首页> 美国卫生研究院文献>Journal of Virology >Immunization with baculovirus-expressed recombinant rotavirus proteins VP1 VP4 VP6 and VP7 induces CD8+ T lymphocytes that mediate clearance of chronic rotavirus infection in SCID mice.
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Immunization with baculovirus-expressed recombinant rotavirus proteins VP1 VP4 VP6 and VP7 induces CD8+ T lymphocytes that mediate clearance of chronic rotavirus infection in SCID mice.

机译:用杆状病毒表达的重组轮状病毒蛋白VP1VP4VP6和VP7免疫可诱导介导SCID小鼠中慢性轮状病毒感染清除的CD8 + T淋巴细胞。

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摘要

Clearance of chronic murine rotavirus infection in SCID mice can be demonstrated by adoptive transfer of immune CD8+ T lymphocytes from histocompatible donor mice immunized with a murine homotypic rotavirus (T. Dharakul, L. Rott, and H.B. Greenberg, J. Virol 64:4375-4382, 1990). The present study focuses on the protein specificity and heterotypic nature of cell-mediated clearance of chronic murine rotavirus infection in SCID mice. Heterotypic cell-mediated clearance was demonstrated in SCID mice infected with EDIM (murine) rotavirus after adoptive transfer of CD8+ T lymphocytes from BALB/c mice that were immunized with a variety of heterologous (nonmurine) rotaviruses including Wa (human, serotype 1), SA11 and RRV (simian, serotype 3), and NCDV and RF (bovine, serotype 6). This finding indicates the serotypic independence of T-cell-mediated rotavirus clearance. To further identify the rotavirus proteins that are capable of generating CD8+ T cells that mediate virus clearance, donor mice were immunized with SF-9 cells infected with a baculovirus recombinant expressing one of the following rotavirus proteins: VP1, VP2, NS53 (from RF), VP4, VP7, NS35 (from RRV), VP6, and NS28 (from SA11). SCID mice stopped shedding rotavirus after receiving CD8+ T cells from mice immunized with VP1, VP4, VP6, and VP7 but not with VP2, NS53, NS35, NS28, or wild-type baculovirus. These results suggest that heterotypic cell-mediated clearance of rotavirus in SCID mice is mediated by three of the major rotavirus structural proteins and by a putative polymerase protein.
机译:SCID小鼠中慢性鼠轮状病毒感染的清除可以通过用鼠类同型轮状病毒免疫的组织相容性供体小鼠的过继转移免疫CD8 + T淋巴细胞来证明(T. Dharakul,L. Rott和HB Greenberg,J. Virol 64:4375- 4382,1990)。本研究的重点是SCID小鼠中慢性鼠轮状病毒感染的细胞介导清除的蛋白质特异性和异型性质。在过继转移BALB / c小鼠的CD8 + T淋巴细胞过继转移后,异种细胞介导的清除率在被EDIM(鼠)轮状病毒感染的SCID小鼠中得到了证明,这些CD8 + T淋巴细胞已用多种异源(非鼠)轮状病毒(包括Wa(人,血清型1), SA11和RRV(猿猴,血清型3),以及NCDV和RF(牛,血清型6)。该发现表明T细胞介导的轮状病毒清除的血清型独立性。为了进一步鉴定能够产生介导病毒清除作用的CD8 + T细胞的轮状病毒蛋白,用感染了表达以下轮状病毒蛋白之一的杆状病毒重组体的SF-9细胞免疫供体小鼠:VP1,VP2,NS53(来自RF) ,VP4,VP7,NS35(来自RRV),VP6和NS28(来自SA11)。从接受VP1,VP4,VP6和VP7免疫但未接受VP2,NS53,NS35,NS28或野生型杆状病毒免疫的小鼠接受CD8 + T细胞后,SCID小鼠停止脱落轮状病毒。这些结果表明,SCID小鼠中轮状病毒异型细胞介导的清除是由三种主要的轮状病毒结构蛋白和推定的聚合酶蛋白介导的。

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