Transcription Factor ZNF683 Inhibits SIV/HIV Replication through Regulating IFNγ Secretion of CD8+ T Cells

Viruses

Tian-Zhang Song¹  Yong-Tang Zheng¹  Ying Lu¹  Hong-Yi Zheng¹  Ren-Rong Tian¹  Ming-Xu Zhang¹  Wei Pang¹ 

[1] Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China;

关键词: lung;    SIVmac239;    slow progressors;    rapid progressors;    northern pig-tailed macaques;    ZNF683;   

DOI  :  10.3390/v14040719

来源: DOAJ

【 摘 要 】

Pulmonary microbial invasion frequently occurs during AIDS progression in HIV patients. Inflammatory cytokines and other immunoregulatory factors play important roles in this process. We previously established an AIDS model of SIVmac239 infection in northern pig-tailed macaques (NPMs), which were divided into rapid progressor (RP) and slow progressor (SP) groups according to their AIDS progression rates. In this study, we performed 16S rDNA and transcriptome sequencing of the lungs to reveal the molecular mechanism underlying the difference in progression rate between the RPs and SPs. We found that microbial invasion in the RP group was distinct from that in the SP group, showing marker flora of the Family XI, Enterococcus and Ezakiella, and more Lactobacilli. Through pulmonary transcriptome analysis, we found that the transcription factor ZNF683 had higher expression in the SP group than in the RP group. In subsequent functional experiments, we found that ZNF683 increased the proliferation and IFNγ secretion ability of CD8+ T cells, thus decreasing SIV or HIV replication, which may be related to AIDS progression in SIVmac239-infected NPMs. This study helps elucidate the various complexities of disease progression in HIV-1-infected individuals.

【 授权许可】

Unknown