Varicella zoster virus as a possible trigger for the development of pityriasis lichenoides et varioliformis acuta: retrospective analysis of our institutional cases.

Although numerous infective agents, including varicella zoster virus (VZV), have been described in association with pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica (PLC), none has been identified consistently in these lesions. We sought to immunohistochemically identify VZV glycoprotein (g)E antigens in the vascular endothelium in PLEVA and PLC lesions, based on our previous observation that gE was detected in the vascular endothelium and eccrine unit up until 2 months and 2.5, respectively, years after herpes zoster (HZ) infection. In five of the six cases of PLEVA, VZV gE was identified in the endothelial cells and eccrine epithelium, as observed in HZ lesions, whereas VZV gE was detected in only one of seven patients with PLC. None of the patients with PLEVA who had VZV gE-positive vascular endothelial cells had experienced previous episodes of HZ. VZV may be one of the aetiological agents for PLEVA while other aetiological factors could exist in PLC.

Detection of varicella-zoster virus antigens in lesional skin of zosteriform lichen planus but not in that of linear lichen planus.

BACKGROUND: Distinctions between 'linear lichen planus' (LP) and 'zosteriform LP' are difficult to determine solely based on clinical findings. OBJECTIVE: The aim of this study is to determine whether the presence of the varicella-zoster virus (VZV) antigens could be used to differentiate the zosteriform LP from the linear LP. METHODS: We immunohistochemically investigated the presence of in vivo localization of VZV antigens in 8 LP lesions (zosteriform LP: n = 5, linear LP: n = 3). RESULTS: We describe 2 cases of zosteriform LP without apparent prior episodes of herpes zoster, in whom VZV antigens were detected in the eccrine epithelium. Further analysis showed that VZV antigens were exclusively detected in the eccrine epithelium in the zosteriform LP lesions, but not in the linear LP lesions. CONCLUSION: Etiological differences exist between zosteriform LP and linear LP. The presence of VZV antigens in lesional skin of the former indicates a possible triggering role of this virus in the pathogenesis of this variant.

Varicella-zoster virus antigen expression of eccrine gland and duct epithelium in herpes zoster lesions.

BACKGROUND: It is well known that varicella-zoster virus (VZV) exhibits tropism for the epidermis and follicular epithelium, while little attention has been paid to eccrine gland and duct involvement by VZV. The presence of herpetic syringitis in immunocompromised hosts suggested the possibility of eccrine gland and duct involvement by VZV. OBJECTIVES: To determine whether VZV antigens could be detected in eccrine gland or duct epithelium of herpes zoster (HZ) lesions obtained at various intervals after the onset of a rash, and whether this expression could also be detected in eccrine units from other inflammatory disease lesions suggestive of VZV infection. METHODS: We investigated immunohistochemically in vivo localization of VZV glycoprotein E (gE) antigen in HZ lesions and control inflammatory disease lesions, using the murine monoclonal antibody directed against the VZV gE. RESULTS: VZV gE was differentially detected in the epidermis, follicular and eccrine epithelium, and dermal infiltrating cells in HZ lesions obtained at various intervals after onset. The VZV gE was most persistently detected in eccrine units, regardless of the age of individual HZ lesions, compared with keratinocytes and follicular epithelium. the ge expression was also observed in other inflammatory disease lesions suggestive of vzv infection. CONCLUSIONS: Immunohistochemical detection of VZV gE in eccrine epithelium can be a subtle clue to the diagnosis of HZ which displays most unusual manifestations, and VZV-related disorders.

Decreased dopamine D receptor binding in essential blepharospasm.

