Although intracellular amastigotes are larger and slightly more elongated than extracellular forms(Barros et al. 1996), they share biochemical and ultrastructural similarities (Andrews et al. 1987, Ley et al. 1988, Villalta and Kierszenbaum 1982) and express similar antigenic stage-specific markers (Andrews et al. 1987, Barros et al. 1997, Pan and McMahon-Pratt 1989, Silva et al. 1998, Verbisck et al. 1998). Studies with strains of T. cruzi I and II, suggest that the expression of the epitopes defined by monoclonal antibodies may vary considerably among intracellular and extracellular amastigotes of the two lineages (Verbisck et al. 1998). Further studies with isolates from chagasic patients tend to confirm this extensive polymorphism (Silva C.V., unpublished observations).
While previous results from the literature have provided conflicting evidence regarding the infectivity of T. cruzi intracellular amastigotes (Carvalho et al. 1981, Ley et al. 1988, Ulisses de Carvalho and De Souza 1986, Umezawa et al. 1985), there are reports that infective extracellular amastigotes resist antibody-independent complement lysis (Iida et al. 1989). We found that intracellular amastigotes (isolated from infected cells) of strains from both T. cruzi I or T. cruzi II groups are highly susceptible to complement lysis and poorly infective to either Vero or HeLa cells, as well as to MDCK cells transfected with Rho GTPases (Barros 1996, Fernandes and Mortara 2004). A plausible explanation for these results is that intracellular amastigotes are committed to growth within a sheltered environment whereas extracellular forms have to cope with a more hostile milieu where they may encounter not only specific antibodies (Andrews 1989) but also complement proteins (Iida et al. 1989). Acquisition of complement resistance and infectivity by extracellular amastigotes is certainly an interesting and as yet poorly understood process that deserves further investigation.
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