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首页> 外文期刊>Microbes and infection >Impaired T-cell differentiation in the thymus at the early stages of acute pathogenic chimeric simian-human immunodeficiency virus (SHIV) infection in contrast to less pathogenic SHIV infection.
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Impaired T-cell differentiation in the thymus at the early stages of acute pathogenic chimeric simian-human immunodeficiency virus (SHIV) infection in contrast to less pathogenic SHIV infection.

机译：与病原性较低的SHIV感染相比，急性病原性嵌合猿猴-人免疫缺陷病毒（SHIV）感染早期胸腺中T细胞分化受损。

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One of the mechanisms by which HIV infection induces the depletion of CD4+ T cells has been suggested to be impairment of T-cell development in the thymus, although there is no direct evidence that this occurs. To examine this possibility, we compared T-cell maturation in the intrathymic progenitors between macaques infected with an acute pathogenic chimeric simian-human immunodeficiency virus (SHIV), which causes profound and irreversible CD4+ T-cell depletion, and macaques infected with a less pathogenic SHIV, which causes only a transient CD4+ T-cell decline. Within 27 days post-inoculation (dpi), the two virus infections caused similar increases in plasma viral loads and similar decreases in CD4+ T-cell counts. However, in the thymus, the acute pathogenic SHIV resulted in increased thymic involution, atrophy and the depletion of immature T cells including CD4(+)CD8(+) double-positive (DP) cells, whereas the less pathogenic SHIV did not have these effects. Ex vivo differentiation of CD3(-)CD4(-)CD8(-) triple-negative (TN) intrathymic progenitors to DP cells was assessed by a monkey-mouse xenogenic fetal thymus organ culture system. Differentiation was impaired in the TN intrathymic progenitors of the acute pathogenic SHIV-infected monkeys, while differentiation was not impaired in the TN intrathymic progenitors of the less pathogenic SHIV-infected monkeys. These differences suggest that dysfunction of thymic maturation makes an important contribution to the irreversible depletion of circulating CD4+ T cells in vivo.
机译：尽管没有直接的证据表明，HIV感染诱导CD4 + T细胞耗竭的一种机制是胸腺T细胞发育受损。为了检验这种可能性，我们比较了感染急性致病性嵌合猿猴-人类免疫缺陷病毒（SHIV）的猕猴与胸腺内祖细胞中T细胞的成熟情况，这种病毒可导致CD4 + T细胞大量耗竭且不可逆转，而猕猴感染的病原性较低SHIV，仅引起短暂的CD4 + T细胞下降。接种后（dpi）27天之内，两次病毒感染导致血浆病毒载量增加相似，而CD4 + T细胞计数减少相似。然而，在胸腺中，急性致病性SHIV导致胸腺退化，萎缩和未成熟T细胞的耗尽，包括CD4（+）CD8（+）双阳性（DP）细胞，而致病性较低的SHIV没有这些效果。通过猴鼠异种胎儿胸腺器官培养系统评估CD3（-）CD4（-）CD8（-）三阴性（TN）胸腺内祖细胞向DP细胞的离体分化。急性致病性SHIV感染的猴子的TN胸腺祖细胞的分化受损，而致病性较低的SHIV感染的猴子的TN胸腺祖细胞的分化不受损。这些差异表明，胸腺成熟功能障碍是体内循环CD4 + T细胞不可逆耗竭的重要原因。

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