This new study suggests that the window of opportunity for intervention in new HIV infection may be day and not weeks after transmission.
The study, published in The Journal of Virology shows that the virus starts to damage the immune system in the first four weeks after infection - establishing a pool of infected CD4 cells far earlier than the three to four weeks originally thought.
The conclusion comes from the study of 30 people who were newly-infected with HIV-1. Plasma from these individuals was sampled every three days for several months - before, during, and after the "ramp-up" phase of infection, when HIV-1 is multiplying rapidly and heading toward its peak viral load. In measuring the levels of four products of CD4 T cell death during this period in these samples, they were able to track and establish a timetable of the virus's destructive path.
The four byproducts of CD4 T cell death include TRAIL (tumor necrosis factor-related apoptosis-inducing ligand), Fas ligand, TNF receptor type 2 and plasma microparticles, tiny bits of cell membrane that are broken up and left floating around in the plasma when the cell dies and breaks apart.
The researchers found that TRAIL levels increased significantly a full week (7.2. days) before peak viral load, which is approximately 17 days after HIV-1 transmission, suggesting that during the earliest period of infection, called the eclipse phase, TRAIL may actually initiate or hasten HIV-1's destruction of CD4 T cells. In contrast, they found that the levels of the other three cell death products were most significantly elevated during peak viral load.
This suggests that any vaccine developed against HIV will have to establish as much immunity as possible before infection and then be followed by a booster than provoked a secondary, broad-based antibody response.
