The formation of persistent, load-bearing attachments to dynamic microtubule tips is fundamental to all kinetochore activities.
Changes in the model parameter values of N, ρ and GP within the admissible range (i.e. leading to the eventual clearance of pathogens by the host or low persistent pathogen load) alters the time scales of the response curves without affecting the overall shape characteristics of the pathogen load and immune response curves.
This would effectively counter the repetitive homeostatic attenuation of the immune response that arises from chronic persistent antigen load and stimulation.
For instance, Thewlis et al. [ 6] observed persistent asymmetric load distribution in TKA patients 6 months after surgery and Levinger et al. [ 2] described proprioceptive deficits that remained for at least 12 months following TKA surgery.
Virological failure was defined as a persistent viral load above 5000 RNA copies/mL on two consecutive measurements, after at least 24 weeks on HAART, in a treatment-adherent child.
It has been suggested that persistent antigen load secondary to chronic infection and high viral replication rate lead to excessive formation of immunocomplexes, and these circulating immunocomplexes deposited in intermediate and small-sized vessels initiate vasculitic processes [ 28, 29].
The 4 children with persistent detectable viral load had no evidence of clinical or immunologic failure, and no children in group B were switched to a second line regimen due to treatment failure during the study period.
We hypothesised that, in contrast to active TB, latently infected individuals would display an immunological signature consistent with persistent low antigen load and long-term immune control, i.e. one dominated by dual IFN-γ/IL-2 secreting effector-memory T cells accompanied by IL-2-secreting central memory T cells.
Virologic failure is defined as a persistent HIV viral load of ≥ 5,000 copies/ml, after at least 24 weeks on ART, in a treatment-adherent child [ 19].
Nevertheless, the success of the treatment is closely related to the continuous use of drugs in order to assure persistent plasma viral load (VL) suppression [ 7, 8].
Our work suggests that under a chronic persistent tumor antigen load, as exists for a late-stage surgically nonresectable cancer patient, the IL2 feedback loop described by McNally et al 12 continuously oscillates between a state of activation and suppression.
