Of Coats and Pockets

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Science  24 Jun 2005:
Vol. 308, Issue 5730, pp. 1843
DOI: 10.1126/science.308.5730.1843c

The protozoan parasite Trypanosoma brucei is responsible for African sleeping sickness. One of the interesting features of its biology is that while multiplying in the bloodstream, the parasite evades immune detection and clearance by expressing on its cell surface a dense coat of variant surface glycoprotein (VSG); this coat is doffed periodically (internalized via the flagellar pocket) and replaced with an antigenically distinct version of VSG.

Sheader et al. examined how trypanosomes respond when the turnover of VSG is blocked by RNA interference. In vitro, trypanosomes deficient for VSG synthesis stalled before the cytokinesis stage of the cell cycle, when the two daughter cells normally would separate. In vivo, arrested trypanosomes were rapidly cleared from the bloodstream of infected mice, even though the total amount of surface VSG had not decreased. It appears that the ongoing manufacture of VSG is monitored by the parasite to maintain a dense surface coat. However, at least in these experiments, the RNAi-treated parasites appeared to be trapped in a slightly compromised coat that can be targeted successfully by the host immune system. — SMH

Proc. Natl. Acad. Sci. U.S.A. 102, 8716 (2005).

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