Biberfeld P, Ensoli B, Stürzl M, Schulz T F
Immunopathology Laboratory, Institution for Oncology-Pathology, Karolinska Institute and Hospital, Stockholm, Sweden.
Curr Opin Infect Dis. 1998 Apr;11(2):97-105. doi: 10.1097/00001432-199804000-00002.
Epidemiological studies have strengthened the case for Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 being the long-sought Kaposi sarcoma agent, but have also pointed to a role for other co-factors. Like other tumour viruses, Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 establishes a latent (persistent) infection in Kaposi sarcoma-spindle (tumorous) cells, but can also undergo lytic replication in these and other cell types. Several latent and lytic viral genes may play a role in the pathogenesis of Kaposi's sarcoma. Although Kaposi sarcoma-associated herpesvirus/human herpesvirus 8 contains at least two genes with transforming properties, it has not yet been shown to be oncogenic in animals. This, and other studies on inflammatory/angiogenic cellular and viral cytokines as well as HIV-Tat, emphasizes the multifactorial complexity of the pathogenesis of Kaposi's sarcoma.
流行病学研究进一步证明了卡波西肉瘤相关疱疹病毒/人类疱疹病毒8就是长期以来寻找的卡波西肉瘤病原体，但也指出了其他协同因素的作用。与其他肿瘤病毒一样，卡波西肉瘤相关疱疹病毒/人类疱疹病毒8在卡波西肉瘤纺锤体（肿瘤性）细胞中建立潜伏（持续）感染，但也可在这些细胞及其他细胞类型中进行裂解复制。一些潜伏和裂解性病毒基因可能在卡波西肉瘤的发病机制中起作用。虽然卡波西肉瘤相关疱疹病毒/人类疱疹病毒8含有至少两个具有转化特性的基因，但尚未证明其在动物中具有致癌性。这一情况以及关于炎性/血管生成性细胞和病毒细胞因子以及HIV-Tat的其他研究，都强调了卡波西肉瘤发病机制的多因素复杂性。
