Torten M, Franchini M, Barlough J E, George J W, Mozes E, Lutz H, Pedersen N C
Department of Medicine, School of Veterinary Medicine, University of California, Davis 95616.
J Virol. 1991 May;65(5):2225-30. doi: 10.1128/JVI.65.5.2225-2230.1991.
Within 6 months of infection with the Petaluma isolate of feline immunodeficiency virus, specific-pathogen-free domestic cats exhibited a decrease in the percentage and number of circulating CD4+ lymphocytes and in the CD4+/CD8+ T-cell ratio, along with a marginally significant depression of pokeweed mitogen-induced lymphocyte proliferation in vitro. There was no loss of responsiveness to concanavalin A during this stage, and the cats were capable of mounting a satisfactory antibody response to a T-dependent, synthetic polypeptide immunogen. The pokeweed mitogen response deficit became clearly demonstrable by 11 to 12 months postinfection. A decline in the lymphocyte proliferative response to concanavalin A and a diminished ability to mount an in vivo antibody response to the T-dependent immunogen evolved by 25 to 44 months postinfection. Virus infection did not affect the ability of cats to mount an antibody response to a T-independent synthetic polypeptide immunogen. These data indicate that feline immunodeficiency virus produces a slowly progressive deterioration of T-cell function but does not affect the ability of B cells to recognize and respond to a T-independent antigenic stimulus.
用猫免疫缺陷病毒佩塔卢马分离株感染无特定病原体的家猫后6个月内，循环CD4+淋巴细胞的百分比和数量以及CD4+/CD8+T细胞比值均下降，同时体外商陆丝裂原诱导的淋巴细胞增殖略有显著抑制。在此阶段，对刀豆蛋白A的反应性没有丧失，并且这些猫能够对依赖T细胞的合成多肽免疫原产生令人满意的抗体反应。感染后11至12个月，商陆丝裂原反应缺陷变得明显。感染后25至44个月，对刀豆蛋白A的淋巴细胞增殖反应下降，对依赖T细胞的免疫原产生体内抗体反应的能力减弱。病毒感染不影响猫对非依赖T细胞的合成多肽免疫原产生抗体反应的能力。这些数据表明，猫免疫缺陷病毒会导致T细胞功能缓慢进行性恶化，但不影响B细胞识别和响应非依赖T细胞的抗原刺激的能力。
