ANALYSIS OF CELLULAR FACTORS AFFECTING RETROVIRUS INFECTION AND GROWTH

逆转录病毒复制已被证明需要病毒和细胞 成分，以及细胞因子或功能已知限制 逆转录病毒感染和生长。这种情况最常发生在 病毒附着和渗透水平，但其他渗透后 影响也已被描述。了解心力衰竭的细胞机制 病毒控制可能在我们开发抗病毒药物的尝试中有用 影响人类逆转录病毒的病毒，如艾滋病毒和HTLVI。这样做的目的是 该项目是描述细胞因子在生长和生长中的作用 限制逆转录病毒感染。此前，我们曾报道过 RD114在猫细胞中的限制不发生在 前驱LtR，因为报告基因与LtR有效地连接在一起 在限制性和允许性牢房中。我们已经扩展了我们的分析 RD114病毒在猫体内生长抑制机制的研究 成纤维细胞，并可显示与内源性RD114的表达有关 MRNAs与限制性表型相关。此外，受限制 细胞表达约gp85kD的RD114糖蛋白分子 而不是RD114转染或感染后预期的gp7O。 RD114受体与修饰的gp7O分子之间的相互作用 可能是RD114病毒传播能力受限的原因 在猫成纤维细胞中。我们还研究了猫科动物的生长 免疫缺陷病毒(FIV)在猫脑源性细胞系G355， 并已表明某些病毒株是产生梭状病毒的 对这些细胞有细胞毒性。干扰分析表明，FIV 在G355细胞上使用与使用的受体不同的受体 由猫科动物内源性和外源性病毒感染。通过以下方式促进细胞融合 复制的C型病毒的存在，并在 含MoS的Mo-MuSV转化细胞。两国的融合 MSV转化的G355细胞提供了一种易于量化的生物学 在贴壁细胞系中检测病毒感染性。

Retrovirus replication has been shown to require both viral and cellular components, and cellular factors or functions are known to restrict retrovirus infection and growth. This occurs most frequently at the level of virus attachment and penetration, but other post-penetration effects have also been described. Understanding cellular mechanisms of viral control may be useful in our attempts to develop antiviral agents which affect human retroviruses, such as HIV and HTLVI. The goal of this project is to characterize the role of cellular factors in the growth and restriction of retrovirus infection. Previously, we had reported that RD114 restriction in feline cells does not occur at the level of the proviral LTR, since reporter genes linked to the LTR function efficiently in both restrictive and permissive cells. We have extended our analysis of the mechanism of restriction of growth of RD114 virus in feline fibroblasts, and can show that the expression of endogenous RD114-related mRNAs correlates with the restricted phenotype. Additionally, restricted cells express RD114 glycoprotein molecules of approximately gp85 kD instead of the expected gp7O following RD114 transfection or infection. Interaction between the RD114 receptor and the modified gp7O molecule is probably responsible for the restricted ability of RD114 virus to spread in feline fibroblasts. We have also studied the growth of feline immunodeficiency virus (FIV) in the cat brain-derived cell line, G355, and have shown that certain strains of the virus are fusigenic and cytotoxic for these cells. Interference analysis indicates that FIV utilizes a receptor on G355 cells which is different from the ones used by feline endogenous and exogenous viruses. Cell fusion is enhanced by the presence of replicating C-type viruses and is further enhanced in cells transformed by the mos-containing Mo-MuSV. The fusion of MSV-transformed G355 cells provides an easily quantifiable biological assay for virus infectivity in an adherent cell line.