**2. Pathogenesis of the HSV keratitis**

General pathogenesis of herpesvirus infections include: active viral replication, state of latency and reactivation. Primary infection, usually in the childhood could be asymptomatic, oral, but also could affect upper respiratory track or ocular surface in the form of the conjunctivitis or blepharoconiunctivitis. After a primary infection, HSV-1 begins a life-long latency in the trigeminal ganglia, where abundant viral RNAs are constantly produced. In order to establish latency, HSV-1 has evolved several mechanism to evade the host immune response. The process is complex based on HSV-1 several viral proteins targeting multiple steps of the cellular DNA-sensormediated antiviral signal pathway of the host. Moreover, it is believed, that viral protein activation varies between immediate period after infection and the late phase of infection. Inhibition of the type I interferon (IFN-I) activity has been described as the main pathogenetic pathway of downregulating the host immune response. Numerous mechanism including: inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, modulating interferon regulatory factor 3 (IRF3), interferon regulatory factor 7 (IRF7) or stimulator of IFN genes (STING) function were identified. Recently a broad attention was brought to the HSV-1 immediate early (IE) protein infected-cell polypeptide 0 (ICP0), which is an E3 ubiquitin ligase, a nuclear phosphoprotein that was described to play an essential role in inhibition of IFN-I production through IRF7 protein expression reduction, thus promoting viral replication, latency, and reactivation. Certain triggering agents, physiological and environmental stress, including ultraviolet exposure, fever, injury, hormonal disruption or immunosuppression could cause viral reactivation in the tissues innervated by the trigeminal ganglion, causing different forms of the HSV keratitis: epithelial, stromal or endothelial. Epithelial keratitis is the most common form of HSV keratitis, but the recurrence infection may also affect other corneal layers. Recurrence varies in frequency between subjects and throughout the life and could cause irreversible corneal damage and decrease in visual acuity, ranging from superficial opacities to serious complications such as corneal perforation and endophthalmitis [6–10].

## **3. Diagnosis**

The diagnosis of HSV keratitis is mainly based on the presence of typical unilateral corneal lesions on the slit lamp examination. However, the clinical diagnosis may be guided by modern imaging techniques, such as optical coherence tomography or confocal microscopy. Also, laboratory testing including polymerase chain reaction (PCR) and novel techniques based on multiplex dot hybridization (MDH) assay or immunochromatographic assay (ICGA) may serve as a potential guide in the diagnostic process.

#### **3.1 Symptoms**

Patients symptoms depend on the clinical form and stage of the disease. Primary infection may be asymptomatic. Recurrent infections symptoms include: foreign

#### *Recent Advances in the Diagnosis and Management of Herpetic Keratitis DOI: http://dx.doi.org/10.5772/intechopen.96898*

body sensation, ocular or ocular adnexa pain, lacrimation, photophobia, decreased vision and conjunctival hyperemia. Symptoms are usually not specific. Although, patient with recurrent keratitis are aware of the symptoms of the recurrent keratitis, which allows for the rapid referral and treatment. Patients with neutrotrophic keratitis due to HSV keratitis may experience only mild symptoms despite the advanced corneal involvement.
