virus and cancer
Jeffrey John
I want to thank all of you who took the time to write me in responce to a
previous message.
In this message I would like to discuss the role of herpes viruses and cancer
and would appreciate any comments hypothesises or therioes any of you may
have.The herpes virus I work with is a herpes viru(Lucke Tumor Herpesvirus) that
infects north americam leopard frogs.It was the first cancer to be associated
with a herpes virus and confirmed using Koch postulates.The primary tumor is a
renal tumor, more specifically the tumor seems to arise from epithelial stem
cells of the proximal tubules of the kidney.
I would like any of your in put as to how you think the genome of the herpes
virus plays its role in causing the infected cells to poliferate uncontolablly
and thus become carcinogentic. Could it be the viral genome codes for proteins
or other produts that bind to domains on the host DNA that turn on those genes
that regulate the cell cycle.Or does the viral DNA itself contain with in its
genome oncogenes that cause the host cell to poliferate under the right
circumstances. Possibly a combination of both?
The tumor I work with also can become metastatic and would appeciate any
comments as to how the herpes viral DNA plays a role if any in this. For my
honors thesis I found through PCR that the virus is found in all secondary
metastatic colonies. Electron microscopic research also supports this data.
Thanks For Your Help!
Jeffrey C. John
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Dirk Dittmer
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The DNA genome of small DNA tumor viruses like SV40 encode transforming
proteins for instance large T antigen. Those have (at least) two functions;
1) to transactivate cellular genes including cell cycle regulatory genes
and 2) to bind directly to cell cycle regulatory proteins. I presume your
virus does something similar. There is a slew of literature on that. A good
one is "Fundamental Virology" or "Virology", by Fields and Kipe Raven
Press. I don't know whether the 1995 edition is already out or will be
later this year.
None of the other herpesviruses is truely transforming, except
Epstein-Barr-Virus.
Yours,
Dirk
--
Dirk Dittmer
Stanford University School of Medicine
Deptartment of Microbiology and Immunology
Fairchild Building
Stanford, CA 94305-5402
FAX: USA-415-725-6997
Telephone: USA-415-723-7393
e-mail: dit...@leland.stanford.edu
Ian A. York
>have.The herpes virus I work with is a herpes viru(Lucke Tumor Herpesvirus) that
>infects north americam leopard frogs.It was the first cancer to be associated
>with a herpes virus and confirmed using Koch postulate
Are you sure about this? I had thought that Marek's disease (of chickens)
was the first tumour to be associated with a herpesvirus; and also,
incidentally, the first tumour for which a vaccine is available.
>I would like any of your in put as to how you think the genome of the herpes
>virus plays its role in causing the infected cells to poliferate uncontolablly
>and thus become carcinogentic.
There are several other herpesviruses which are associated with tumours,
and it seems likely that they use different mechanisms of oncogenesis. I
don't think any are very well understood. Epstein-Barr virus, of course,
is the best example in humans. There are quite a few reviews and papers
on this. Herpes simplex virus, particularly type 2, has also been linked
to cancer. The linkage is mostly epidemiological (in that people infected
with HSV2 are more likely to get cervical cancer; the risk ratio is
unspectacular but is moderately convincing, I think. Not all studies find
such an association). HSV2 also can cause transformation of cells in
vitro at low frequency. In this case it seems to use a 'hit-and-run'
mechanism, in that the transformed cells don't maintain any herpes
sequences. Mechanism is unknown. The 'hit-and-run' hypothesis is being
suggested for the putative Kaposi's Sarcoma Herpes Virus as well, in that
despite the recent epidemiological links between KSHV and some forms of
KS, KS cell lines in vitro apparently don't have the KSHV genome
detectable. This is all quite controversial right now, I think.
In sum, different herpes viruses appear to use different mechanisms, and
these mechanisms are poorly understood. I could speculate, but I don't
think there's enough known for these speculations to be more than general
statements of principal.
There are some fairly obvious starting points for your project, I think,
and I assume that at least some have been done or are under way (does the
viral genome stick around? All of it, or just part? And other fairly
classical tricks and approaches.)
--
Ian York (yo...@mbcrr.harvard.edu)
Dana-Farber Cancer Institute, 44 Binney St., Boston MA 02115
Phone (617)-632-3921 Fax (617)-632-2627
C. Roy Keys
My interest in projects such as yours stems from a general desire
to understand the process of development of cancers and to seek
measures to cure and prevent, though I am not a researcher or
scientist. I should like to call your attention to a proposal that
I have circulated on the internet, and to which I have had very
little response as yet. In the proposal, which I will append to
this message, I seek to interest competent researchers in an
investigation of the proposition that cancers are indeed viral in
origin, but that the process of "infection" may be much more
complicated than the introduction of the virus from outside the
organism. In other words, the notion to be investigated is that
pathogenic agents may develop within the organism itself.
I begin with a lengthy quote from the 1946 self-published
monograph by O.C. Gruner, former pathologist to the Royal Victoria
Hospital and research fellow at McGill University in Montreal. The
monograph is entitled An Interpretation of Cancer. I think that Dr.
Gruner's comments are especially germane to the research you are
conducting, and offer a fresh viewpoint on the problem.
