TABLE 1.
Variations in the levels of BCL-2 family members in cell subsets during HIV infectiona
| Cell subset | Level variation during: |
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|---|---|---|---|---|---|---|
| Acute HIV infection |
Chronic HIV infection |
ART therapy |
||||
| BCL-2 | Other homologs | BCL-2 | Other homologs | BCL-2 | Other homologs | |
| CD4+ T cells | ||||||
| Proapoptotic | ↓BCL-2 | ↑BAX | ↓BCL-2 | |||
| Antiapoptotic | ↑BCL-2 | Levels restored to normal | ||||
| ↑BCL-2 in infected TFH cells | ↑BCL-2 in latently infected central memory CD4 cells | |||||
| ↑BCL-2 in infected TN, TReg, and PD-1low cells |
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| CD8+ T cells | ||||||
| Proapoptotic | ↓BCL-2 | ↓BCL-2 | ↓BCL-XL | |||
| Antiapoptotic | ↑BCL-2 in elite controllers | ↑BCL-2 response to IL-7 | ||||
| Monocytes | ↓BCL-2 | ↑BCL-2, allowing for survival of infected cells | ||||
| Macrophages, antiapoptotic | ↑BCL-2 | ↑BCL-XL | ↑BIM (paradoxically increased survival) | |||
| ↓BAD and BAX | ||||||
| Dendritic cells | ||||||
| Myeloid | ↑BCL-2 in tissue | |||||
| ↓BCL-2 in circulation | ||||||
| Plasmacytoid | ↑BCL-2 in circulation | |||||
a
BCL-2 and its family members have demonstrated different susceptibilities to HIV-induced modulations in their levels across the different immune cell subsets at different stages of infection.TN, naive T cell; TReg, regulatory T cells; PD-1low, cells expressing low levels of the PD-1 ligand.