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来自急性感染猫的免疫球蛋白G可阻断黏膜猫免疫缺陷病毒感染。

IgG from acutely infected cats blocks mucosal feline immunodeficiency virus infection.

作者信息

Burkhard Mary Jo, Hoover Edward A

机构信息

Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210, USA.

出版信息

Vet Immunol Immunopathol. 2005 Jun 15;106(1-2):87-95. doi: 10.1016/j.vetimm.2005.01.008.

DOI:10.1016/j.vetimm.2005.01.008
PMID:15910995
Abstract

We have previously shown an absence of detectable systemic or local infection in cats exposed to an infectious (100 TCID(50)) feline immunodeficiency virus (FIV) plasma inoculum via either the rectal or vaginal mucosa. In contrast, this same plasma inoculum was infectious via parenteral inoculation. Moreover an equivalent dose of cell-free tissue culture-origin virus inoculum infected 100% of cats by either the rectal or vaginal exposure route. To evaluate this phenomena, we used a tissue culture system to identify a heat-stable factor in the plasma of cats acutely (3 weeks) infected with FIV that blocked infection of naive peripheral blood mononuclear cells (PBMC) by either cell-free or cell-associated FIV in vitro. A single application of as little as a 1:200 dilution of either heparinized or Alsevier's anticoagulated plasma effectively inhibited production of FIV p26 in culture over a 21-day co-culture period. Depletion of antibody using a protein A column abrogated the inhibitory effect of FIV plasma against in vitro FIV infection. Co-inoculation of heat-inactivated plasma with 400 TCID(50) FIV-B-2542 cell-free supernatant virus onto the vaginal mucosa of two cats resulted in complete inhibition of infection in one cat and increased time to infection in the second. Thus, antibody found in the plasma of cats acutely infected with FIV blocks cell-associated and cell-free infection, inhibits virus production in previously infected cells, and reduces mucosal transmission efficiency in vivo. Extrapolation may help explain the relatively inefficient mucosal transmission of human immunodeficiency virus-1 (HIV) and other lentiviruses.

摘要

我们之前已经表明,通过直肠或阴道黏膜暴露于感染性(100个组织培养感染剂量50%,TCID(50))猫免疫缺陷病毒(FIV)血浆接种物的猫,未检测到全身性或局部感染。相比之下,相同的血浆接种物经肠胃外接种具有传染性。此外,等量的无细胞组织培养来源病毒接种物通过直肠或阴道暴露途径可使100%的猫感染。为了评估这种现象,我们使用一种组织培养系统来鉴定急性(3周)感染FIV的猫血浆中的一种热稳定因子,该因子在体外可阻断无细胞或细胞相关FIV对未感染外周血单个核细胞(PBMC)的感染。在21天的共培养期内,单次应用低至1:200稀释的肝素化或阿尔斯维尔抗凝血浆可有效抑制培养物中FIV p26的产生。使用蛋白A柱去除抗体可消除FIV血浆对体外FIV感染的抑制作用。将热灭活血浆与400个TCID(50) FIV-B-2542无细胞上清液病毒共同接种到两只猫的阴道黏膜上,结果一只猫的感染完全被抑制,另一只猫的感染时间延长。因此,急性感染FIV的猫血浆中的抗体可阻断细胞相关和无细胞感染,抑制先前感染细胞中的病毒产生,并降低体内黏膜传播效率。由此推断可能有助于解释人类免疫缺陷病毒1型(HIV)和其他慢病毒相对低效的黏膜传播。

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