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，细胞因子或功能是已知的限制 逆转录病毒感染和生长。 这种情况最常发生在 病毒附着和渗透的水平，但其他渗透后 还描述了效果。 了解细胞机制 病毒控制可能有助于我们开发抗病毒药物 它会影响人类逆转录病毒，例如艾滋病毒和HTLVI。这个目标 该项目是表征细胞因子在生长和 限制逆转录病毒感染。 此前，我们曾报道， 猫细胞中的RD 114限制不会发生在 前病毒LTR，因为报告基因连接到LTR功能有效 在限制性和允许性细胞中。 我们扩展了我们的分析 RD 114病毒在猫体内抑制生长机理的研究 成纤维细胞，并可以显示内源性RD 114相关的表达， mRNA与限制性表型相关。 此外，限制 细胞表达约gp 85 kD的RD 114糖蛋白分子 而不是RD 114转染或感染后预期的gp 70。 RD 114受体和修饰的gp 7 O分子之间的相互作用是 可能是RD 114病毒传播能力受限的原因 在猫的成纤维细胞中。 我们还研究了猫科动物的生长 免疫缺陷病毒（FIV）在猫脑衍生细胞系G355中的作用， 并且已经证明某些病毒株是融合基因型的， 对这些细胞有毒性。 干扰分析表明，FIV 利用G355细胞上的受体，其与所用的受体不同 由猫内源性和外源性病毒引起。 细胞融合被增强， 复制C型病毒的存在，并进一步增强， 用含Mo-MuSV的Mo-MuSV转化的细胞。 的融合 MSV转化的G355细胞提供了一种易于定量的生物学特性。 粘附细胞系中病毒感染性的测定。

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.