Biological complexity:how toxoplasmosis parastizes (Introduction)

by David Turell , Friday, November 25, 2016, 01:15 (2921 days ago) @ David Turell

The parasite produces a protein to block antibodies from its host:

http://phys.org/news/2016-11-toxoplasma.html

"The parasite Toxoplasma gondii is a silent success. It infects up to 95% of people in many regions of the world, and most of them never know it, due to the parasite's artful manipulation of its host's immune response. Toxoplasma keeps the immune response low enough so that it can thrive, but high enough so that its human hosts generally live healthy lives and can incubate parasites.

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"'The parasite rewires the host's inflammatory response," says Matthew Bowler, who led the research at EMBL. "It completely subverts the chain reaction that would normally trigger our body's defenses."

"When a cell in your body detects a parasite, it sets off a chain reaction. Inside that cell, a series of molecules activate each other until a protein called p38α is activated and moves into the cell's nucleus. There, it turns on the genes that trigger the inflammatory response. Among other things, the purpose of that response is to eliminate the pathogen. One would expect parasites like Toxoplasma to want to subdue that response, but Mohamed-Ali Hakimi and colleagues at IAB discovered a few years ago that Toxoplasma secretes a protein, GRA24, which does just the opposite: it activates and controls our inflammatory response.

"Bowler and Hakimi discovered that GRA24 bypasses the cell's chain reaction, activating p38α directly, and pulling it into the nucleus to turn on inflammatory response genes. Using a combination of techniques, they found that the Toxoplasma protein attaches itself much more strongly to p38α than the cell's own proteins do. So by producing a protein that binds directly, and very tightly, to p38α, Toxoplasma controls the level of the inflammatory response and sustains it by making it inaccessible to the proteins that would usually turn it off. This is why Toxoplasma isn't considered a serious health threat except for pregnant women and people with compromised immune system."

Life cycle:

http://web.stanford.edu/group/parasites/ParaSites2006/Toxoplasmosis/lifecycle.html

"T. gondii primarily exists in three forms: oocysts, tachyzoites, and bradyzoites. Oocysts are only produced in the definitive host, members of the family Felidae. When passed in feces and then ingested, the oocysts can infect humans and other intermediate hosts. They develop into tachyzoites, which are the rapidly multiplying trophozoite form of T. gondii. They divide rapidly in cells, causing tissue destruction and spreading the infection. Tachyzoites in pregnant women are capable of infecting the fetus. Eventually tachyzoites localize to muscle tissues and the CNS where they convert to tissue cysts, or bradyzoites. This is thought to be a response to the host immune reaction. Ingestion of cysts in contaminated meat is also a source of infection, as bradyzoites transform back into tachyzoites upon entering a new host."

Comment: The primary host is cats where eggs are developed, but the parasite cycles through other animals. Look at the diagram in the Stanford site. Ask yourself how this could have evolved step by step. Toxoplasmosis needs the blocking molecule to survive throughout the lifecycle. Logically it had to have this defensive molecule when it started its lifestyle. Note also the giant molecule it uses seen in the first article given here. How did the parasite develop this molecule before entering its first host and experience the immune system present? It has to be saltation.