Puma lentivirus is controlled in domestic cats after mucosal exposure in the absence of conventional indicators of immunity.
Puma lentivirus is controlled in domestic cats after mucosal exposure in the absence of conventional indicators of immunity.
复制标题
在没有常规免疫指标的情况下，家猫粘膜暴露后美洲狮慢病毒得到控制。
DOI：
10.1128/jvi.79.5.2797-2806.2005
复制
发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Vandewoude,Sue
中科院分区：
文献类型：
--
作者：
Terwee,JulieA;Yactor,JenniferK;Sondgeroth,KerryS;Vandewoude,Sue
很高比例的自由放养美洲狮(Felis Concolor)感染了猫慢病毒(美洲狮慢病毒，猫免疫缺陷病毒PCO[FIV-PCO]，在这里被称为PLV)，但没有疾病的证据。与家猫FIV相比，PLV在非肠道感染后可在家猫中建立生殖性感染，但它不会导致T细胞调节失调。在此，我们报道了经鼻腔感染PLV的猫，在缺乏相关的特异性免疫反应的情况下，可迅速清除外周血单核细胞(PBMC)前病毒载量。将4只无特定病原体的猫分成两组，每组4只，分别通过黏膜(口鼻)或肠外(静脉)途径感染PLV。路线。所有动物在感染后3周内PBMC培养阳性和PCR阳性，血清转换，未表现出临床疾病，但3至4只口鼻感染动物在3个月内清除了循环前病毒DNA。在持续感染的动物中，抗体效价达到了更高的水平。在黏膜接种的动物中，PLV抗原诱导的增殖略强，但在细胞毒性T淋巴细胞反应或细胞因子谱方面，两组之间没有差异。在所有在尸检中检测到病毒的动物中，病毒的分布主要是胃肠道的，而不是淋巴的。病毒清除的可能机制包括跨越粘膜表面所需的病毒适合性的差异，持久性的阈值剂量要求，或未检测到的灭菌宿主免疫反应。这是首次报道在出生后暴露于血清阳性的动物中控制生产性猫科动物或灵长类慢病毒感染。这一观察的机制将为控制免疫缺陷疾病提供线索，并可能促使重新检查疫苗诱导的针对人类免疫缺陷病毒和其他慢病毒的免疫。
A high percentage of free-ranging pumas (Felis concolor) are infected with feline lentiviruses (puma lentivirus, feline immunodeficiency virus Pco [FIV-Pco], referred to here as PLV) without evidence of disease. PLV establishes productive infection in domestic cats following parenteral exposure but, in contrast to domestic cat FIV, it does not cause T-cell dysregulation. Here we report that cats exposed to PLV oro-nasally became infected yet rapidly cleared peripheral blood mononuclear cell (PBMC) proviral load in the absence of a correlative specific immune response. Two groups of four specific-pathogen-free cats were exposed to PLV via the mucosal (oro-nasal) or parenteral (i.v.) route. All animals were PBMC culture positive and PCR positive within 3 weeks postinfection and seroconverted without exhibiting clinical disease; however, three or four oro-nasally infected animals cleared circulating proviral DNA within 3 months. Antibody titers reached higher levels in animals that remained persistently infected. PLV antigen-induced proliferation was slightly greater in mucosally inoculated animals, but no differences were noted in cytotoxic T-lymphocyte responses or cytokine profiles between groups. The distribution of virus was predominantly gastrointestinal as opposed to lymphoid in all animals in which virus was detected at necropsy. Possible mechanisms for viral clearance include differences in viral fitness required for crossing mucosal surfaces, a threshold dose requirement for persistence, or an undetected sterilizing host immune response. This is the first report of control of a productive feline or primate lentivirus infection in postnatally exposed, seropositive animals. Mechanisms underlying this observation will provide clues to containment of immunodeficiency disease and could prompt reexamination of vaccine-induced immunity against human immunodeficiency virus and other lentiviruses.