A naturally occurring species-specific defense against viruses, interferon is synthesized intracellularly and increases resistance to viral infection. Synthetic analogues such as polyinosinic acid–polycytidylic acid have induced patients to form their own interferon.
Topically administered interferon (off-label) is ineffective in the treatment of epidemic keratoconjunctivitis caused by adenovirus. Likewise, interferon alone has little effect on herpes simplex keratitis. In combination, however, it seems to act as a topical adjuvant to traditional antiviral therapy in resistant herpes simplex keratitis. In one study of patients with herpes simplex keratitis, interferon used in conjunction with acyclovir yielded significantly faster healing time than treatment with acyclovir alone (5.8 vs 9.0 days, respectively). Interferon also speeds the healing of epithelial defects when used in combination with trifluridine. The dosage of interferon (30 million IU/mL) is 2 drops per day for the first 3 days of treatment.
Interferon also has been shown to inhibit vascular endothelial cell proliferation and differentiation. It is particularly effective in the treatment of juvenile pulmonary hemangiomatosis, which was fatal before the development of interferon. Interferon alfa-2b (off-label), administered subconjunctivally, intralesionally, and/or topically, is a treatment option for conjunctival intraepithelial neoplasia and invasive squamous cell carcinoma (see BCSC Section 8, External Disease and Cornea). Intralesional administration of interferon is reported to be especially effective in ocular Kaposi sarcoma.
Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.