Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes

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...

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Main Authors: Jingting Zhu, Lingyan Yang, Qibo Zhang, Jia Meng, Zhi-Liang Lu, Rong Rong
Format: Article
Language:English
Published: MDPI AG 2020-03-01
Series:Viruses
Subjects:
Online Access:https://www.mdpi.com/1999-4915/12/4/381
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author Jingting Zhu
Lingyan Yang
Qibo Zhang
Jia Meng
Zhi-Liang Lu
Rong Rong
author_facet Jingting Zhu
Lingyan Yang
Qibo Zhang
Jia Meng
Zhi-Liang Lu
Rong Rong
author_sort Jingting Zhu
collection DOAJ
description 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.
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spelling doaj.art-bcd24ac45e934c25821ee0c5f3fb33e52023-11-19T20:13:45ZengMDPI AGViruses1999-49152020-03-0112438110.3390/v12040381Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T LymphocytesJingting Zhu0Lingyan Yang1Qibo Zhang2Jia Meng3Zhi-Liang Lu4Rong Rong5Department 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, ChinaVRL-China, Suzhou 215123, ChinaDepartment of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool L69 7BE, UKDepartment 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, ChinaDepartment 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, ChinaDepartment 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, ChinaAutophagy 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.https://www.mdpi.com/1999-4915/12/4/381SRVautophagyapoptosisautophagosomeviral replication
spellingShingle Jingting Zhu
Lingyan Yang
Qibo Zhang
Jia Meng
Zhi-Liang Lu
Rong Rong
Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
Viruses
SRV
autophagy
apoptosis
autophagosome
viral replication
title Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
title_full Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
title_fullStr Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
title_full_unstemmed Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
title_short Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
title_sort autophagy induced by simian retrovirus infection controls viral replication and apoptosis of jurkat t lymphocytes
topic SRV
autophagy
apoptosis
autophagosome
viral replication
url https://www.mdpi.com/1999-4915/12/4/381
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AT jiameng autophagyinducedbysimianretrovirusinfectioncontrolsviralreplicationandapoptosisofjurkattlymphocytes
AT zhilianglu autophagyinducedbysimianretrovirusinfectioncontrolsviralreplicationandapoptosisofjurkattlymphocytes
AT rongrong autophagyinducedbysimianretrovirusinfectioncontrolsviralreplicationandapoptosisofjurkattlymphocytes