Reggeti F, Ackerley C, Bienzle D
Department of Pathobiology, University of Guelph, Guelph, ON N1G 2W1, Canada.
The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada.
J Gen Virol. 2008 Jan;89(Pt 1):277-287. doi: 10.1099/vir.0.83161-0.
The lymphotropic lentiviruses feline immunodeficiency virus (FIV) and human immunodeficiency virus (HIV) enter cells by sequential interaction with primary receptors CD134 or CD4, respectively, and subsequently with chemokine receptors. The host-cell range for FIV is broader than that for HIV, but whether this is a function of receptor expression is unknown. Lack of reagents specific to feline molecules has limited detection and analysis of receptors and their interaction with viral components. Here, the expression of CD134 and CXCR4 on feline T and B lymphocytes, dendritic cells (DCs) and macrophages was examined and the kinetics of FIV replication were assessed. Quantification of CD134 mRNA by real-time PCR indicated expression in all leukocytes, with significantly more transcripts in CD4(+) lymphocytes than in other leukocytes. Antibodies against human CD134 bound inconsistently to feline leukocytes. CXCR4 was detected with antibody clone 12G5 on the surface of monocyte-derived cells only, but gene transcripts were present in all cells, with the highest copy number in lymphocytes. CXCR4 expression decreased and CD134 expression increased with cell activation in lymphocytes. A subtype B biological isolate of FIV infected DCs, macrophages and lymphocytes, with the highest replication in CD4(+) lymphocytes, whilst cloned FIV P14 infected all cells, but replicated less efficiently. Although viral replication was lower in DCs and macrophages than in lymphocytes, DCs expressed specific receptors and were infected productively with FIV, as indicated by viral ultrastructure and DNA detection. These results may implicate altered function of DCs in the induction of specific immunity against FIV.
亲嗜性慢病毒猫免疫缺陷病毒（FIV）和人类免疫缺陷病毒（HIV）分别通过与主要受体CD134或CD4依次相互作用，随后与趋化因子受体相互作用而进入细胞。FIV的宿主细胞范围比HIV更广，但这是否是受体表达的一种功能尚不清楚。缺乏针对猫科动物分子的特异性试剂限制了对受体及其与病毒成分相互作用的检测和分析。在此，检测了猫T淋巴细胞、B淋巴细胞、树突状细胞（DC）和巨噬细胞上CD134和CXCR4的表达，并评估了FIV复制的动力学。通过实时PCR对CD134 mRNA进行定量分析表明，所有白细胞中均有表达，CD4(+)淋巴细胞中的转录本明显多于其他白细胞。抗人CD134抗体与猫白细胞的结合不一致。仅在单核细胞衍生细胞表面用抗体克隆12G5检测到CXCR4，但所有细胞中均存在基因转录本，淋巴细胞中的拷贝数最高。在淋巴细胞中，随着细胞活化，CXCR4表达降低，CD134表达增加。FIV的B亚型生物学分离株感染了DC、巨噬细胞和淋巴细胞，在CD4(+)淋巴细胞中的复制最高，而克隆的FIV P14感染了所有细胞，但复制效率较低。尽管DC和巨噬细胞中的病毒复制低于淋巴细胞，但DC表达特异性受体并被FIV有效感染，病毒超微结构和DNA检测表明了这一点。这些结果可能暗示DC在诱导针对FIV的特异性免疫中的功能改变。
