Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, 111 Ren'ai Road, Suzhou Dushu Lake Science and Education Innovation District, Suzhou Industrial Park, Suzhou 215123, China.
Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool L69 7BE, UK.
Viruses. 2020 Mar 31;12(4):381. doi: 10.3390/v12040381.
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.
自噬和细胞凋亡是两种重要的进化上保守的宿主防御机制,可抵抗病毒入侵和发病。然而,在 T 淋巴细胞的病毒感染过程中,这两种途径之间的关联仍有待阐明。猴 D 型逆转录病毒(SRV)是致命性猴获得性免疫缺陷综合征(SAIDS)的病原体,它可以表现出类似于人类获得性免疫缺陷综合征的疾病特征。在这项研究中,我们证明了新分离的 SRV 亚型 SRV-8 的感染会触发 Jurkat T 淋巴细胞中的自噬和凋亡途径。在感染 SRV-8 后,自噬蛋白 LC3 和 p62/SQSTM1 与 procaspase-8 相互作用,这可能是导致 caspase-8/-3 级联激活和 SRV-8 感染的 Jurkat 细胞凋亡的原因。我们的研究结果表明,T 淋巴细胞对 SRV 感染的自噬反应促进了 T 淋巴细胞的凋亡,而这反过来又可能是 SRV 感染过程中 T 淋巴细胞丢失的潜在发病机制。