Journal article
HIV associated cell death: Peptide-induced apoptosis restricts viral transmission
- Abstract:
- The human immunodeficiency virus (HIV) is still a global pandemic and despite the successful use of anti-retroviral therapy, a well-established cure remains to be identified. Viral modulation of cell death has a significant role in HIV pathogenesis. Here we sought to understand the major mechanisms of HIV- induced death of lymphocytes and the effects on viral transmission. Flow cytometry analysis of lymphocytes from five latent HIV-infected patients, and HIV IIIB-infected MT2 cells demonstrated both necrosis and apoptosis to be the major mechanisms of cell death in CD4+ and CD4-/CD8- lymphocytes. Significantly, pro-apoptotic tumor necrosis factor (TNF) peptide (P13) was found to inhibit HIV-related cell death and reduced viral transmission. Whereas pro-necrotic TNF peptide (P16) had little effect on HIV-related cell death and viral transmission. Understanding mechanisms by which cell death can be manipulated may provide additional drug targets to reduce the loss of CD4+ cells and the formation of a viral reservoir in HIV infection
- Publication status:
- Published
- Peer review status:
- Peer reviewed
Actions
Access Document
- Files:
-
-
(Preview, Version of record, pdf, 2.6MB, Terms of use)
-
- Publisher copy:
- 10.3389/fimmu.2023.1096759
Authors
- Publisher:
- Frontiers Media
- Journal:
- Frontiers in Immunology More from this journal
- Volume:
- 14
- Pages:
- 1096759-1096759
- Article number:
- 1096759
- Publication date:
- 2023-02-22
- DOI:
- EISSN:
-
1664-3224
- ISSN:
-
1664-3224
- Language:
-
English
- Keywords:
- Pubs id:
-
1333233
- Local pid:
-
pubs:1333233
- Source identifiers:
-
W4321498180
- Deposit date:
-
2026-05-05
- ARK identifier:
This ORA record was generated from metadata provided by an external service. It has not been edited by the ORA Team.
Terms of use
- Copyright date:
- 2023
- Licence:
- CC Attribution (CC BY)
If you are the owner of this record, you can report an update to it here: Report update to this record