Studies on the entry of simian 40 (SV40) virus by Pelkmans and coworkers [52–54] have documented that caveolae can actually play a role in nonconstitutive endocytosis. Thus, after binding of SV40 virus to the cell surface via the MHC class I molecule, the virus particles move laterally in the plasma membrane to end up in caveolae. Although these caveolae are initially immobile, the virus initiates a complex signaling cascade leading to a profound disorganization of the cortical actin cytoskeleton and a transient recruitment of the GTP-binding protein dynamin known to be involved in membrane fission (see Section 4.8). Importantly, without SV40-stimulation, less than 10% of the caveolae were associated with dynamin.
These changes, in turn, resulted in a wave of incoming caveolar vesicles containing virus where reorganized actin filaments formed “tails” necessary for internalization of the SV40-containing caveolae [53]. Subsequently, the virus was delivered
to caveosomes (see Section 4.7) and transported further downstream to the endoplasmic reticulum (ER). However, a delay of several hours then occurs before caveolin returns from the caveosomes to the plasma membrane in vesicles now devoid of virus particles [52].
It is interesting to note that antibody-induced crosslinking of MHC class I moleules (the SV40 receptor) results in an accumulation of MHC class I clusters in small uncoated surface invaginations” identical to caveolae, as reported 25 years go by Huet and coworkers. No clusters were found in clathrincoated pits. From he caveolae-like invaginations the clusters were apparently internalized and delivred to lysosomes [55]. It is therefore tempting to speculate that it is the samen derlying mechanism that is responsible for caveolae-mediated uptake of SV40 virus particles after their binding to MHC class I and of MHC class I clusters
enerated by antibody crosslinking.
Source:: lipid raft and C. Fielding, J.C. Jhonwilley and Son
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