Effect of HIV on T-cells
From this article:


  Researchers found that when the virus productively infects the few permissive CD4 T cells present, death occurs through apoptosis mediated by an enzyme called caspase-3. But when HIV abortively infects nonpermissive CD4 T cells, death occurs by pyroptosis, which depends on the activation of caspase-1. It turns out that the vast majority—roughly 95 percent—of CD4 T cell death in lymphoid tissues is driven by caspase-1-mediated pyroptosis.


When it comes to macrophages, however:


  macrophages are much more resistant to cytopathic effects of lentiviral replication than for example activated CD4+ T cells [23, 24, 25], and HIV-1 has evolved sophisticated mechanisms to prolong the life span of infected macrophages [24, 26]. Especially long-lived macrophages may therefore harbor the virus for long time periods, thus constituting HIV-1 reservoirs and posing a major obstacle to virus eradication from infected individuals.


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