I wonder if you can help me or point me to the right place...
I've been given a task to produce an animation showing obligate chain
termination by a drug on the target DNA of a herpes virus.
I need to show the virus infecting a cell, inserting its DNA, and then
ACV (Acyclovir?) entering the cell, going through viral thymidine kinase
interacting with cellular enzymes and then inserting itself into the
viral DNA and performing an "obligate chain termination"...
This excerpt from the "Expert Opinion in Herpes", (Issue 2 ISSN0969-7659)
was offered by my client but contains far too little information to be
able to reconstruct an animation. All of the illustrations are very
diagrammatical and abstract, and I would like to create something that
is informative, and at least a bit more realistic!
Sounds like a pretty tall order on a Pentium 90... but armed with a little
more knowledge, I think I can do it using my range of software.
All I need is some idea of the scale of a typical cell, (its structure,
texture etc) and the scale and structure of a herpes virus / human DNA
and other cell structures and some idea of what the DNA looks like
macroscopically, so I can zoom in and animate the reactions. (I have
a 12-base DNA fragment from PDB, but that's going into a little too much
detail - I'm not intending to render a genome fly-by yet!).
"Herpesvirus-HIV interactions
~~~~~~~~~~~~~~~~~~~~~~~~~~~~
The possible co-factor roles of herpesviruses in HIV pathogenesis
remain topical, especially with respect to the apparent effects of
acyclovir in delaying death from AIDS. At the 18th International
Herpesvius Workshop, all the data in this area involved in vitro systems.
It should be remembered that in vitro systems do not necessarily
mimic the in vivo studies. Hence, clinical strains of CMV were shown
to enhance macrophage trophic HIV-strain production in co-infected
macrophages between 3- to 40-fold. This effect segregated with human
CMV virions. However, a separate report showed that human CMV was able
to repress HIV replication. Two presentations demonstrated genetic
elements in the HHV-6 genome that up-regulate HIV transcription. First
Dr Z Yi, University of Miami School of Medicine, USA reported that ORF-A
transactivates the HIV LTR through the NF-kB sites. Dr J Rosenthal,
George Town University, Washington DC, USA reported that the 283 amino
acid ORF-1 gene transactivates both the HIV LTR and the interleukin-2
receptor promoter. Interestingly, the ORF-1 product was able to
reactivate a tat-defective HIV-1 pro-virus from latently infected
cervical cells in vitro.
Since HHV-7 uses the CD4 receptor for entry into cells, the possibility
of a negative co-factor role for HHV-7 was explored by Dr Paolo Lusso,
National Cancer Institute, Bethesda, MD, USA at the HHV-6/HHV-7 satellite
workshop. Pre-treatment of CD4+ T-cells with HHV-7 for 48 hours led to
a reduction in HIV-1 infection, presumably via the down-regulation of
cell surface CD4. In contrast to the other herpesviruses, transactivation
of HIV by HHV-7 has not been detected."
(very simple graphic of extracellular HHV-7 and HIV competing for the
CD4 receptor sticking out from the cross-sectional surface of a cell.)
(One day I'd love to animate DNA from first principles of atomic and
molecular interaction, put them all together and watch it happen!
I've experimented with 80 or so atoms attracting and repelling each
other to form structures and raytracing the results - very pretty, as
they wobble around and break up when hit by stray atoms, but lacks
realism owing to not knowing the actual forces and how they change
with various bondings etc.)
I have less than a week to come up with some previews.
Cheers
Andy.
--
+---------------------------------------------------------------------------+
| Haveland-Robinson Associates | Email: andy at osea.demon.co.uk |
| 17 Williams Way, Pondtail, Fleet, | ahaveland at cix.compulink.co.uk |
| Hampshire, GU13 9EU, England. | Tel. 0252-811670 Fax 811714 |
+---------------------------------------------------------------------------+
>>> Some dream of doing great things, while others stay awake and do them <<<
