(a) those regulatory T cells are selected that have V regions with complementarity to as many helper T cells as possible, and (b) helper T cells are selected not only on the basis of their V regions having some affinity for MHC class II, but also on the basis of the V regions having some affinity for the selected regulatory T cell V regions. The helper T cells and regulatory T cells that are co-selected are then a mutually stabilizing construct, and for a given mouse genome, more than one such mutually stabilizing set can exist. This resolution of the I-J paradox leads to some testable predictions. However, considering the importance of the (unfound) I-J determinant for the theory, the I-J paradox solution is still subject to strong criticism, e.g.Falsifiability. Relevance for understanding HIV pathogenesis An immune network model for HIV pathogenesis was published in 1994 postulating that HIV-specific T cells are preferentially infected (Hoffmann, 1994, op cit.). The publication of this paper was followed in 2002 with the publication of a paper entitled "HIV preferentially infects HIV specific CD4+ T cells." Under the immune network theory, the main cause for progression to AIDS after HIV infection is not the direct killing of infected T helper cells by the virus. Following an infection with HIV that manages to establish itself, there is a complex interaction between the HIV virus, the T helper cells that it infects, and regulatory T cells. These three quasispecies apply selective pressure on one another and co-evolve in such a way that the viral epitopes eventually come to mimick the V regions of the main population of T regulatory cells. Once this happens, anti-HIV antibodies can bind to and kill most of the host's T regulatory cell population. This results in the dysregulation of the immune system, and eventually to other further anti-self reactions, including against the T helper cell population. At that point, the adaptive immune system is completely compromised and AIDS ensues. Hence in this model, the onset of AIDS is primarily an auto-immune reaction triggered by the cross-reaction of anti-HIV antibodies with T regulatory cells. Once this induced auto-immunity sets in, removing the HIV virus itself (for instance via HAART) would not be sufficient to restore proper immune function. The co-evolution of the quasispecies mentioned above will take a variable time depending on the initial conditions at the time of infection (i.e. the