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1. Routes of Transmission

The Herpes Simplex Virus is transmitted mainly through contact with mucous membranes or damaged skin. The routes of infection depend on the viral type (HSV-1 or HSV-2) and patient age:

• Contact-Domestic Route (mainly for HSV-1):

– Infection occurs via direct contact with affected skin, mucous membranes, or saliva of an infected person.

– Auto-inoculation is possible by transferring the virus from the lips, nose, or other areas to the eye via hands, towels, contact lenses, or cosmetics.

• Sexual Route (typical for HSV-2):

– Virus is transmitted sexually, which less frequently causes ophthalmic herpes but can lead to neonatal infections.

• Vertical Transmission:

– HSV-2 is transmitted from mother to child during childbirth. In newborns, herpetic keratitis is often accompanied by generalized infection.

• Rare Routes:

– Aerosol transmission (possible in laboratory or medical settings).

– Blood transfusion (in exceptional cases).

2. Primary Infection

Primary infection occurs upon the first contact with the virus.

Viral entry:

HSV enters through microtraumas of skin or mucous membranes, binding to specific receptors (nectin-1, HVEM) on the cell surface.

Once inside, the virus releases DNA into the host cell nucleus where viral replication begins.

Clinical features:

Most patients experience a subclinical primary infection without pronounced symptoms.

Ophthalmic manifestations may include acute epithelial keratitis or herpetic conjunctivitis.

Immune response:

Primary infection stimulates innate immunity. Type I interferons (IFN-α, IFN-β) inhibit viral replication, and neutrophils and macrophages destroy infected cells.

After the acute phase, the virus migrates along sensory nerve endings to regional ganglia, where latency is established.

3. Latency and Reactivation

HSV latency is a key mechanism enabling lifelong viral persistence.

Latent infection:

Viral DNA is maintained in the nucleus of trigeminal nerve neurons as an episome, not integrated into host DNA.

Latency is supported by expression of non-coding transcripts (Latency-Associated Transcripts, LAT) that suppress viral replication and block apoptosis of infected neurons.

Triggers of Reactivation:

HSV reactivates under factors disrupting immune control:

• Physical: ultraviolet radiation, eye trauma, surgical interventions.

• Immunological: immunosuppression (e.g., HIV, chemotherapy), viral or bacterial infections.

• Emotional: stress, fatigue.

• Hormonal: hormonal shifts in women, menstruation.