A protein called SAMHD1, produced by dendritic cells, provides resistance of immune cells against HIV. Researchers are currently investigating the mechanism by which SAMHD1 resists HIV infection, but it's been proposed that this protein destroys the free flowing dNTPs, thus depleting virus infected cells of building blocks to replicate the viral genome. This process is termed Nucleotide pool depletion. Or in the words of Dr. Landau "SAMHD1 essentially starves the virus." But the viruses have their own escape strategies - they evolved to not infect SAMHD1 producing cells, but to infect CD4 T-cells, which do not produce such protective proteins. In addition, HIV and related viruses have developed Protein X that directly attacks SAMHD1, allowing it to infect dendritic cells.
I found this article interesting because it has profound therapeutic implications. If we could develop a drug to increase SAMHD1 production in naturally non-producing cells, such as CD4 T cells, therefore counter-attacking HIV's immune evading strategies. In addition, understanding how viral protein X interacts and destroys SAMHD1 could pave the way to developing drugs that prevent viral destruction of these crucial genes.