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首页> 美国卫生研究院文献>Journal of Virology >CD8+ and CD20+ Lymphocytes Cooperate To Control Acute Simian Immunodeficiency Virus/Human Immunodeficiency Virus Chimeric Virus Infections in Rhesus Monkeys: Modulation by Major Histocompatibility Complex Genotype
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CD8+ and CD20+ Lymphocytes Cooperate To Control Acute Simian Immunodeficiency Virus/Human Immunodeficiency Virus Chimeric Virus Infections in Rhesus Monkeys: Modulation by Major Histocompatibility Complex Genotype

机译：CD8 +和CD20 +淋巴细胞协作以控制恒河猴的急性猿猴免疫缺陷病毒/人类免疫缺陷病毒嵌合病毒感染：主要组织相容性复杂基因型的调节。

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We have previously described two isogenic molecularly cloned simian immunodeficiency virus/human immunodeficiency virus chimeric viruses (SHIVs) that differ from one another by 9 amino acids and direct distinct clinical outcomes in inoculated rhesus monkeys. SHIVDH12R-Clone 7, like other highly pathogenic CXCR4-tropic SHIVs, induces rapid and complete depletions of CD4+ T lymphocytes and immunodeficiency in infected animals. In contrast, macaques inoculated with SHIVDH12R-Clone 8 experience only partial and transient losses of CD4+ T cells, show prompt control of their viremia, and remain healthy for periods of time extending for up to 4 years. The contributions of CD8+ and CD20+ lymphocytes in suppressing the replication of the attenuated SHIVDH12R-Clone 8 and maintaining a prolonged asymptomatic clinical course was assessed by treating animals with monoclonal antibodies that deplete each lymphocyte subset at the time of virus inoculation. The absence of either CD8+ or CD20+ cells during the SHIVDH12R-Clone 8 acute infection resulted in the rapid, complete, and irreversible loss of CD4+ T cells; sustained high levels of postpeak plasma viremia; and symptomatic disease in Mamu-A*01-negative Indian rhesus monkeys. In Mamu-A*01-positive animals, however, the aggressive, highly pathogenic phenotype was observed only in macaques depleted of CD8+ cells; SHIVDH12R-Clone 8 was effectively controlled in Mamu-A*01-positive monkeys in the absence of B lymphocytes. Taken together, these results indicate that both CD8+ and CD20+ B cells contribute to the control of primate lentiviral infection in Mamu-A*01-negative macaques. Furthermore, the major histocompatibility complex genotype of an infected animal, as exemplified by the Mamu-A*01 allele in this study, has the additional capacity to shift the balance of the composite immune response.
机译：先前我们已经描述了两种等基因分子克隆的猿猴免疫缺陷病毒/人类免疫缺陷病毒嵌合病毒（SHIV），它们彼此相差9个氨基酸，并且在接种的恒河猴中具有不同的临床效果。与其他高致病性的CXCR4嗜性SHIV一样，SHIVDH12R-Clone 7可以诱导感染动物的CD4 + T淋巴细胞快速，完全耗尽和免疫缺陷。相比之下，接种SHIVDH12R-Clone 8的猕猴只经历CD4 + T细胞的部分和短暂损失，显示出对病毒血症的迅速控制，并且可以持续长达4年的时间保持健康。通过用单克隆抗体处理动物，评估了CD8 + 和CD20 + 淋巴细胞在抑制减毒的SHIVDH12R-Clone 8的复制和维持无症状的临床过程中的作用。在接种病毒时会耗尽每个淋巴细胞亚群。在SHIVDH12R-Clone 8急性感染期间，没有CD8 + 或CD20 + 细胞会导致CD4 +迅速，完全和不可逆转地丢失 sup> T细胞；高峰后血浆病毒血症持续高水平；和Mamu-A * 01阴性印度恒河猴的症状性疾病。然而，在Mamu-A * 01阳性动物中，仅在耗竭CD8 + 细胞的猕猴中观察到具有攻击性的高致病性表型。在没有B淋巴细胞的情况下，在Mamu-A * 01阳性的猴子中SHIVDH12R-Clone 8得到了有效控制。综上所述，这些结果表明CD8 + 和CD20 + B细胞均有助于控制Mamu-A * 01阴性猕猴的灵长类慢病毒感染。此外，如本研究中的Mamu-A * 01等位基因所示，感染动物的主要组织相容性复杂基因型具有改变复合免疫反应平衡的额外能力。

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