Pathogenesis of human immunodeficiency virus-related Kaposi's sarcoma.
Pathogenesis of human immunodeficiency virus-related Kaposi's sarcoma.
复制标题
人类免疫缺陷病毒相关卡波西肉瘤的发病机制。
DOI：
10.1097/00001622-199210000-00010
复制
发表时间：
1992
影响因子：
3.4
通讯作者：
S. Miles
中科院分区：
文献类型：
--
作者：
S. Miles
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.
