exon boundaries in two large Tunisian families.ResultsA novel deletion SLC4A11 mutation (p. Leu479del; c.1434_1436del) is responsible for CHED in both analysed families. This non-frameshift mutation was found in a homozygous state in affected members and heterozygous in non-affected members. In silico analysis largely support the pathogenicity of this alteration that may leads to stromal oedema by disrupting the osmolarity balance. Being localised to a region of alpha-helical secondary structure, Leu479 deletion may induce protein-compromising structural rearrangements.ConclusionTo the best of our knowledge, this is the first clinical and genetic study exploring CHED in Tunisia. The present work also expands the list of pathogenic genotypes in SLC4A11 gene and its associated clinical diagnosis giving more insights into genotype–phenotype correlations.

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Incidence of Fungal Infection in Positive Donor Rim Cultures after Corneal Transplantation

Ocular Immunology and Inflammation ◽

10.1080/09273948.2020.1841806 ◽

2021 ◽

pp. 1-5

Author(s):

Julia Shatten ◽

Roheena Kamyar ◽

Deepinder Dhaliwal ◽

Regis P. Kowalski ◽

Vishal Jhanji

Keyword(s):

Fungal Infection ◽

Corneal Transplantation

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Assessment of antiviral activity, efficacy, and toxicity of prostaglandin A2 in a rabbit model of herpetic keratitis.

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.40.10.2327 ◽

1996 ◽

Vol 40 (10) ◽

pp. 2327-2331 ◽

Cited By ~ 11

Author(s):

W J O'Brien ◽

J L Taylor ◽

H Ankel ◽

G Sitenga

Keyword(s):

Antiviral Activity ◽

Cultured Cells ◽

Rabbit Model ◽

Herpetic Keratitis ◽

Human Cornea ◽

Latently Infected ◽

Blood Aqueous Barrier ◽

Prostaglandin A2 ◽

Simplex Virus ◽

Pharmacologically Active

Prostaglandin A2 (PGA2) inhibited the replication of herpes simplex virus type 1 in rabbit and human cornea stromal cells at concentrations of 1 to 5 microM while causing significant toxicity at 55 to 150 microM. Despite favorable therapeutic indices in cultured cells, PGA2 was not effective as a therapeutic agent in the treatment of herpetic keratitis in a rabbit model. The sequelae of disease appeared more severe in animals receiving PGA2 than in untreated or placebo-treated controls. The recovery of virus from tissues of latently infected rabbits was not affected by therapy. PGA2 therapy alone induced breakdown of the blood-aqueous barrier, indicating that pharmacologically active concentrations of drug were achieved in the eye. Thus, PGA2 had antiviral activity, but its proinflammatory effects appeared to be more detrimental than beneficial in the treatment of herpetic keratitis.

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