Conventional (Western) Method of Ocular Herpes Treatment

The approach to managing patients with ocular herpes employed in Europe, the USA and several Asian countries boils down to the following combination: chemotherapy agent + corticosteroid.

I. Chemotherapy drugs

In 1962, H.E. Kaufman introduced the first chemotherapy agent aimed at ocular herpes, IDU. In 1978, Acyclovir (also known as Zovirax) was developed. IDU has almost no place in modern ophthalmology, with the most popular chemotherapy drugs being Acyclovir, Cidofovir and Foscarnet.

The mechanism of action of these agents is associated with inhibition of viral replication inside cells to a greater (Acyclovir) or lesser (other drugs) extent.

However, their toxicity is so high that it often mitigates the therapeutic effect. Among the disadvantages of chemotherapy agents are:

  • high toxicity and severe allergic reactions:
    • local: edema up to chemosis, redness, irritation of the eyelids and other ocular structures, inflammation of the iris, hypotony (Cidofovir),
    • systemic: nephrotoxicity, neurotoxicity, anemia, severe headache, vomiting, ulceration of the genitourinary tract (Foscarnet),
  • emergence of resistant viral strains,
  • efficacy limited to superficial forms of herpes,
  • limited specificity; for instance, Acyclovir is only effective against HSV and varicella- zoster.

To be fair, Acyclovir has several advantages over other chemotherapy agents and is an effective antiviral drug. It is an irreplaceable “antiviral shield” for patients after corneal grafting for ocular herpes.

The combination of Acyclovir and Poludan is the gold standard for ocular herpes. According to A.A. Kasparov (1991), combined use of these two drugs with different mechanisms of action provided a synergistic effect which translated into shorter treatment courses and increased recovery rates.

II. Corticosteroids (Dexamethasone, Hydrocortisone, etc.)

It is now well known that steroids promote herpes infection in the cornea and are thus unacceptable as monotherapy without antiviral agents.


  • inhibit interferon and antibody production in ocular tissues which means they undermine natural defenses and
  • thus lead to activation of the virus (as it is no longer kept at bay) and dangerous complications:
    • chronicity - the patient cannot recover as the disease keeps returning,
    • worsening of the initial condition - rapidly progressing necrosis of the cornea, lens involvement (complicated cataract), keratouveitis,
    • increase in intraocular pressure and secondary glaucoma,
  • inhibit normal immune response and thus pave the way to secondary bacterial infection, which leads to purulent inflammation (hypopyon keratitis), ulceration and corneal melting,
  • slow down healing by suppressing regenerative processes in tissues.

It is these steroid-complicated forms of herpes simplex keratitis that are the leading causes of blindness and disability as a result of rapid development of severe leucoma and corneal perforation with subsequent complicated cataract, secondary glaucoma and endophthalmitis.

The latter two complications along with acute retinal necrosis are frequent causes of irreversible blindness associated with ocular herpes.

Summing up, the first component (chemotherapy drugs) leads to severe toxic reactions and gives rise to resistant viral strains, while the second (steroids) compromises the immune system, activates the virus, hampers regeneration and promotes secondary bacterial infection resulting in severe complications and even blindness.