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Biomedical subjects

R Muraki

Publications and source records attributed to R Muraki.

11 recordsLinked to original sources
PubMed2001

Pathway of viral spread in herpes zoster: detection of the protein encoded by open reading frame 63 of varicella-zoster virus in biopsy specimens.

Reactivation of varicella-zoster virus (VZV) in the dorsal root or trigeminal ganglia causes herpes zoster. The pathway of viral spread from the ganglia to the skin and also within the skin is not yet completely understood. Histological studies have revealed that each skin lesion in herpes zoster progresses sequentially through the stages of erythema, vesicles, pustules and finally ulceration. An immunohistochemical study of the early skin lesions of herpes zoster demonstrated a high incidence of hair follicle involvement and the main localization of the virus at the isthmus. This evidence suggests that VZV initially spreads from the ganglia through myelinated nerves, which predominantly end around the isthmus of hair follicles. To further investigate the viral spread within the skin, we analyzed the sequential appearance of the immediate early proteins encoded by ORF 63 of VZV (IE63), using an anti-IE63 antibody raised by immunization of rabbits with a recombinant protein. This antibody could detect IE63 in a western blot analysis of infected cells and also in immunohistochemical analysis of the skin lesions of herpes zoster. IE63 initially appeared in the nuclei of the follicular epithelial cells and basal or parabasal epidermal cells. Later, the nuclei and cytoplasm of cells in the epidermis and hair follicles became positive. IE63 remained in the virus-infected cells even during their degeneration. When we examined the hair follicles in the early erythematous lesions, cells positive for IE63 were predominantly distributed around the isthmus. In addition, some lymphocytes around the blood vessels were also positive for IE63, but these cells were seldom positive for the structural antigen. Thus, these observations suggest that VZV arriving through myelinated nerves infects not only permissive cells, but also non-permissive cells in the involved skin of herpes zoster.

Animals↗
PubMed1996

Hair follicle involvement in herpes zoster: pathway of viral spread from ganglia to skin.

Herpes zoster is caused by reactivation of varicella-zoster virus (VZV) persisting in dorsal root or trigeminal ganglia. To clarify the pathway of viral spread from the ganglia to skin, 16 biopsy specimens of early skin lesions of herpes zoster obtained from the face and trunk of 13 patients were studied histologically and immunohistochemically using monoclonal antibodies to the structural proteins of VZV. VZV-infected cells were detected in the hair follicles in 10 of the 16 specimens and in the epidermis in 2 specimens. Infected cells were localized in the isthmus of every involved follicle (12/12), frequently in the stem (8/10) and infundibulum (6/10), and never in the bulb. The high frequency of follicular involvement in herpes zoster suggests that VZV spreads to the area of skin innervated by myelinated nerves, which end around the isthmus of hair follicles and sebaceous glands.

Antigens, Viral↗
PubMed1993

[A case of progressive systemic sclerosis with Sjögren's syndrome presenting with coma, convulsion and bilateral thalamic hypodensity on computed tomography].

A 35-year-old female with progressive systemic sclerosis (PSS) and Sjögren's syndrome developed consciousness disturbance and generalized seizure after the episode of fever and erythema lasting for 3 weeks. Neurological examination disclosed deep coma and spastic tetraplegia with pathological reflexes. Laboratory data showed mild anemia, severe hypoproteinemia, hypoalbuminemia and increase of protein content in the cerebrospinal fluid. Cranial CT scans obtained after convulsion revealed diffuse brain swelling and bilateral symmetrical hypodensity involving the thalami and posterior limbs of the internal capsule. High-dose corticosteroid therapy and osmotherapy with correction of hypovolemia were started, because severe dehydration, hypoalbuminemia and cerebral vasculitis were suspected to change the vascular permeabilities. Neurological symptoms and CT findings were rapidly improved. Cerebral angiography 4 weeks after convulsion showed definite angitis. The patient was discharged 9 weeks after convulsion. In our case, a possible cause of the characteristic CT findings may be the disturbance of cerebral venous return due to hypovolemia and vasculitis. High-dose corticosteroid therapy may be recommended in patients with collagen disease, who show the bilateral symmetrical thalamic hypodensity on CT scans.

Adult↗
PubMed1992

Immunohistochemical study of skin lesions in herpes zoster.

Thirty-seven biopsy skin tissues of herpes zoster taken from 27 patients were analysed immunohistochemically using two monoclonal antibodies detecting either nucleocapsid or glycoproteins of varicella-zoster virus (VZV) on paraffin sections of formalin fixed tissues. Skin lesions of herpes zoster were divided clinically into four stages: erythematous, vesicular, pustular and ulcerative. In the erythematous stage, VZV antigens, if detected, were found only within ballooning cells in the lower epidermis or follicular epithelium. In the vesicular stage, antigens were detected in the cells around and within the intraepidermal vesicles and in histiocytes or fibrocytes of the dermis in all cases and in the endothelial or perineural cells in 10 of 14 cases. In the pustular stage, the antigens were observed in degenerated or necrotic keratinocytes and multinucleated giant cells within pustules and some necrotic cells in the dermis. In the ulcerative stage, the viral antigens were detected only at the ulcer margin and around the hair shaft in 2 of 7 cases. These results suggest that VZV initially involves the epidermis in the erythematous stage, subsequently invades the dermis in the vesicular stage, and disappears in the early ulcerative stage.

Antigens, Viral↗
PubMed1991

Differentiation disorders of keratinocytes in seborrheic keratosis (acanthotic type).

Since the differential disorder of keratinocytes in seborrheic keratosis remains to be elucidated, the differentiation of seborrheic keratosis (acanthotic type) was examined immunohistochemically using a lectin and two anti-keratin monoclonal antibodies. A lectin, peanut agglutinin (PNA), and anti-keratin monoclonal antibody, 34 beta B4, recognize the whole epidermis except for the basal layer in the normal epidermis. In seborrheic keratosis (acanthotic type), cells unstained with either PNA or 34 beta B4 were found throughout the entire tumor. In the upper part of the tumor, some cells appeared to undergo keratinization without expressing the differential markers recognized by PNA or 34 beta B4. Another anti-keratin monoclonal antibody, 34 beta E12, stained the tissues in the same way as in the normal epidermis. Thus it was indicated that, in seborrheic keratosis (acanthotic type), although differentiation was partially maintained, some cells might undergo maturation without expressing the differentiation markers recognized by PNA or 34 beta B4.

Aged↗
PubMed1986

Antibody responses to early antigens of varicella-zoster virus (VZV) during varicella and zoster.

The antibody responses to membrane and early antigens and thymidine kinase of varicella-zoster virus (VZV) were studied in sera during both varicella and zoster by a test with fluorescent antibody to membrane antigen (FAMA), staining the biochemically transformed cells by the immunofluorescent technique and neutralization of virus-specific thymidine kinase activity, respectively. Similar increases in FAMA antibody titers were demonstrated in sera from patients with varicella and zoster. IgM was detected in both groups, but appeared earlier during varicella than during zoster. Furthermore, the antibody titers to early antigens and virus-specific thymidine kinase were higher in patients with zoster than in those with varicella. These data suggest that different types of antibody responses occur during varicella and zoster.

Adolescent↗