Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection

Area of Science:

• Virology
• Immunology
• Cell Biology

Background:

• Herpes simplex virus type 1 (HSV1) is a widespread human pathogen causing oral lesions and serious ocular diseases like herpes stromal keratitis and acute retinal necrosis.
• HSV1 establishes lifelong latency in neurons, evading host immune responses.
• Programmed cell death (PCD) pathways (apoptosis, necroptosis, pyroptosis) are critical innate immune mechanisms for eliminating infected cells and regulating inflammation.

Purpose of the Study:

• To review key studies on programmed cell death (PCD) pathways manipulated by HSV1.
• To elucidate how HSV1 subverts host cell death mechanisms to establish infection and modulate inflammation.
• To correlate cell death pathways with HSV1 infection outcomes, particularly ocular diseases.

Main Methods:

• Review of existing literature on HSV1, programmed cell death (PCD), and ocular diseases.
• Analysis of studies detailing HSV1's strategies to evade or manipulate host cell death pathways.
• Synthesis of information on the role of apoptosis, necroptosis, and pyroptosis in HSV1 pathogenesis.

Main Results:

• HSV1 has evolved multiple strategies to evade or manipulate host PCD pathways, including apoptosis, necroptosis, and pyroptosis.
• These evasion strategies allow HSV1 to subvert viral clearance and modulate inflammatory responses.
• Dysregulation of cell death contributes to persistent infection and the development of severe ocular manifestations.

Conclusions:

• HSV1 actively manipulates host programmed cell death (PCD) pathways to ensure its survival and persistence.
• Targeting HSV1's manipulation of PCD offers potential therapeutic strategies for managing viral infections and preventing ocular disease.
• Further research into the intricate interplay between HSV1 and host cell death is essential for developing effective treatments.