Hi everyone,
Having seen the thread initiated by Leonard regarding viral
attachment I thought I might try and extend it by enquiring about viral
fusion and entry following attachment. The story so far is that the virus
possesses the same charge as the cell, so polybrene or DEAE dextran is
added to the medium to reduce the repulsion between the two. Following
this, the virus slowly finds its way to the cell by diffusion and binds to
it. SOme of the bound viruses are not bound in a specific manner and come
off the cell and drift away to find another cell. Others are bound to a
particular receptor via the surface protein on the virus surface.
Now for the second part. Upon reading the literature, I am
led to believe that extent of viral binding does not correlate very well
with transfection efficiency. If that is the case, then why is this so?
Is it because viral fusion and entry does not occur each time a virus
binds
to the cell even though the binding is specific? Or is there a mistake in
presuming that a majority of bound viruses are bound to the cell via the
receptor?
I came across the theory in a book by Dimmock and Primrose that
some of the viral surface proteins are more effective at inducing
binding and subsequent entry than others even though for all intents and
purposes they appear the same! I am not sure if they were the first (I
doubt it) to propose this theory, but does the theory hold water? At first
glance it does seem to explain why you could have bound virus and still no
transfection. Does a similar situation exist with non-enveloped viruses
too? i.e. virus binds to the cell but does nothing more than that?
Finally, are there any thoughts about what is so special about
these receptors?
Rajesh
Rajesh Krishnamurthy E-mail: krishnam at mit.edu
Department of Chemistry : krishnam at gulag.mit.edu
MIT (617)253-7660
Cambridge, MA 02139
