**1. Introduction**

The long-neglected disease called American trypanosomiasis or Chagas disease (CD) was first described in 1909 by the Brazilian doctor Carlos Chagas and it currently affects millions of people throughout the world. Its causative agent is the protozoan parasite *Trypanosoma cruzi* (Kinetoplastidae: Trypanosomatidae) found in more than 150 species of domestic and wild mammals that act as reservoirs [1, 2]. There are several transmission routes to humans such as the inoculation of parasites present in the feces of a hematophagous insect vector of the Triatominae subfamily or consumption of contaminated food with these feces, blood transfusions, organ transplants, and congenital [3]. The infection has a self-limiting acute phase with evident or absent parasitemia and may go unnoticed in many infected individuals. Some patients succumb during the acute phase of the disease, while others develop an adaptive immune response that generally controls the infection. If the parasite cannot be completely eradicated, the infection can last a lifetime and, if left untreated, presents potentially life-threatening complications such as chronic chagasic cardiomyopathy (CCC), which can present itself in its acute form or after a latency period that can extend for decades [4]. The persistence of the parasite in the host for such long periods indicates that it must surpass the host's immune response mechanisms, of which apoptosis is among the most important. Interestingly, *T. cruzi* is capable of inducing or preventing apoptosis of host cells as needed [5]. In this work, we describe the basic aspects of Chagas disease and analyze the role of apoptosis in the infection by this protozoan parasite.
