BUTTING IN: HIV integrates genetic material into the genome of a host’s memory T cells, frequently at sites of so-called Alu repeats (above, left panel). Although these cells are suspected of harboring intact, latent viral DNA, researchers have found that clones of an infected T cell have short, dysfunctional integrations and thus likely do not compose the HIV reservoir that can replicate if a patient stops antiretroviral therapy (above, right panel).© KIMBERLY BATTISTA
The paper
L.B. Cohn et al., “HIV-1 integration landscape during latent and active infection,” Cell, 160:420-32, 2015.
Antiretroviral treatments have transformed HIV infection from a death sentence to a manageable, though lifelong, condition. But remove the drugs that prevent the virus from replicating, and the infection comes roaring back. Although scientists have long known that somewhere in the bodies of HIV-positive people a latent reservoir of virus lies in wait, ready to replicate when conditions are right, researchers have struggled to locate it. One of the more popular latent-reservoir hypotheses is that the virus integrates into the genome of a memory T cell. That cell then divides many times, creating clones of the original integration that serve as an on-demand virus-making factory.
To test this ...
