Miles S A
University of California, Los Angeles.
Curr Opin Oncol. 1992 Oct;4(5):875-82. doi: 10.1097/00001622-199210000-00010.
Infection with the human immunodeficiency virus-1 is associated with a marked increase in the incidence of Kaposi's sarcoma. Recent studies suggest that the risk of Kaposi's sarcoma in human immunodeficiency virus infection is increased with oral-fecal contact and that a sexually transmitted agent possibly related to human papillomavirus-16 could be involved. Exposure to this or another sexually transmitted agent apparently alters both the morphology and growth regulation of the Kaposi's sarcoma progenitor cells. These changes include the expression of the alpha chain of the interleukin-6 receptor with the acquisition of an interleukin-6-dependent autocrine growth loop. Subsequent perturbation of multiple cytokines during human immunodeficiency virus infection, including Oncostatin-M, interleukin-1 beta and tumor necrosis factor-alpha alters the subsequent growth of Kaposi's sarcoma. These studies suggest that control of cytokine perturbations or the underlying human immunodeficiency virus-1 infection should result in a significant reduction in the rate of growth of acquired immunodeficiency syndrome-related Kaposi's sarcoma.
人类免疫缺陷病毒1型感染与卡波西肉瘤的发病率显著增加有关。最近的研究表明，人类免疫缺陷病毒感染时卡波西肉瘤的风险会因口粪接触而增加，并且可能涉及一种与人类乳头瘤病毒16型相关的性传播因子。接触这种或另一种性传播因子显然会改变卡波西肉瘤祖细胞的形态和生长调控。这些变化包括白细胞介素-6受体α链的表达以及获得白细胞介素-6依赖性自分泌生长环。在人类免疫缺陷病毒感染期间多种细胞因子的后续紊乱，包括制瘤素-M、白细胞介素-1β和肿瘤坏死因子-α，会改变卡波西肉瘤的后续生长。这些研究表明，控制细胞因子紊乱或潜在的人类免疫缺陷病毒1型感染应会使获得性免疫缺陷综合征相关卡波西肉瘤的生长速度显著降低。
