AN EXPERIMENTAL-STUDY OF PRIMARY FELINE IMMUNODEFICIENCY VIRUS-INFECTION IN CATS AND A HISTORICAL COMPARISON TO ACUTE SIMIAN AND HUMAN-IMMUNODEFICIENCY-VIRUS DISEASES
AN EXPERIMENTAL-STUDY OF PRIMARY FELINE IMMUNODEFICIENCY VIRUS-INFECTION IN CATS AND A HISTORICAL COMPARISON TO ACUTE SIMIAN AND HUMAN-IMMUNODEFICIENCY-VIRUS DISEASES
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DOI：
10.1016/0165-2427(94)90156-2
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发表时间：
1994-11-01
影响因子：
1.8
通讯作者：
PEDERSEN, NC
中科院分区：
文献类型：
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作者：
DUA, N;REUBEL, G;PEDERSEN, NC
16 只青春期无特定病原体的猫接种了猫免疫缺陷病毒 (FIV) 的 Petaluma 株，然后在感染后 5、10、21、28、42、56、70 和 84 天的时间点各对两只猫进行尸检。淋巴结肿大从第10天开始逐渐增加并持续整个过程。发热、轻度至重度不适、厌食、腹泻、脱水和全身酸痛等总体临床症状出现在第 42 天左右，在第 56 天达到顶峰，并在感染后第 70-84 天消失。白细胞减少症最初伴有轻度淋巴细胞减少症，后来伴有轻度淋巴细胞减少症和严重中性粒细胞减少症，在感染后 14-28 天出现，在第 56 天达到最低点，此后持续存在。 CD4(+):CD8(+) T细胞比率在第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细胞百分比的增加所致。显着的组织病理学病变包括感染后 56-70 天之间的骨髓增生；从第 42 天开始出现胸腺炎，伴有皮质退化和滤泡增生；第 42 天左右开始外周和肠系膜淋巴结、脾脏和扁桃体淋巴样增生；伤寒从第 56 天起最为明显，间质性肾炎和肺炎在第 42 天后最为严重。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 相关病毒血症在感染后 42-56 天达到峰值，此后突然下降。血液白细胞感染后 5 天即可检测到前病毒 DNA，其他器官感染后 10 天即可检测到前病毒 DNA。中枢神经系统、肺、胸腺、扁桃体和肠系膜淋巴结是病毒最早定位的部位。 FIV 衣壳蛋白抗体在感染后 14 天出现，并在第 42-56 天达到峰值水平。 FIV 感染初级阶段发生的异常与急性猿猴和人类免疫缺陷病毒引起的疾病所描述的异常一致。
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.