Drago F, Ranieri E, Malaguti F, Battifoglio M L, Losi E, Rebora A
Institute of Dermatology, University of Genoa, Italy.
Dermatology. 1997;195(4):374-8. doi: 10.1159/000245991.
Clinical evidence suggests a viral etiology for pityriasis rosea (PR).
To evaluate human herpesvirus (HHV)-6 and HHV-7 as candidates for the etiology of PR.
Blood and skin tissue from 12 patients with acute PR, and 12 patients with other dermatoses were studied, as well as blood samples from 25 healthy persons. Serum interferon (IFN)-alpha and IFN-gamma were analyzed by ELISA. Analysis of morphological changes in cocultured peripheral blood mononuclear cells (PBMC) and electron microscopy (EM) to identify viral particles were performed. Polymerase chain reaction (PCR) with specific primers for HHV-6 and HHV-7 DNA sequences was performed on the plasma and PBMC of patients and healthy controls and on the skin of patients with PR and other skin diseases.
PR plasma contained detectable IFN-alpha and IFN-gamma, whereas plasma from controls did not. PBMC from PR patients showed ballooning cells and syncytia after 7 days in culture whereas PBMC from controls and recovered PR patients did not. This cytopathic effect was also documented in a PR patient who relapsed and in Sup-T1 cell cultures inoculated with the cell-free supernatant from centrifuged cultured PBMC; in this supernatant, herpesvirus, virions were detected by EM, PCR identified HHV-7 DNA in PBMC, plasma and skin from all patients with active PR and in the PBMC only of 5 patients tested 10-14 months later. Weaker signals of HHV-7 DNA were detected in PBMC of 11 controls, but not in their plasma. Skin was negative for HHV-7 in all control specimens.
Although the detection of HHV-7 DNA in PBMC and tissues does not prove directly a causal role, HHV-7 DNA in cell-free plasma corresponds to active replication which supports a causal relationship. We propose that PR is a clinical presentation of HHV-7 reactivation.
临床证据提示玫瑰糠疹(PR)的病毒病因。
评估人疱疹病毒(HHV)-6和HHV-7作为PR病因的可能性。
研究了12例急性PR患者、12例其他皮肤病患者的血液和皮肤组织,以及25名健康人的血样。通过酶联免疫吸附测定(ELISA)分析血清α干扰素(IFN)和γ干扰素。进行共培养外周血单个核细胞(PBMC)的形态学变化分析及电子显微镜(EM)检查以识别病毒颗粒。采用针对HHV-6和HHV-7 DNA序列的特异性引物,对患者和健康对照者的血浆及PBMC以及PR患者和其他皮肤病患者的皮肤进行聚合酶链反应(PCR)。
PR患者血浆中可检测到α干扰素和γ干扰素,而对照组血浆中未检测到。PR患者的PBMC在培养7天后出现气球样细胞和多核巨细胞,而对照组和康复的PR患者的PBMC未出现。一名复发的PR患者以及接种了经离心培养的PBMC无细胞上清液的Sup-T1细胞培养物中也记录到了这种细胞病变效应;在此上清液中,通过EM检测到疱疹病毒、病毒体,PCR在所有活动性PR患者的PBMC、血浆和皮肤中以及仅在10 - 14个月后检测的5例患者的PBMC中鉴定出HHV-7 DNA。在11名对照者的PBMC中检测到较弱的HHV-7 DNA信号,但在其血浆中未检测到。所有对照标本的皮肤HHV-7检测均为阴性。
虽然在PBMC和组织中检测到HHV-7 DNA并不能直接证明其因果关系,但无细胞血浆中的HHV-7 DNA对应于活跃复制,这支持了一种因果关系。我们提出PR是HHV-7再激活的一种临床表现。