In article <33E76C67.7F6 at hkstar.com>, Chui Yiu Loon <chuiyl at hkstar.com> wrote:
>direct cell-cell contact. How successful is that strategy will in the
>end have to hang on to how sensitive is the host cell in detecting
>abnormality inside itself. Therefore, the crucial question remains: how
>does a cell start to know it has got an infection?
This is one of the reasons I'm dubious about the "danger" hypothesis.
Although there are certainly some viruses which lead cells to produce
'danger' signals, it's not clear to me that all do. Perhaps more
significantly, if the 'danger' signals were more important than the
'non-self' signals, then you'd predict that viruses (in their quest to
evade teh immune system) would put more emphasis on blocking 'danger'
signals than on blocking 'non-self' signals. While some viruses do block
cytokines (particularly acute viruses, such as many of the pox viruses)
the classic chronic viruses (herpesviruses, and to some extent
adenoviruses) have massive armament directed against the MHC class I
antigen processing pathway--i.e. they target the non-self pathway, rather
than the danger system.
Note that herpes simplex virus, for example, almost totally blocks the
induction of cytotoxic T lymphocytes in humans, and this effect is
probably due to its blockade of MHC class I, rather than any effect on
cytokines.
To me this suggests that non-self is a more important signal than danger.
I recognize that it's suggestive rather than definitive, though.
Ian
--
Ian York (iayork at panix.com) <http://www.panix.com/~iayork/>
"-but as he was a York, I am rather inclined to suppose him a
very respectable Man." -Jane Austen, The History of England
