Biomod/2011/MIT/Origami/GP120
For Meeting 8/10/11
What we went over at the last meeting was that the relatively low number of envelope spikes with an uneven distribution on the surface of the virion made it harder for antibodies to simultaneously bind two spikes at once, making it harder to neutralize the virion and mount an effective immune response. The question was why were these spikes so unevenly distributed and as I understood it, if it was possible to find where these were ultimately anchored. Previously, I had mentioned that it was something like GP120(Extracellular)----->GP41(transmembrane)------>Cytoplasmic tail of GP41 Now, I found that there is a protein called Tail Interacting Protein 47(TIP47) that interacts with that cytoplasmic tail of GP41 as well. The same TIP47 interacts with the viral matrix, acting as a linker. So the complete connection between them is something more along the lines of: GP120(Extracellular)-------->GP41(Transmembrane)------>GP41 Cytoplasmic Tail------->TIP47 Linker--------->P17 protein composing HIV matrix Overexpression of TIP47 results in an increase in the number of incorporated envelope spikes, while silencing of it results in impaired infectivity through lack of said spikes. link
