Cellular Invasion: Pathogen DNA Takes Up Residence in Cells
I’ve been doing a lot of work lately knocking out cells that have been internally infected with pathogens. They cause chronic problems and never function right. Terminating them with electronic frequencies is the only way to get rid of some persistent problems.
The authors of a current paper found parasite DNA embedded in host cells. A letter to the editor noted that this problem is probably found in many disease entities. It is interesting to see tentative findings in my home laboratory confirmed in academic research centers.
Letter to the Editor:
Re: “Chagas parasite invades genome”: I think the authors of this paper have been rather modest and have underplayed the importance of their finding that “Typanosomacruzi kinetoplast DNA [is] found in the genomes of infected patients and animals.” It could be because their laboratory is dedicated to work on Chagas Disease, and they did not want to give an impression of straying away from it.
The finding has immediate relevance to many other obligate or facultative intracellular pathogens of humans and animals:
– Mycobacterium tuberculosis (Tuberculosis)
– Mycobacterium leprae (Leprosy)
– Listeria monocytogenes (Listeriosis)
– Salmonella typhi (Typhoid Fever)
– Shigella dysenteriae (Bacillary dysentery)
– Yersinia pestis (Plague)
– Brucella species (Brucellosis)
– Legionella pneumophila (Pneumonia)
– Rickettsiae (Typhus; Rocky Mountain Spotted Fever)
– Chlamydia (Chlamydia; Trachoma)
In my opinion, the top two items in the above list are of great importance, and it might be worthwhile for researchers to carry out studies similar to those of Nitz et al. on the possibility of the DNA of the pathogen “invading” the host genome.
T.S. Raman, retired biochemist
New Delhi, India
Chagas parasite invades genome: Typanosoma cruzi kinetoplast DNA found in the genomes of infected patients and animals
By David Secko, New Scientist, 23 Jul 2004
How infection with Typanosomacruzi—an intracellular parasite that can hide out in the cells of the body—results in the development of chronic Chagas disease has been a mystery. Now a study in the July 23 Cell reports the integration of T.cruzi DNA into the genomes of infected patients, as well as chicken and rabbit animal models, suggesting that horizontal gene transfer may play a role in T.cruzi host–parasite interactions.
T. Cruzi infects some 16 to 18 million people in Latin America, and one third of these infections are estimated to result in chronic Chagas disease, which may not manifest itself until decades after an initial infection. A “major controversy” in the area of chronic Chagas disease research has been whether the presence of the parasite or an autoimmune reaction is its potential cause, said David Campbell, from the University of California, Los Angeles, who was not involved in the Cell study.