广泛反应性Th肽诱导的淋巴细胞增殖反应对马传染性贫血病毒的攻击没有保护作用。

Darrilyn G Fraser, Steve R Leib, Bao Shan Zhang, Robert H Mealey, Wendy C Brown, Travis C McGuire
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引用次数: 12

摘要

研究了5种脂肽免疫对马传染性贫血病毒(EIAV)攻击的影响,其中3种含有辅助性t淋巴细胞(Th)表位,2种含有Th和细胞毒性t淋巴细胞(CTL)表位。与免疫前相比,EIAV脂肽免疫马的外周血单个核细胞对Th肽有显著的增殖反应,这种反应归因于位点221至245 (Gag 221-245)、Gag 250-269和Pol 326-347的显著反应;然而,没有一致的CTL反应。在EIAV脂肽免疫的马中,显著的增殖反应允许测试假设,免疫反应将增强EIAV攻击后的Th和CTL反应,并减轻病毒载量和临床疾病的严重程度。病毒攻击后1周,EIAV脂肽免疫组对Th肽的增殖反应明显增加,而对照组则没有。攻击两周后,与对照组相比,EIAV脂肽免疫组对病毒感染的细胞靶标发生了显著的CTL反应。这些Th和CTL反应没有显著改变病毒RNA拷贝数/ml或疾病严重程度。因此,在病毒攻击后早期,脂肽诱导的增殖反应和增强的Th和CTL反应无法控制攻击病毒载量和临床疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lymphocyte proliferation responses induced to broadly reactive Th peptides did not protect against equine infectious anemia virus challenge.

The effect of immunization with five lipopeptides, three containing T-helper (Th) epitopes and two with both Th and cytotoxic T-lymphocyte (CTL) epitopes, on equine infectious anemia virus (EIAV) challenge was evaluated. Peripheral blood mononuclear cells from EIAV lipopeptide-immunized horses had significant proliferative responses to Th peptides compared with those preimmunization, and the responses were attributed to significant responses to peptides Gag from positions 221 to 245 (Gag 221-245), Gag 250-269, and Pol 326-347; however, there were no consistent CTL responses. The significant proliferative responses in the EIAV lipopeptide-immunized horses allowed testing of the hypothesis that Th responses to immunization would enhance Th and CTL responses following EIAV challenge and lessen the viral load and the severity of clinical disease. The EIAV lipopeptide-immunized group did have a significant increase in proliferative responses to Th peptides 1 week after virus challenge, whereas the control group did not. Two weeks after challenge, a significant CTL response to virus-infected cell targets occurred in the EIAV lipopeptide-immunized group compared to that in the control group. These Th and CTL responses did not significantly alter either the number of viral RNA copies/ml or disease severity. Thus, lipopeptide-induced proliferative responses and enhanced Th and CTL responses early after virus challenge were unable to control challenge virus load and clinical disease.

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