Several million people in Latin America are estimated to have Chagas disease, although most will not know that they are infected. The disease is caused by the protozoan Tryptanosoma cruzi and is transmitted by the bite of the blood-sucking beetles known as ‘kissing bugs’ because of their tendency to bite close to the mouth. Although the disease typically produces very mild symptoms in the early stages, chronic disease can lead to severe damage to the heart and GI tract and is often fatal. Severe disease and death occur many years after initial infection – even when the parasites are no longer present – and Brazilian scientists speculated that T. cruzi DNA might be retained in the body and that the resulting genomic alterations could explain the rejection of heart tissue by the host immune system. An unusual feature of virulent T. cruzi is that extra-nuclear mitochondrial DNA known as the kinetoplast (kDNA) accounts for 15-30% of the total cellular DNA. The kDNA is made up of thousands of minicircles which can insert into the genome of an infected individual. Depending on where the parasitic DNA is inserted, it can affect genes involved in cell communication, correct function of the immune system and even our sense of smell. The parasitic DNA can also be incorporated into the DNA of sperm and eggs and so can appear in the genome of children who have never themselves been in direct contact with the parasite.
Although it has been known for some time that the human genome contains significant amounts of viral DNA that have evolved with us over millions of years, the new research suggests that the transfer of mitochondrial DNA from T. cruzi to the human population may also be contributing to human genetic diversity. The parasite is especially well placed to fulfil this role since it infects millions of people, many of whom will migrate to other continents, infects many species of wild animals, and rarely kills its human victims below the age of forty.
The study is published in PLoS ONE.