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

Abstract

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.

Characterizing the Pathogenicity and Immunogenicity of Simian Retrovirus Subtype 8 (SRV-8) Using SRV-8-Infected Cynomolgus Monkeys

“…SRV-8 infection elicited dynamic changes in various host genes [ 40 ]. The pathobiological mechanism of the diseases induced by SRV-8 infection is still unknown.…”

A Review on Zoonotic Pathogens Associated with Non-Human Primates: Understanding the Potential Threats to Humans

“…Togami et al found that zidovudine and tenofovir disoproxil fumarate, in sub-micromolar to nanomolar dosages, potently inhibit SRV-4 infection; conversely, non-nucleoside reverse transcriptase inhibitors and protease inhibitors showed no activity against SRV-4 [ 67 ]. Human infection with SRV has no clear clinical manifestations [ 68 ]; however, to prevent virus transmission, PCR is performed and model animals are regularly tested for viral antibodies, and animals that test positive for the virus are immediately removed.…”

Treatment of Parkinson’s disease using focused ultrasound with GDNF retrovirus-loaded microbubbles to open the blood–brain barrier

“…After incubation at room temperature for 30 min, the microbubbles were washed twice by the floating method to wash off the unbound virus particles and obtain the pLXSN-GDNF microbubble contrast agent. Four sample aliquots were taken from the virus solution, washing the supernatant each time and microbubble solution binding virus, in which the virus quantity was detected by real-time (fluorescence) quantitative PCR, and the adhesion efficiency of the virus and microbubbles was determined [17]. The preparation and detection methods for pLXSN-EGFP microbubbles were the same as those above.…”