Читать книгу Herpetic keratitis: from symptoms to recovery - - Страница 6

1. Corneal Infection (Primary Infection)

The virus penetrates the corneal epithelial cells, causing their destruction:

Viral replication:

• In infected cells, the virus utilizes host mechanisms for reproduction.

• New viral particles are released, infecting neighboring cells.

Cellular damage:

• The cytotoxic effect of the virus leads to the death of epithelial cells and formation of characteristic dendritic ulcers.

Role of the immune system:

• Local activation of innate immunity causes influx of neutrophils and release of pro-inflammatory cytokines (IL-1, TNF-α).

• Immune mechanisms protect against systemic viral spread but may cause additional tissue damage.

2. Chronic Inflammation (Stromal Keratitis)

During reactivation, the virus affects deeper layers of the cornea:

• Immune response:

– Reactivation activates T cells, which infiltrate the stromal layers and trigger production of pro-inflammatory cytokines (IFN-γ, IL-17).

– Antibodies against viral antigens may cause complement-dependent stromal damage.

• Neovascularization:

– Chronic inflammation stimulates growth of blood vessels within the cornea, disrupting its transparency.

• Scarring:

– Fibrosis of the stroma due to inflammation leads to persistent reduction of visual acuity.

3. Endothelial Lesions and Keratouveitis

In severe recurrences, the deep corneal layers and anterior chamber are involved:

• Endothelial keratitis:

– Stromal edema and endothelial damage impair corneal hydration.

• Keratouveitis:

– Anterior chamber inflammation may be accompanied by elevated intraocular pressure and secondary glaucoma development.

Modern Concepts of Pathogenesis

See Appendix (QR code linking to Source No.7)

1. Role of Genetic Predisposition:

• Genetic polymorphisms in immune response genes such as TLR3 and IFNL3 may increase the risk of severe herpetic keratitis.

2. Corneal Microbiome:

• Alterations in the ocular surface microbiota are associated with frequent recurrences.

3. Epigenetic Mechanisms:

• Studies indicate that epigenetic changes in trigeminal nerve neurons can modulate HSV latency and reactivation.

Conclusion

The etiology and pathogenesis of herpetic keratitis involve complex interactions among viral factors, immune response, and host conditions. Deep understanding of these processes allows development of new approaches for treatment and prevention, minimizing recurrence risk and long-term complications.