Among the pathogens that have developed a variety of strategies to
overcome the host immune system, is the causative agent of Chagas disease,
Trypanosoma cruzi. During a long co-evolution process, the parasite has learned how
to live in many different environments, including vertebrate and invertebrate hosts. The
parasite has also evolved many invasive strategies, including several different ways to
enter the host and also the capacity to target different host tissues. An acute systemic
response arises in the host after the rapid parasite colonization, interfering with both
innate and adaptive immunity. The capacity of T. cruzi to interfere with humoral and
cellular immune responses is demonstrated by the expression of different sets of
molecules called virulence factors. Among them, the role of antioxidant enzymes,
cruzipain, the Tc85/transialidase superfamily, mucins, MASPs, GPI anchors,
complement regulatory proteins and others are discussed in this chapter. The
expression of parasite-specific virulence factors allows T. cruzi to overcome host
immunity successfully and also to invade and disseminate in many different
mammalian hosts. However, the picture that has emerged suggests that the basis and
mechanisms of parasite virulence could be more complex than expected. Different
aspects such as parasite genetic diversity, the effects of polyparasitism and the potential
effects that vertebrate and invertebrate hosts have on parasite virulence and the
outcome of natural or experimental infection by T. cruzi should be taken into account
in futures studies to understand T. cruzi virulence.
Keywords: Complement regulatory proteins, CRP, GPI anchor, Immune evasion,
MASPs, Mucins, Siglec, Small mucin-like gene, Tc85, Trans-sialidase.
