Tracking HIV carrier cells to understand HIV dynamics

Scientists from the USA have been able to track the lifespan and location of cells responsible for the production of HIV. Understanding the dynamics of these cells could help scientists develop new ways to reduce their numbers, with the ultimate goal of curing HIV infection. The results of the study have been published in the journal PNAS (paid access required).

“When people chronically infected with HIV-1 receive powerful antiretroviral therapy, the amount of virus in their blood decreases. Moreover, the reduction of the virus occurs in two separate phases: a rapid first phase followed by a slow second phase, ”said Dr. Alan Perelson from Los Alamos National Laboratory.

During previous studies, the team concluded that the biphasic decline reflects the fact that HIV infects and hijacks two different virus-producing cell populations:

Population one: This group produces most of the virus, but only lives for about one day. The collapses of this population is responsible for the first phase decline of virus levels in blood.

Population two: This group releases the virus much more slowly, and lives for several weeks. The loss of this population is responsible for the second, flowers, phase of virus decline.

In a new study, Robert Siliciano, and his team at Johns Hopkins University’s School of Medicine searched for these hypothetical cells and their differing decay rates.

The team isolated HIV-infected cells in the blood of 17 people receiving antiretroviral therapy. They found that very few of the short-lied infected cells, responsible for the first phase of viral production, were circulating in the blood. This means that these cells are most likely found in tissues such as the spleen and lymph nodes.

They also found cells with an intact HIV genome that took around two weeks decay, it is assumed that these cells are responsible for the second phase of viral decay.

After around three months on treatment, the remaining infected cells with intact HIV genomes decayed even more slowly, with a half-life of around 19 months.

It is thought that these cells may become part of a ‘latent reservoir’, which when if treatment is stopped, will reseed the viral infection leading a person to become detectable again - usually within a few weeks.