Human adenovirus (HAdV) is the most common cause of infectious conjunctivitis, accounting for up to 75% of all conjunctivitis cases and affecting people of all ages and demographics. In addition to ocular complications, it can cause systemic infections in the form of gastroenteritis, respiratory disease, and dissemination in immunocompromised individuals. HAdV causes lytic infection of the mucoepithelial cells of the conjunctiva and cornea, as well as latent infection of lymphoid and adenoid cells. Epidemic keratoconjunctivitis (EKC) is the most severe ocular manifestation of HAdV infection, in which the presence of subepithelial infiltrates (SEIs) in the cornea is a hallmark feature of corneal involvement. SEIs have the tendency to recur and may lead to long-term visual disability. HAdV persistence and dissemination are linked to sporadic outbreaks of adenoviral keratoconjunctivitis. There is no FDA-approved antiviral for treating adenoviral keratoconjunctivitis, and as such, solutions should be proffered to handle the challenges associated with viral persistence and dissemination. Several treatment modalities have been investigated, both systemically and locally, to not only mitigate symptoms but reduce the course of the infection and prevent the risk of long-term complications. These options include systemic and topical antivirals, in-office povidone-iodine irrigation (PVI), immunoglobulin-based therapy, antiinflammatory therapy, and immunotherapy. More recently, combination PVI/dexamethasone ophthalmic formulations have shown favorable outcomes and were well tolerated in clinical trials for the treatment of EKC. Possible, future treatment considerations include sialic acid analogs, cold atmospheric plasma, N-chlorotaurine, and benzalkonium chloride. Continued investigation and evaluation of treatment are warranted to reduce the economic burden and potential long-term visual debilitation in affected patients. This review will focus on how persistence and dissemination of HAdV pose a significant challenge to the management of adenoviral keratoconjunctivitis. Furthermore, current and future trends in prophylactic and therapeutic modalities for adenoviral keratoconjunctivitis will be discussed.

Allergic conjunctivitis is predominantly an immunoglobulin E-mediated hypersensitivity reaction to environmental allergens. Allergic diseases affect >30% of the world’s population, of which 40% report associated ocular manifestations. Cellular and soluble mediators play a major role in the pathophysiology of allergic conjunctivitis. Mast cells, which are major effector cells of allergic conjunctivitis, undergo activation and degranulation to release histamine, tryptase, prostaglandins, leukotrienes, and cytokines. These mediators play important roles in immunopathological mechanisms that generate the clinical manifestations of allergic conjunctivitis. These clinical features include conjunctival hyperaemia, chemosis, tearing, itching, papillae, mucus discharge, and eyelid oedema. Histamine mediates the early phase of the allergic immune response, whereas lipid mediators and cytokines are involved in the late phase of the immunopathology of allergic conjunctivitis. Current management of allergic conjunctivitis includes non-pharmacological approaches such as allergen avoidance and palliative therapy, whereas pharmacological therapeutic modalities may include antihistamine–mast cell stabiliser combination ophthalmic formulations and allergen-specific immunotherapy. Furthermore, as cellular and soluble mediators play a pivotal role in the immunopathogenesis and immunopathology of allergic conjunctivitis, development of immunotherapeutic and pharmacotherapeutic agents specific to these mediators can enhance the therapeutic index and safety profile of anti-allergy treatment.