Timely HAART initiation may pave the way for a better viral control

In this article we use a computational model and clinical data to identify the role of HAART timing on the residual capability to control HIV rebound after treatment suspension. Analyses of clinical data from three groups of patients initiating HAART respectively before seroconversion (very early), during the acute phase (early) and in the chronic phase (late), evidence differences arising from the very early events of the viral infection.The computational model allows a fine grain assessment of the impact of HAART timing on the disease outcome, from acute to chronic HIV-1 infection. Both patients' data and computer simulations reveal that HAART timing may indeed affect the HIV control capability after treatment discontinuation. In particular, we find a median time to viral rebound that is significantly longer in very early than in late patients.A timing threshold is identified, corresponding to approximately three weeks post-infection, after which the capability to control HIV replication is lost. Conversely, HAART initiation occurring within three weeks from the infection could allow to preserve a significant control capability. This time could be related to the global triggering of uncontrolled immune activation, affecting residual immune competence preservation and HIV reservoir establishment.The question of when antiretroviral therapy has to be initiated remains a challenging issue. Recent studies show that the early immune response to HIV-1 infection is likely to be an important factor in determining the clinical course of disease [1]. The first weeks following HIV-1 transmission are extremely dynamic. They are associated with rapid damage to generative immune cell micro-environments and with immune responses that partially control the virus. Following HIV-1 infection, the virus first replicates locally in the mucosa and then is transported to draining lymph nodes where further amplification occurs. This initial phase of infection, until the systemic viral dis