No abstract available.
Herpesviridae* ; Herpesvirus 7, Human ; Herpesvirus 8, Human ; Humans*

In this study, the author explored the role of interferon regulatory factor 7 (IRF7) and latent membrane protein 1 (LMP1) on the regulation of antigen presenting molecules in B-lymphoblastoid cell lines. First, the author observed the endogenous expression of IRF7 and LMP1 in paired EBV-positive B-lymphoblastoid cell lines, Sav I and Sav III, which represent EBV type I and type III latency, respectively. The Sav I cell, which does not express LMP1, showed very low levels of endogenous IRF7 in the cytoplasm. However, Sav III cells, which express large amounts of LMP1, contained high levels of endogenous IRF7 in both the cytoplasm and the nucleus. The expression of surface MHC class I antigen was 7.8-fold higher in Sav III compared with Sav I cells when measured by fluorescence activated cell sorter (FACS) analysis. To understand whether IRF7 is involved in regulation of MHC I and TAP1, LMP1 or IRF7 were expressed by cotransfection in DG75 cells. Levels of TAP1 protein were up-regulated by LMP1 and IRF7 alone, and by LMP1 co expression with IRF7, the expression level was highest after co-transfection of LMP1 with IRF7. TAP1 promoter activity was also up-regulated to 2.4, 2.0, 3.2-fold by LMP1, by IRF7, and by LMP1 plus IRF7, respectively. Surface expression of MHC class I antigen was up-regulated by LMP1 alone and LMP1 plus IRF7, but not by IRF7 alone. These results suggest that IRF7 induces the expression of TAP1, but not MHC class I antigen and that LMP1 and IRF7 have additive effects on the expression of TAP1 protein.
Cell Line* ; Cytoplasm ; Fluorescence ; Herpesvirus 4, Human ; Interferon Regulatory Factor-7 ; Membrane Proteins

In this study, the author explored the role of interferon regulatory factor 7 (IRF7) and latent membrane protein 1 (LMP1) on the regulation of antigen presenting molecules in B-lymphoblastoid cell lines. First, the author observed the endogenous expression of IRF7 and LMP1 in paired EBV-positive B-lymphoblastoid cell lines, Sav I and Sav III, which represent EBV type I and type III latency, respectively. The Sav I cell, which does not express LMP1, showed very low levels of endogenous IRF7 in the cytoplasm. However, Sav III cells, which express large amounts of LMP1, contained high levels of endogenous IRF7 in both the cytoplasm and the nucleus. The expression of surface MHC class I antigen was 7.8-fold higher in Sav III compared with Sav I cells when measured by fluorescence activated cell sorter (FACS) analysis. To understand whether IRF7 is involved in regulation of MHC I and TAP1, LMP1 or IRF7 were expressed by cotransfection in DG75 cells. Levels of TAP1 protein were up-regulated by LMP1 and IRF7 alone, and by LMP1 co expression with IRF7, the expression level was highest after co-transfection of LMP1 with IRF7. TAP1 promoter activity was also up-regulated to 2.4, 2.0, 3.2-fold by LMP1, by IRF7, and by LMP1 plus IRF7, respectively. Surface expression of MHC class I antigen was up-regulated by LMP1 alone and LMP1 plus IRF7, but not by IRF7 alone. These results suggest that IRF7 induces the expression of TAP1, but not MHC class I antigen and that LMP1 and IRF7 have additive effects on the expression of TAP1 protein.
Cell Line* ; Cytoplasm ; Fluorescence ; Herpesvirus 4, Human ; Interferon Regulatory Factor-7 ; Membrane Proteins

BACKGROUND: Pityriasis rosea is a common, acute self-limiting papulosquamous disorder in which many studies suggest viral causative factors in its pathogenesis. Recently, the link between pityriasis rosea and the reactivation of human herpes virus-6 (HHV-6) and HHV-7 infection has been suggested. This evidence suggests that targetting HHV-6 or HHV-7 may be an effective treatment for pityriasis rosea. OBJECTIVE: We treated pityriasis rosea patients with oral famciclovir to investigate the effect of oral famciclovir in pityriasis rosea. METHODS: A case group of seventeen patients with pityriasis rosea were treated with oral famciclovir (250 mg 3 times daily for 7 days). Clinical evaluation at 0, 1 & 2 weeks was undertaken. A skin biopsy and polymerase chain reaction analysis of HHV-6 from a skin specimen were performed. We analyzed 19 patients with pityriasis rosea who were treated with topical steroid and oral antihistamines retrospectively and considered them as the control group. RESULTS: On the 7th day after oral famciclovir treatment was started, pityriasis rosea had regressed completely in 3 patients (17.6%) and had regressed partially in 9 patients (52.9%). On the 14th day, 12 patients (70.6%) had achieved more than partial regression. On the 7th day, systemic symptoms had improved in all 9 patients. Clearance of skin lesions was achieved in average 7.57 days in patients who had regressed completely after 14 days' treatment. Histological examination of patients was compatible with pityriasis rosea and polymerase chain reaction analysis of HHV-6 was negative in all 8 patients. Compared with the control group, the treatment for patients in the case group seemed to have better effects, but statistical analysis failed to show any significant differences between the two groups. CONCLUSION: Famciclovir was not effective in the treatment of pityriasis rosea, but further investigation is needed.
Biopsy ; Herpesvirus 6, Human ; Herpesvirus 7, Human ; Histamine Antagonists ; Humans ; Pityriasis Rosea* ; Pityriasis* ; Polymerase Chain Reaction ; Retrospective Studies ; Skin ; Skin Diseases, Papulosquamous

