I’m a Biologist, and the stuff I’ve read about herpes simplex can fill a book, but we can have a very short discussion on how herpes looks like and gain a better understanding of this strange disease.
Herpes Simplex Morphology
All Herpes Simplex Virus are marked by the formation of large, pink-to-purple (Cowdry Type A) intracellular inclusions that contain intact and disrupted virions and push darkly stained host cell chromatin to the edges of the nucleus. Although cell and nuclear size increase only slightly, herpesvirus produces inclusion-breeding multi-nucleated syncytia, which are diagnostic in smears and blister fluid.
HSV-1 and HSV-2
HSV-1 and HSV-2 cause lesions ranging from self-limited cold sores and gingivostomatitis to the dangerous disseminated visceral infections and encephalitis. Fever blisters or cold sores favor the facial skin around mucosal orifices (lips, nose), where their distribution is frequently bilateral and independent of skin dermatomes, Intraepithelial edema and ballooning degeneration of epidermal cells, often burst and crust over, but some may result in superficial ulcerations.
Gingivostomatitis is usually encountered in children and is caused by HSV-1, it is a vesicular eruption extending from tongue to retro-pharynx and causing cervical lymphadenopathy. Coxsackievirus also causes oral vesicular eruptions in children, although the lesions are milder and limited to the pharynx and tonsils.
HSV causes two forms of corneal lesions. Herpes epithelial keratitis shows typical viral-induced cytolysis of the superficial epithelium and is sensitive to anti-viral drugs. In contrast, herpes stromal keratitis shows infiltrate of mononuclear cells around keratinocytes and endothelial cells, leading to neovascularization, scarring, opacification of the cornea, and eventual blindness. This is an immunological reaction to the HSV infection and responds to corticosteroid therapy.