Relevance of Intracellular Replication to the Evolution of Chagas Disease

Why does GM1 induce a potent beneficial response to experimental Chagas disease?

“…itself corresponds to an intracellular time of three days, which is consistent with the practice of waiting five days to collect second generation parasites in vitro. N r is not far from the result we previously estimated ͑N r = 13.8͒ for the experiment of El Bouhdidi et al (1994) with BALB/c mice infected with the Tehuantepec strain of T. cruzi (Sibona et al, 2007) and it is consistent with the results ͑N r Ϸ 30͒ of a recent in vitro experiment using the CL strain (Coimbra et al, 2007). We remark that a higher in vitro value of N r is not surprising because of the better feeding of (and weaker constraints on) cells in a monolayer culture.…”

“…Since blood parasites are the infective forms, antibodies become a central part of the host defense against T. cruzi. Our basic model is built upon the following assumptions: These assumptions are embodied in a set of first-order equations that describe the evolution of the various populations (Sibona et al, 2005;Sibona et al, 2007). If N antibody species are present, the equation for the total number of circulating trypomastigotes, n͑t͒, is dn͑t͒ dt…”

“…The parameters ⍀ and N r can be related to the mean amastigote duplication time by considering a Malthusian model for the amastigote replication dynamics (Sibona et al, 2005;Sibona et al, 2007). A simple calculation yields…”

“…The model accurately predicts all possible outcomes of the disease: healing, death, and chronic infection, with stationary or quasi-cyclical populations (Condat et al, 2003). It also reproduces experimental data and permits us to estimate the damage generated by direct parasitic action (Sibona et al, 2007). This model was used to investigate diverse situations of interest, such as the action of parasite-released decoys, the influence of immune reaction delays, and the effects of an increase in the antibody efficiency (Sibona et al, 2005).…”