Autophagy and apoptosis are two important evolutionarily conserved host defense mechanisms against viral invasion and pathogenesis. However, the association between the two pathways during the viral infection of T lymphocytes remains to be elucidated. Simian type D retrovirus (SRV) is an etiological agent of fatal simian acquired immunodeficiency syndrome (SAIDS), which can display disease features that are similar to acquired immunodeficiency syndrome in humans. In this study, we demonstrate that infection with SRV-8, a newly isolated subtype of SRV, triggered both autophagic and apoptotic pathways in Jurkat T lymphocytes. Following infection with SRV-8, the autophagic proteins LC3 and p62/SQSTM1 interacted with procaspase-8, which might be responsible for the activation of the caspase-8/-3 cascade and apoptosis in SRV-8-infected Jurkat cells. Our findings indicate that autophagic responses to SRV infection of T lymphocytes promote the apoptosis of T lymphocytes, which, in turn, might be a potential pathogenetic mechanism for the loss of T lymphocytes during SRV infection.

中文翻译：

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猿猴逆转录病毒感染诱导的自噬控制Jurkat T淋巴细胞的病毒复制和凋亡。

自噬和凋亡是抵抗病毒入侵和发病机制的两个重要的进化上保守的宿主防御机制。然而，在T淋巴细胞的病毒感染过程中两种途径之间的关联仍有待阐明。猿猴D型逆转录病毒（SRV）是致命猿猴后天免疫机能丧失综合症（SAIDS）的病原体，它可以表现出与人类后天免疫机能丧失综合症相似的疾病特征。在这项研究中，我们证明了SRV-8（一种新分离的SRV亚型）的感染触发了Jurkat T淋巴细胞的自噬和凋亡途径。在被SRV-8感染后，自噬蛋白LC3和p62 / SQSTM1与procaspase-8相互作用，这可能是caspase-8 / -3级联的激活以及SRV-8感染的Jurkat细胞凋亡的原因。