Kano Y, Shiohara T
Kyorin University School of Medicine, Mitaka, Tokyo, Japan.
J Dermatol Sci. 2000 Apr;22(3):196-204. doi: 10.1016/s0923-1811(99)00085-7.
Human cytomegalovirus (CMV) is a member of the herpes family of viruses. After primary infection, it undergoes latency/persistence. Significant progress has been made in the last few years in detecting CMV. The most available approach to the diagnosis of CMV infection is the direct detection of CMV antigen in nuclei of peripheral blood leukocytes, an assay known as pp65 direct antigenemia test. CMV infection is well controlled in the immunocompetent hosts; however, there are various immunological changes in immune function during and after recovery from CMV infections. Characteristic changes in lymphocyte subsets occur during CMV infection, mainly involving expansion and activation of CD8+ T lymphocytes and NK cells. On the other hand, CMV has an array of immune escape strategies for establishing a life long latent state: CMV inhibits major histocompatibility complex (MHC) class I expression within infected cells and impairs IFN-gamma-induced MHC class II-dependent antigen presentation by macrophages; it can also encode proteins that can interfere with the presentation of viral peptide antigens to T cells. While cutaneous manifestations of CMV seen in immunocompromised patients have been extensively reported, those in adult immunocompetent individuals have received relatively little attention: in this setting the primary CMV infection appears as CMV mononucleosis. At the time of occurrence of the mononucleosis syndrome, a variety of extracutaneous and cutaneous manifestations occur. These clinical symptoms are not the direct consequence of proliferation of CMV in given tissues but indicative of the immunological response toward CMV. The incidence of the appearance of eruptions in CMV mononucleosis is variable. Certain drugs given in the early stage of this disease play an important role in the development of eruption, just as with the ampicillin rashes in the Epstein-Barr virus mononucleosis. Although the mechanism by which drugs trigger the development of rashes in patients with CMV mononucleosis is unknown, it is assumed that CMV is likely to be a potential amplifier of drug rashes induced by activation of drug-specific T cells. By improving methods for detection of CMV, we can recognize that many types of eruptions other than CMV mononucleosis could be induced by primary infection or reactivation of CMV.
人巨细胞病毒（CMV）是疱疹病毒家族的成员。初次感染后，它会进入潜伏/持续状态。在过去几年中，CMV检测取得了重大进展。诊断CMV感染最常用的方法是直接检测外周血白细胞细胞核中的CMV抗原，该检测方法称为pp65直接抗原血症试验。CMV感染在免疫功能正常的宿主中得到很好的控制；然而，在CMV感染期间及恢复后，免疫功能会发生各种免疫变化。CMV感染期间淋巴细胞亚群会发生特征性变化，主要涉及CD8 + T淋巴细胞和NK细胞的扩增和激活。另一方面，CMV有一系列免疫逃逸策略来建立终身潜伏状态：CMV抑制受感染细胞内主要组织相容性复合体（MHC）I类表达，并损害巨噬细胞中IFN-γ诱导的MHC II类依赖性抗原呈递；它还可以编码能够干扰病毒肽抗原向T细胞呈递的蛋白质。虽然免疫功能低下患者中CMV的皮肤表现已被广泛报道，但成年免疫功能正常个体中的皮肤表现相对较少受到关注：在这种情况下，原发性CMV感染表现为CMV单核细胞增多症。在单核细胞增多症综合征发生时，会出现各种皮肤外和皮肤表现。这些临床症状不是CMV在特定组织中增殖的直接后果，而是对CMV免疫反应的指示。CMV单核细胞增多症中皮疹出现的发生率各不相同。在这种疾病的早期给予某些药物在皮疹的发生中起重要作用，就像在EB病毒单核细胞增多症中的氨苄青霉素皮疹一样。虽然药物引发CMV单核细胞增多症患者皮疹发展的机制尚不清楚，但推测CMV可能是药物特异性T细胞激活诱导的药物皮疹的潜在放大器。通过改进CMV检测方法，我们可以认识到除CMV单核细胞增多症外，许多类型的皮疹可能由CMV的原发性感染或再激活引起。