OBJECTIVES: The purpose of this study was to investigate whether dopamine D(2) receptor binding was altered in the striatum of essential blepharospasm patients. METHODS: Striatal dopamine D(2) receptor binding was measured with positron emission tomography and [(11)C]raclopride. We studied eight drug-naive patients with bilateral blepharospasm and eight age-matched normal controls. RESULTS: The uptake indices in the blepharospasm group were significantly reduced by 11.7% in the caudate (P < 0.005), 11.6% in the anterior putamen (P < 0.0001), and 10.3% in the posterior putamen (P < 0.005) relative to the control group. CONCLUSIONS: This study indicates decreased dopamine D(2) receptor binding in the entire striatal region of blepharospasm patients. The findings suggest that decreased dopamine D(2) receptor binding might be one of the predisposing factors that leads to the dysfunction of the motor circuit, resulting in the loss of broad inhibition of unwanted movements during an intended movement in blepharospasm patients.

Mutations in a hydrophilic part of the core gene of hepatitis C virus in patients with hepatocellular carcinoma in China.

We investigated the association between hepatocellular carcinoma (HCC) and the genomic characteristics of the hepatitis C virus (HCV) isolated from residents of the inshore region of the Yangtze River, an area that has one of the highest incidence of HCC in China. We determined the genomic heterogeneity of HCV, and the sequence divergence of the HCV core gene in individuals with chronic hepatitis and HCC. HCV genotype II was predominant among these isolates, which were homologous to other Chinese and Japanese HCV isolates. The rate of nucleotide substitutions in the core gene was significantly greater for isolates from HCC patients than for those from individuals with chronic hepatitis. The nucleotide substitutions were unevenly scattered along the core gene; a cluster of missense mutations was apparent in the region encoding the second hydrophilic domain of the core protein. The rate of occurrence of missense mutations per nucleotide substitution was significantly greater in this clustering variable region (CVR) of the core gene than in the remaining core gene sequence. These observations suggest that mutations in the CVR may be involved in the pathogenesis of chronic HCV infection during hepatocellular carcinogenesis.

Detection of different quasispecies of hepatitis C virus core region in cancerous and noncancerous lesions.

The quasispecies of hepatitis C virus (HCV) core region in non-cancerous and cancerous hepatocellular carcinoma (HCC) lesions, respectively, of 7 patients with hepatocellular carcinoma were studied. Multiple fluorescence based-polymerase chain reaction (PCR)-single strand conformation polymorphism exhibited a different set and a larger number of quasispecies in cancerous portions than those in non-cancerous portions. DNA sequencing of PCR-amplified core region substantiated an accumulation of nucleotide substitutions, and a greater number of quasispecies in cancerous portions than those in non-cancerous portions. The deduced amino acid sequences disclosed that at the peptide position 45, Ser is dominant in non-cancerous lesions, and Gly in cancerous lesions, respectively. Thus, HCV in hepatocellular carcinoma includes a large number of specific quasispecies presumably due to their vigorous proliferation. A different set of quasispecies with the amino acid change is presumed to be related to the hepatocarcinogenesis.

Virological features of hepatitis C virus infection in patients with liver diseases in the inshore area of the Yangtze River.

The prevalence, genotypes, coinfection and putative core gene sequence of hepatitis C virus (HCV) were investigated in the inshore area of the Yangtze River, where hepatocellular carcinoma (HCC) is thought to be very common. Most patients with liver diseases were infected with hepatitis B virus (HBV), but the incidence of anti-HCV was very low, being 3.4% in patients with acute hepatitis, and approximately 7% in those with chronic liver diseases. The rate of coinfection with HBV and HCV in patients with HCC was 4.5%, which was similar to that in Shanghai (5.6%), but lower than that in Yangzhou (31.2%), Beijing (26.8%) and Zhejiang (28.6%). Of 124 patients with non-A, non-B (NANB) liver disease, 15 (12.1%) were positive for anti-HCV. HCV genotype analysis in 41 HCV-RNA-positive patients with liver diseases showed that genotype II was dominant (85.4%), followed by genotype III (7.3%) and II+III (7.3%). No genotype I or IV was found. The genome sequences of the HCV putative core gene from two patients with chronic hepatitis were more closely similar to those of previous isolates from Japan and China, than to that of an American isolate. These results suggest that HCV infection is not an important etiological factor for liver diseases, and that the HCV isolates in China are from the same subgroup as those in Japan.