In response to
> "Teenage males are highly susceptible to infection by a sports car =
virus
> (scv). This virus becomes integrated into the host's genome but is =
latent.=20
> As affluence manifests itself by the accretion of fatty tissue, the =
viral
> genome is activated and causes the expression of brain specific =
cytokines."
I asked my baby brother who understands these things if he could =
translate into English. For those who want to know, the real, simple =
explanation follows. To me, it says that there should be a long term =
market for Morgans!
-----Original Message-----
From: GANN A [SMTP:a.gann@lancaster.ac.uk]
Sent: Wednesday, May 28, 1997 9:58 AM
To: Simon Orebi Gann
Subject:=09
Dear Simon,
Yes, this sounds about right. The model for all such viral infections =
is, of course, bacteriophage lambda, which - as is apparently the case =
with scv - can, on infecting its host, develope as a lysogen =
(integrating its genome (DNA) into that of the host where it it =
expresses (reads the gene for) a repressor which switches off all the =
virus' other genes - but stimulates the expression of its own. Thus =
integrated, the (latent) viral genome is passively replicated (copied) =
as part of that cell's genome when the host cell divides; this produces =
two infected cells. This dormant condition can be maintained for many =
generations until suitable conditions outside the cell tell the virus =
that the more violent, lytic route to replication would be worth a try. =
The signal is received via intracellular signalling pathways I won't =
bore you with, but which exist to keep the (normally uninfected) cell =
informed about extracellular conditions; the virus has simply designed =
its repressor in such a way that it will be inactivated when these =
pathways are activated. This means the virus swithes on all its lytic =
genes, excises its genome from the host cell genome, copies it about a =
hundred times, packages each in viral coat proteins (encoded by the =
recently expressed viral genes) and bursts the cell, releasing all the =
viral particles to infect a hundred new, previously uninfected cells. =
The signal to do this is healthy growth conditions which tend to suggest =
there will be plenty of new, healthy cells to infect. If a new virus =
infects a cell already carrying an integrated virus OF EXACTLY THE SAME =
TYPE, the repressor being made by the reident virus blocks the incoming =
one from doing any damage.
Many mammalian viruses can grow as 'lysogens' in this way, including HIV =
of course. But in this case, the virus can make new viruses that bud =
from the cell without killing it. These mammalian viruses, and =
derivatives of lambda known as defective lambda prophages, can sit in =
the host genome for ever and express genes without excising their =
genomes and killing the cell. And as these viruses can even pick up =
host genes in their own genome as they move from cell to cell, they =
might - once integrated and activated (perhaps years later) - express =
all sorts of new functions within the host cell, changing its character =
for better (by providing useful functions the cell lacked) or worse (by, =
for example, upsetting the cells normal growth control by expressing =
growth activating genes which can lead to cancer). In the case of scv =
this allegedly includes a cytokine that specifically activates cells =
within the brain that convince the organism that driving very fast while =
sitting very close to the ground is a jolly fine thing.
Hope this is of some help.
Alexander
>
>=20
|