When the malaria-causing Plasmodium parasite first slips into the human bloodstream, injected by the bite of an infected mosquito, it does not immediately target red blood cells. Instead, it seeks refuge inside the liver and rapidly reproduces, copying itself as many as 30,000 times in the span of 48 hours.
After building strength in numbers, the parasite leaves the liver and escapes into the blood stream, invading red blood cells and triggering the devastating disease.
After arriving at the liver, Plasmodium forces its way into liver cells, stealing a bit of the cell membrane to form a small pouch inside the cell. This pouch, called a vacuole, provides a safe harbor while the parasite grows and divides, stealing nutrients and proteins from the host cell along the way.
“The liver stage is a checkpoint, a bottleneck, where it goes from a few dozen parasites to many thousands of parasites, which are released from the liver into the blood where it is amplified into hundreds of billions of parasites.”
Researchers show that liver-stage Plasmodium relies on a host protein called aquaporin-3 to survive and copy itself. Inhibiting the function of aquaporin-3 may provide a new way to keep Plasmodium from proliferating and prevent malaria before symptoms start.
Source: https://www.sciencedaily.com/releases/2018/05/180522152117.htm