Autor: |
Ploemen IH; Department of Medical Microbiology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands., Croes HJ, van Gemert GJ, Wijers-Rouw M, Hermsen CC, Sauerwein RW |
Jazyk: |
angličtina |
Zdroj: |
PloS one [PLoS One] 2012; Vol. 7 (12), pp. e50772. Date of Electronic Publication: 2012 Dec 05. |
DOI: |
10.1371/journal.pone.0050772 |
Abstrakt: |
The proteins P52 and P36 are expressed in the sporozoite stage of the murine malaria parasite Plasmodium berghei. Δp52&p36 sporozoites lacking expression of both proteins are severely compromised in their capability to develop into liver stage parasites and abort development soon after invasion; presumably due to the absence of a parasitophorous vacuole membrane (PVM). However, a small proportion of P. berghei Δp52&p36 parasites is capable to fully mature in hepatocytes causing breakthrough blood stage infections. We have studied the maturation of replicating Δp52&p36 parasites in cultured Huh-7 hepatocytes. Approximately 50% of Δp52&p36 parasites developed inside the nucleus of the hepatocyte but did not complete maturation and failed to produce merosomes. In contrast cytosolic Δp52&p36 parasites were able to fully mature and produced infectious merozoites. These Δp52&p36 parasites developed into mature schizonts in the absence of an apparent parasitophorous vacuole membrane as shown by immunofluorescence and electron microscopy. Merozoites derived from these maturing Δp52&p36 liver stages were infectious for C57BL/6 mice. |
Databáze: |
MEDLINE |
Externí odkaz: |
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