Huang Y Q, Li J J, Kim K S, Nicolaides A, Zhang W G, Le J, Poiesz B J, Friedman-Kien A E
Department of Microbiology, New York University Medical Center, NY 10016.
AIDS. 1993 Mar;7(3):317-22. doi: 10.1097/00002030-199303000-00002.
HIV-1 transcripts have been detected in AIDS-related Kaposi's sarcoma (KS) tissues within the factor XIIIa + dermal dendrocytes present in the tumor. Various cytokines and growth factors have been shown to influence the growth of KS-derived cells in vitro. HIV-1 preferentially infects CD4+ cells and has also been found to infect some CD4- cells in vitro. The susceptibility of cultured KS cells in vitro to infection with HIV-1 and the expression of interleukin (IL)-1 beta, IL-6 and basic fibroblast growth factor (bFGF) after exposure to HIV-1 was examined.
The susceptibility of two different KS-derived cell cultures to HIV-1 infection was examined by the expression of p24 antigen, detection of proviral sequence and electron microscopy. The expression of IL-1 beta, IL-6 and bFGF was detected by enzyme-linked immunosorbent assay and reverse transcriptase polymerase chain reaction.
KS-derived cells can be infected by HIV-1 in vitro. Both KS-derived cells were found to express CD4 mRNA. The expression of IL-1 beta and IL-6 was increased, whereas the expression of bFGF was not stimulated after exposure of KS cells to HIV-1.
These experiments describe the in vitro infection of KS-derived cells by HIV-1 and the expression of various cytokines and growth factor following infection. The increased production of cytokines observed following such infection may be involved in the pathogenesis of AIDS-related KS.
在艾滋病相关卡波西肉瘤(KS)组织中肿瘤内存在的因子ⅩⅢa + 真皮树突状细胞内已检测到HIV-1转录本。多种细胞因子和生长因子已被证明在体外可影响KS来源细胞的生长。HIV-1优先感染CD4+细胞,并且在体外也已发现它能感染一些CD4-细胞。检测了体外培养的KS细胞对HIV-1感染的易感性以及暴露于HIV-1后白细胞介素(IL)-1β、IL-6和碱性成纤维细胞生长因子(bFGF)的表达。
通过p24抗原的表达、前病毒序列的检测和电子显微镜检查,检测两种不同的KS来源细胞培养物对HIV-1感染的易感性。通过酶联免疫吸附测定和逆转录聚合酶链反应检测IL-1β、IL-6和bFGF的表达。
KS来源的细胞在体外可被HIV-1感染。发现两种KS来源的细胞均表达CD4 mRNA。KS细胞暴露于HIV-1后,IL-1β和IL-6的表达增加,而bFGF的表达未受到刺激。
这些实验描述了HIV-1对KS来源细胞的体外感染以及感染后多种细胞因子和生长因子的表达。这种感染后观察到的细胞因子产生增加可能参与了艾滋病相关KS的发病机制。