Yoon K J, Wu L L, Zimmerman J J, Hill H T, Platt K B
Veterinary Diagnostic Laboratory, College of Veterinary Medicine, Iowa State University, Ames 50011, USA.
Viral Immunol. 1996;9(1):51-63. doi: 10.1089/vim.1996.9.51.
Infection of porcine alveolar macrophages by the porcine reproductive and respiratory syndrome virus (PRRSV) was significantly enhanced in vitro by antibody raised against the PRRSV isolate ISU-P (p < 0.01). Increased yields and infection rates were highly correlated (r = 0.95) and the ratio of yield to infection rate was greater than 1.4, suggesting that more than one mechanism was responsible for enhanced infection. Antibody-dependent enhancement (ADE) of infection was also demonstrated in vivo using a completely randomized block design (n = 16). The mean level and duration of viremia were greater (p < 0.05) in pigs injected with subneutralizing amounts of PRRSV-specific IgG prior to virus challenge than in control pigs injected with normal IgG. In contrast, virus replication was significantly (p < 0.01) inhibited in pigs with neutralizing antibody titers of 4 log2. The period of time that subneutralizing levels of antibody can persist and contribute to ADE of PRRSV infection was estimated in 4 pigs injected with PRRSV-specific IgG to yield an initial neutralizing antibody titer of 3.8 log2. Neutralizing activity declined to undetectable levels by day 37 postinjection (PI). ADE activity was first detected in undiluted sera on day 20 PI and persisted through day 62 PI. Western immunoblot analysis of sera collected between days 37 and 62 PI detected antibodies specific for the 15-kDa nucleocapsid and 26-kDa glycosylated envelope proteins. These results strongly suggest that ADE has the potential to contribute to the pathogenesis of PRRSV infection and is mediated by antibody specific for the 26-kDa envelope protein.
针对猪繁殖与呼吸综合征病毒（PRRSV）分离株ISU - P产生的抗体，在体外可显著增强PRRSV对猪肺泡巨噬细胞的感染（p < 0.01）。产量增加与感染率高度相关（r = 0.95），产量与感染率之比大于1.4，这表明增强感染是由多种机制引起的。使用完全随机区组设计（n = 16）在体内也证实了感染的抗体依赖性增强（ADE）。在病毒攻击前注射亚中和量PRRSV特异性IgG的猪，其病毒血症的平均水平和持续时间比注射正常IgG的对照猪更高（p < 0.05）。相反，中和抗体效价为4 log2的猪中病毒复制受到显著抑制（p < 0.01）。对4头注射PRRSV特异性IgG以产生初始中和抗体效价为3.8 log2的猪，估计了亚中和水平抗体持续存在并促进PRRSV感染ADE的时间。中和活性在注射后第37天（PI）降至无法检测的水平。ADE活性在注射后第20天在未稀释血清中首次检测到，并持续到注射后第62天。对注射后第37天至62天收集的血清进行的western免疫印迹分析检测到针对15 kDa核衣壳蛋白和26 kDa糖基化包膜蛋白的特异性抗体。这些结果强烈表明，ADE有可能促成PRRSV感染的发病机制，并且由针对26 kDa包膜蛋白的抗体介导。