Herpes zoster (HZ), or shingles, is caused by the reactivation of latent varicella-zoster virus (VZV) from the sensory ganglia when VZV-specific T-cell immunity is decreased because of aging or immunosuppression. In the present study, we developed HZ DNA vaccine candidates encoding VZV proteins and cytokine adjuvants, such as IL-7 and IL-33. We immunized C57BL/6 mice with DNA plasmids encoding VZV glycoprotein E (gE), immediate early (IE) 63, or IE62 proteins and found that robust VZV protein-specific T-cell responses were elicited by HZ DNA vaccination. Co-administration of DNA plasmids encoding IL-7 or IL-33 in HZ DNA vaccination significantly enhanced the magnitude of VZV protein-specific T-cell responses. Protective immunity elicited by HZ DNA vaccination was proven by challenge experiments with a surrogate virus, vaccinia virus expressing gE (VV-gE). A single dose of HZ DNA vaccine strongly boosted gE-specific T-cell responses in mice with a history of previous infection by VV-gE. Thus, HZ DNA vaccines with IL-7 and IL-33 adjuvants strongly elicit protective immunity.
Aging ; Animals ; DNA* ; Ganglia, Sensory ; Glycoproteins ; Herpes Zoster* ; Herpesvirus 3, Human ; Immunosuppression ; Interleukin-33* ; Interleukin-7* ; Mice ; Plasmids ; T-Lymphocytes ; Vaccination ; Vaccines, DNA* ; Vaccinia virus

OBJECTIVE: To investigate the cytokine/chemokine profile in patients with Epstein-Barr virus (EBV)-related hemophagocytic lymphohistiocytosis (HLH), and assess the prognostic value of survival. METHODS: Serum levels of thirty-eight cytokines/chemokines were measured by multiple cytokine assay kit in EBV-related HLH patients, EBV-infected patients, and controls. The expression profile of cytokines/chemokines was compared among groups. The changes of cytokine/chemokine expression in active and remission stage of EBV-related HLH patients were also compared, and the prognostic values for survival were evaluated. RESULTS: Serum levels of interferon-α2 (IFN-α2), interleukin (IL)-6, and IL-7 in EBV-related HLH patients were 33.67(23.23-68.78) pg/ml, (74.95±25.53) pg/ml, and 35.35(19.50-63.55) pg/ml, respectively, which were significantly higher than those in EBV-infected patients［IFN-α2: 16.07(9.87-29.63); IL-6: 55.91±20.29; IL-7: 20.40(13.35-31.40)］ and controls ［IFN-α2: 11.02(4.67-21.25); IL-6:42.64±13.41; IL-7: 16.95(14.95-33.78)］(all P<0.05). Serum levels of IL-8, IL-9, and marcophage-derived chemokine (MDC) in EBV-related HLH patients were 11.00(7.50-15.27) pg/ml, 81.30(40.79-111.0) pg/ml, and (512.6±128.7) pg/ml, respectively, which were significantly higher than those in controls ［IL-8: 6.80(5.56-8.38); IL-9: 41.30(29.82-67.91); MDC: 384.1±156.6］(all P<0.05), but there was no remarkable differences compared with EBV-infected patients (P>0.05). Serum IFN-α2, IL-6, IL-7, IL-8, IL-9, and MDC in survival and death groups of EBV-related HLH patients were analyzed by receiver operating characteristic curve with area under curve of 0.781, 0.778, 0.633, 0.805, 0.562, and 0.657, respectively (P=0.019, 0.021, 0.269, 0.015, 0.607, and 0.190). IFN-α2, IL-6, and IL-8 had good predictive effect on survival. Serum level of IFN-α2, IL-6, and MDC of EBV-related HLH patients in remission stage were significantly lower than those in active stage (P<0.05), while IL-7, IL-8, and IL-9 were not different (P>0.05). CONCLUSION IFN-α2, IL-6, IL-7, IL-8, IL-9, and MDC may take part in the pathogenesis of EBV-related HLH.
Humans ; Lymphohistiocytosis, Hemophagocytic/complications* ; Herpesvirus 4, Human ; Cytokines/metabolism* ; Epstein-Barr Virus Infections/complications* ; Interleukin-6 ; Clinical Relevance ; Interleukin-7 ; Interleukin-8 ; Interleukin-9 ; Chemokines ; Interferons

Interferon regulatory factor 7 (IRF7) is one of the transcriptional factors for the activation of type I Interferon (IFN) genes. It is known that IRF7 and the latent membrane protein 1 (LMP1) of Epstein-Barr virus (EBV) are highly expressed in EBV type III latency cells, and LMP1 induces mRNA expression of IRF7. In this study, the expression pattern of endogenous IRF7 was observed in several B cell lines with or without EBV infection by immunofluorescence staining. IRF7 was localized in the cytoplasm of EBV-negative B cells and EBV type I latency B cell lines. However, IRF7 was located both in the cytoplasm and nucleus of EBV type III latency cell lines. In the Jijoye cell (type III latency cell), IRF7 was colocalized with LMP1 in the cytoplasm in a capping configuration, and their interaction was confirmed by co-immunoprecipitation of LMP1 and IRF7. This colocalization was confirmed by co-transfection of IRF7 and LMP1 plasmids in EBV-negative B cells. These results suggest that the IRF7 and LMP1 interact with each other, and this may relate to the mechanism whereby LMP1 exerts functional effects in B-lymphocytes.
Viral Matrix Proteins/*biosynthesis/metabolism ; Trans-Activation (Genetics) ; Signal Transduction ; RNA, Messenger/metabolism ; Plasmids/metabolism ; Microscopy, Fluorescence ; Interferon Regulatory Factor-7/*biosynthesis ; Immunoprecipitation ; Humans ; Herpesvirus 4, Human/metabolism ; *Gene Expression Regulation ; Cytoplasm/metabolism ; Cell Line, Tumor ; B-Lymphocytes/metabolism/virology