Viral Kerato-Uveitis with Choroidal Vitiligo.

Purpose: To describe unusual fundus findings in typical varicella zoster (VZV) kerato-uveitis.Methods: Observational, retrospective case study of five patients diagnosed with VZV kerato-uveitis.Results: Four out of five cases had a history of typical herpes zoster ophthalmicus skin rash over the forehead. All five patients had stromal keratitis, granulomatous keratic precipitates, and mild-moderate anterior chamber reaction, and two cases had typical VZV-iris atrophic changes. All cases demonstrated clear vitreous and multiple hypopigmented choroidal lesions (MHCL) with indistinct borders only in the affected eyes. Imaging studies failed to demonstrate evidence of active or resolved choroiditis. MHCL remained status quo in all including two cases who had recurrences of kerato-uveitis.Conclusion: We describe previously unreported novel fundus finding, MHCL in typical VZV-kerato-uveitis cases. We presume MHCL are due to loss of melanin from choroidal melanocytes secondary to the VZV infection and propose a term "choroidal vitiligo" to describe these novel fundus findings.

Differential responses of normal human melanocytes to intra- and extracellular dsRNA.

Viral factor has been implicated in the etiopathogenesis of vitiligo. To elucidate the effects of viral double-stranded RNA (dsRNA) on melanocytes and to explore the underlying mechanisms, primary cultured normal human melanocytes were treated with synthetic viral dsRNA analog poly(I:C). The results demonstrated that poly(I:C)-triggered apoptosis when transfected into melanocytes, while extracellular poly(I:C) did not have that effect. Intracellular poly(I:C)-induced melanocyte death was decreased by RIG-I or MDA5 siRNA, but not by TLR3 siRNA. Both intracellular and extracellular poly(I:C) induced the expression of IFNB, TNF, IL6, and IL8. However, extracellular poly(I:C) demonstrated a much weaker induction capacity of cytokine genes than intracellular poly(I:C). Further analysis revealed that phosphorylation of TBK1, IRF3, IRF7, and TAK1 was differentially induced by intra- or extracellular poly(I:C). NFκB inhibitor Bay 11-7082 decreased the induction of all the cytokines by poly(I:C), suggesting the ubiquitous role of NFκB in the process. Poly(I:C) treatment also induced the phosphorylation of p38 and JNK in melanocytes. Both JNK and p38 inhibitors showed suppression on the cytokine induction by intra- or extracellular poly(I:C). However, only the JNK inhibitor decreased the intracellular poly(I:C)-induced melanocyte death. Taken together, this study provides the possible mechanism of viral factor in the pathogenesis of vitiligo.

Hepatitis C and cutaneous alterations / Hepatite C e alterações cutâneas

While most of those infected with hepatitis C virus (HCV) are asymptomatic or only develop liver manifestations, a significant percentage evolves with autoimmune and lymphoproliferative disorders, resulting in a clinical condition called HCV syndrome. This work involving case studies of six patients with hepatitis C and varied skin manifestation aimed to report skin lesions occurring with HCV infection and its treatment. Skin manifestations in hepatitis C have been based on epidemiological studies. This justifies the need for studies that correlate HCV infection and its treatment with skin manifestations.

A maioria dos infectados pelo vírus da hepatite C (VHC) é assintomática ou apresenta somente manifestações hepáticas, porém uma significativa porcentagem evolui com desordens autoimunes e linfoproliferativas resultando na síndrome da hepatite C. Este trabalho envolve seis estudos de casos de pacientes com hepatite C e várias manifestações cutâneas, visando relacionar lesões dermatológicas ao VHC e ao seu tratamento. Manifestações dermatológicas na hepatite C têm sido baseadas em estudos epidemiológicos. Isto justifica a necessidade de estudos que correlacionem infecção pelo VHC e seu tratamento com as manifestações dermatológicas.

Hepatitis C and cutaneous alterations.

While most of those infected with hepatitis C virus (HCV) are asymptomatic or only develop liver manifestations, a significant percentage evolves with autoimmune and lymphoproliferative disorders, resulting in a clinical condition called HCV syndrome. This work involving case studies of six patients with hepatitis C and varied skin manifestation aimed to report skin lesions occurring with HCV infection and its treatment. Skin manifestations in hepatitis C have been based on epidemiological studies. This justifies the need for studies that correlate HCV infection and its treatment with skin manifestations.

Disseminated vitiligo developing around Kaposi sarcoma nodules in an AIDS patient.

Vitiligo and other autoimmune disorders are increasingly being reported in a background of immunosuppression. Viral-induced immune activation and molecular mimicry are the proposed mechanisms for the development of autoimmune diseases in individuals infected with human immunodeficiency virus (HIV). An association of vitiligo with Kaposi sarcoma (KS) rarely has been reported. The development of vitiligo preferentially around KS lesions in a patient with AIDS is unusual. We report a case of disseminated vitiligo that developed around KS nodules in a patient with AIDS.

Segmental vitiligo following encephalitis.

We describe a rare account of a patient who developed segmental vitiligo within several months of an episode of viral encephalitis. This case provides further support to the neuronal hypothesis in the etiology of segmental vitiligo. A literature review of the neuronal theory and pathogenesis of vitiligo is further discussed.

Herpesvirus connection in the expression of autoimmune vitiligo in Smyth line chickens.

The Smyth line (SL) chicken is an animal model for human vitiligo, a common acquired depigmentary disorder affecting about 1-2% of people worldwide. The vitiligo-like depigmentation in SL chickens typically develops when the birds are between 6 and 14 weeks of age and may affect 70-95% of hatch mates. The development of SL vitiligo is considered to depend on two interacting components, namely an inherent melanocyte defect and an autoimmune reaction to melanocytes. Recently, a role for an environmental factor in the expression of vitiligo was suggested by the observation that only 10% of SL chicks imported from the University of Massachusetts (UM) and reared in isolation at biosecurity level 2 (BSL 2) at the University of Arkansas (UA) exhibited vitiligo. Following further assessment of environmental differences between UA and UM SL chickens, three environmental factors that may have influenced the expression of SL vitiligo were identified. Included were housing condition, status of Mycoplasma synoviae infection, and turkey herpesvirus (HVT) vaccination status. Studies were subsequently conducted at UA and UM to assess the role of these environmental factors in the expression of SL vitiligo. M. synoviae infection was not found necessary for vitiligo expression in SL chickens. However, HVT emerged as a strong candidate for an important environmental factor in SL vitiligo. The connection between HVT and SL vitiligo was confirmed for both BSL 2 and conventional housing. Therefore, the observations reported here suggest a strong causative link between HVT infection and SL vitiligo.