HIV, the virus that causes AIDS, does its damage by decimating immune cells. But it also lies dormant in some cells, creating a reservoir that can restart an active infection long after the active virus has been cleared by treatments. This is apparently what happened to a child from Mississippi who was thought to have been cured of infection following antiviral treatments.
Researchers may now have found one of the reasons that it’s so hard to clear out these reservoirs of infected cells. As part of the infection process, HIV normally inserts a copy of itself into a cell’s chromosomes. By chance, some of these insertions cause the cell to grow faster, ensuring that more copies of the virus are around to cause trouble.
The researchers, who are all based in Seattle, took a pretty simple approach to discover this: they sampled cells from HIV patients who were receiving long-term antiviral treatment, looking for the sites of HIV insertion. In these patients, viral replication was suppressed by the drugs, often for periods of over a decade. Therefore, any viruses researchers found were from those cells that had quiescent viruses inserted into their genome.
In some ways, HIV works like a tumor. Cancer cells have mutations that often affect cell growth. When we try and hit this with chemotherapy, tumor cells with a selective advantage that allows them to survive will continue to grow.
HIV inserts randomly into a cell’s DNA, sometimes close to a gene. If that gene happens to be one of the growth genes , the HIV will alter the cell’s metabolism much as cancer mutations do.
So, even when drugs are used to control the HIV, the cells with HIV insertions next to growth genes still manage to survive.
It is not just enough to have drugs that stop HIV from replicating We may have to figure out how to deal with specific insertion points and how to deal with those cells.