The pathogenesis of acute retinal necrosis is characterized by retinal inflammation due to ocular viral infection. Particles from Herpes simplex virus 1 (HSV-1), Herpes simplex virus 2 (HSV-2), and Varicella zoster virus (VZV) infiltrate the retina through various locations of epithelial penetration, including the skin, conjunctiva, cornea, and nasal cavity. Acute retinal necrosis develops from HSV-1, HSV-2, and VZV due to the viruses' ability to transmit and replicate in the central nervous system (CNS), as well as their ability to transport anterograde through the optic nerve, establish latency, reactivate, and cause retinal inflammation. For Caucasian populations, possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens is correlated to genetic predisposition to ARN. For Japanese populations, possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens is correlated to genetic predisposition to ARN. Acute retinal necrosis is associated with the following ocular conditions: progressive outer retinal necrosis, uveitis, cytomegalovirus retinitis, toxoplasmic chorioretinitis, and endophthalmitis.
Acute retinal necrosis pathophysiology
Acute retinal necrosis risk factors
Acute retinal necrosis laboratory findings
Acute retinal necrosis causes
Diabetic retinopathy pathophysiology
Acute retinal necrosis other imaging findings
Acute retinal necrosis epidemiology and demographics
Acute retinal necrosis diagnostic criteria