Dua N, Reubel G, Moore P F, Higgins J, Pedersen N C
Department of Medicine and Epidemiology, School of Veterinary Medicine University of California, Davis 95616.
Vet Immunol Immunopathol. 1994 Nov;43(4):337-55. doi: 10.1016/0165-2427(94)90156-2.
Sixteen adolescent specific pathogen free cats were inoculated with the Petaluma strain of feline immunodeficiency virus (FIV) and two cats were then necropsied at each of 5, 10, 21, 28, 42, 56, 70, and 84 day time points following infection. Lymphadenopathy gradually increased starting at Day 10 and persisted for the duration. Gross clinical signs of fever, mild to severe malaise, anorexia, diarrhea, dehydration, and generalized soreness appeared around Day 42, peaked at Day 56, and disappeared by Days 70-84 post-infection. Leukopenia, associated initially with a mild lymphopenia and later by both a mild lymphopenia and a severe neutropenia, appeared 14-28 days following infection, troughed at Day 56, and persisted thereafter. The CD4+:CD8+ T cell ratio started to decrease around Day 28, reaching a nadir at Days 56-70. This decrease was due to a decline in the absolute numbers and percentage of CD4+ T cells and an increase in the percentage of CD8+ T cells. Significant histopathologic lesions included myeloid hyperplasia between Days 56-70 post-infection; thymitis with cortical involution and follicular hyperplasia starting at Day 42; lymphoid hyperplasia of peripheral and mesenteric nodes, spleen and tonsils beginning around Day 42; typhlitis most evident from Day 56 onward, and an interstitial nephritis and pneumonitis that was most intense after Day 42. Virus was isolated from peripheral blood mononuclear cells (PBMC) beginning 2 weeks post-infection, and plasma viremia appeared 1 week later. Plasma and PBMC-associated viremia peaked at 42-56 days following infection and decreased abruptly thereafter. Proviral DNA was detectable as early as 5 days after infection in blood leukocytes and after 10 days in other organs. The central nervous system, lungs, thymus, tonsils and mesenteric lymph nodes were the earliest sites of virus localization. Antibodies to the FIV capsid protein appeared 14 days following infection and reached peak levels by Days 42-56. Abnormalities occurring during the primary stage of FIV infection were consistent with those described for acute simian and human immunodeficiency virus-induced disease.
16只青春期无特定病原体猫接种了猫免疫缺陷病毒（FIV）的佩塔卢马毒株，然后在感染后的第5、10、21、28、42、56、70和84天这几个时间点，每次对2只猫进行尸检。淋巴结病从第10天开始逐渐加重，并持续整个病程。发热、轻至重度不适、厌食、腹泻、脱水和全身酸痛等明显临床症状在第42天左右出现，在第56天达到峰值，在感染后第70 - 84天消失。白细胞减少最初与轻度淋巴细胞减少有关，随后与轻度淋巴细胞减少和重度中性粒细胞减少均有关，在感染后14 - 28天出现，在第56天降至最低点，并在此后持续存在。CD4⁺:CD8⁺ T细胞比值在第28天左右开始下降，在第56 - 70天达到最低点。这种下降是由于CD4⁺ T细胞的绝对数量和百分比下降以及CD8⁺ T细胞百分比增加所致。显著的组织病理学病变包括感染后第56 - 70天的骨髓增生；从第42天开始的伴有皮质萎缩和滤泡增生的胸腺炎；从第42天左右开始的外周和肠系膜淋巴结、脾脏和扁桃体的淋巴样增生；从第56天起最明显的盲肠炎，以及在第42天后最严重的间质性肾炎和肺炎。感染后2周开始从外周血单核细胞（PBMC）中分离出病毒，1周后出现血浆病毒血症。血浆和PBMC相关的病毒血症在感染后42 - 56天达到峰值，此后急剧下降。感染后5天在血液白细胞中以及10天后在其他器官中可检测到前病毒DNA。中枢神经系统、肺、胸腺、扁桃体和肠系膜淋巴结是最早的病毒定位部位。感染后14天出现针对FIV衣壳蛋白的抗体，并在第42 - 56天达到峰值水平。FIV感染初期出现的异常与急性猿猴和人类免疫缺陷病毒所致疾病中描述的异常一致。
