Th1 regulatory events by infectious pathogens, herpes zoster and herpes simplex viruses: prospects for therapeutic options for atopic eczema

Abstract

Infections caused by viral and bacterial pathogens are typically perceived as harmful, such as in cases of herpes zoster and herpes simplex virus infections. However, clinical observation of an improvement in atopic skin lesions upon herpes virus infection has been noted, particularly at the site of varicella and Kaposi's varicelliform eruption. Th1 immune cells and cytokines, mobilized and induced for protection against infectious pathogens, are expected to improve Th2 dominant atopic symptoms. This study focuses on Th1 immunoregulatory events mediated by infectious pathogens, particularly herpes viruses. Immunoregulatory events induced by herpes viruses may have a potential therapeutic value for treating atopic eczema.

Herpez Zoster in Teens

“…The diagnosis of shingles is generally based on the clinical picture with the establishment of the diagnosis with the presence of prodromal symptoms in the form of pain, typical dermatomal distribution, the presence of clustered vesicles or in some cases papules found, several groups of lesions fill the dermatome, especially where there are sensory nerves, there is no history of similar rashes in the same distribution (getting rid of herpes simplex zosteriformis), and pain and allodinia (pain arising with a stimulus which normally does not cause pain) at the area of the rash (Horiuchi, 2022). Shingles usually begins with prodromal symptoms for 2-4 days, namely systemic (fever, dizziness, malaise), and local (muscle pain, itching, aches).…”

Atopic Dermatitis and the Risk of Infection in End-Stage Renal Disease

“…Some of the genes linked to the process of AD include those encoding proteins involved in the differentiation of keratinocytes and the maintenance of the skin barrier [10]. With an impaired epidermal barrier, there is dysregulation of the skin microbiome as seen by the increased Staphylococcus aureus colonization [11]. The combination of skin-barrier defects, an overactive immune system, and skin-microbiome dysfunction allows for an increased risk of viral and bacterial infections [12].…”