VZV-Associated Site-Specific Psoriatic Eruption: Koebnerization and Possible Isotopic Response

Background The Koebner phenomenon in psoriasis is predominantly attributed to a keratinocyte-centred mechanism (EGFR-ERK/JNK → CCL20/CXCL8) induced by mechanical trauma [1]. Psoriatic eruptions localized to sites previously affected by varicella or herpes zoster are rare but repeatedly reported; depending on the trigger, they may represent classical Koebnerization, Wolf's post-herpetic isotopic response, or an overlap of both, and this paper distinguishes between them rather than assuming a single mechanism. Hypothesis (I) a neurogenic axis in which VZV-associated neuritis and local tissue injury are hypothesized — not yet demonstrated — to engage sensory neuroimmune signalling, releasing substance P (SP) and CGRP from cutaneous sensory nerve endings and activating dermal dendritic cells (NK-1 and CGRP receptors) to secrete IL-23/IL-12, converging on the same downstream node as the established keratinocyte mechanism; (II) an independent experimental agenda proposing that, if a measurable population of circulating or skin-accessible phagocytes carrying persistent vaccine-derived aluminum exists in a given adult patient, the inflammatory signal generated by a primary varicella infection could recruit CCR2+ monocytes to skin by a pathogen-independent mechanism, with age treated as a possible modifier rather than a defining requirement. Evidence Four independent case reports (1969–2015) document psoriatic eruptions localized to sites of varicella or herpes zoster. Axis I is supported by general cutaneous neuroimmunology literature, not by studies dedicated to VZV, and the isotopic-response literature offers a competing explanation for the zoster-associated cases. Axis II lacks any clinical case combining varicella with aluminum exposure and lacks direct evidence of a distal biopersistent-aluminum phagocyte pool in vaccinated adults; a separate set of case reports describes temporally associated psoriatic onset after aluminum-adjuvanted vaccination alone, without establishing aluminum, rather than antigen or nonspecific immune activation, as the causal component. Population-level data on childhood vaccine aluminum and chronic disease exist but study a different population, exposure window, and outcome set, and are not treated here as bearing directly on this hypothesis. Conclusions We present both axes with explicit epistemic labelling (established / hypothesized / contradictory or unstudied) and formulate five testable predictions, most but not all admitting a clean positive/falsification pair.