Begin Quote:
Stage 3. The Stage of Malignancy
29.--The growth which has formed along the lines indicated is not
necessarily "malignant", whatever its microscopic structure. We
know that "lumps" may occur for a long time in the breast, for
instance, and then start growing. We know that a "villous
growth" in the bladder may remain innocent for a long time, and
then start "infiltrating"; that a warty growth in the larynx
may show no sign of "malignancy" for a long period of time.
This means that malignancy is superadded. How? By the
development of a virus in it. This virus can be formed de novo
in the cancer cells (in which case it would be called a
ferment, or "enzyme") or it may be introduced from
without--presumably from another person (directly or
indirectly, like malaria). In both cases, secondary deposits
begin to appear and we must ascribe this to the presence of the
virus, rather than to cancer cells. (See section 68).
On this view, the cancerous growth is the place where the virus
is incubated. Local lymph-stasis gives the necessary time for
the agent to establish itself. Then, liberated from the cells
into the intercellular fluids, the "germ" enters the lymphatic
roots and finally spread through the body (Handley). Undue
surgical manipulation both before and during an operation
facilitates this liberation of the virus; and furthermore, as
Percy pointed out, as long as surgical technique does not
include adequate post-operative drainage through an open wound,
metastasis formation is inevitable.
The various organisms ("germs") which can be found in cancer
tissues and in the blood and excreta--for the most part
dismissed as unimportant "contaminants" or "concomitants"--are
associated with necrotic changes and putrefactive break-down in
the tumour. To those who recognize pleomorphism, such organisms
are later developments, and there is nothing incongruous in the
fact of their being unable to start cancerous development
either in the same patient or in other persons, or in
exprimental animals. Rappin's "microbe de sortie" is apparently
non-pathogenic simply because the effective phase is
ultra-microscopic or intracellular, especially in the spleen;
it is the virus form which is significant for the spread of
cancer (see 23, iii, and v; 68 and 73).
To repeat, various very definite and clean-cut factors
(nutritional errors, intoxications, past infections), give rise
to flocculations in the intercellular spaces, and the vis
medicatrix naturae accounts for the local tumour growth. If the
conditions are not rectified, virus development supervenes. The
tumour now manifests the well-known characteristics of
malignancy. (Sections 57, 62, 68, 72 justify this view, so
divergent from academic teaching.)
30.--The practical importance of this interpretation of the
cancerous process is easily perceived. First, the public should
be warned of the contributory factors (section 23) so that they
can at least take some precautions. When stage 2 is reached,
the physician in his turn should at once act similarly, for,
despite all the propaganda of the Societies for the Control of
Cancer, surgical and even radiological measures are never
instituted immediately (i.e. the same day) and every hour means
more and more progress of the disease. Secondly, a patient in
the third stage is not only approaching the end of life, but is
a source of dissemination--despite official insistence to the
contrary. The time between "infection" and appearance of a
growth is so long (the best analogy being provided by leprosy)
that few will associate the two.
Yet, on the basis of this thesis, the whole disease would stop
if the specific "pathogen" could be "resolved" (that is, first
made soluble, then completely cleared out through the normal
emunctories). The virus could not survive.
End Quote.
It is further evident from Dr. Gruners remarks that any means that
can prevent the emergence of pathogenic viral forms within the
organism would be an effective defense against cancers, while a
cure would be provided if the virus could be destroyed during the
process of infection. In the former, live blood analysis under
dark field microscopy could be a significant factor, while the
frequency instrument developed by Rife has already been proven an
effective means of destroying cancer-causing viruses, and could
likely also be effective against HIV.
I close with a repeat of the proposal made earlier.
Aims: This is a proposal for parallel lab research to identify
minute particles in the plasma of the blood, which earlier
researchers have associated with the onset of malignancies.
Collaborators are sought in the hope that they may attempt to
reproduce these results.
Prerequisites: The preliminary analysis requires the following
setup: A good quality light microscope with 100 watt halogen
light source, 100x objective with diaphragm, and a Naessens-type or
other substage condenser suitable for high magnification dark
field work, i.e. 1000+ X).
Background:
Beale, in "The Microscope in Medicine" (1878) notes: "If we examine
blood with the highest powers, not only do we meet with extremely
minute corpuscules, but many of these are so transparent that they
could not have been seen at all under lower power." (p. 256).
These particles are the microzymes of Antoine Bechamp (1860s),
the protits of Guenther Enderlein (1925), and the somatids of
Gaston Naessens (1980). Their developmental forms (assuming as
did Bechamp, Enderlein, Gruner, Rife, Naessens and others, that
they are pleomorphic) include the pathogenic microbes that
constitute the viral, bacterial and fungal etiological forms of
cancers. A viral origin of cancers was discussed by Barnard et
al. in the Lancet (July 18, 1925, as reported in Scientific
American, October 1925). Rife and collaborators published some
of their findings in Science and in the journal of California
and Western Medicine, with reports in the Franklin Institute
and Smithsonian magazines. Gruner in CMAJ and a series of
monographs. Enderlein in articles in German scientific journals
during and after the first world war and in a book which
appeared in 1925. The first chapters of Bechamp's book "The
Third Element of the Blood" can be obtained from the Sumeria
WWW site.
Procedure:
Blood samples can be obtained readily by pricking the meaty
portion of the right middle digit (after swabbing with alcohol) and
touching gently to a slide. Do not contact the finger, only the
bead of blood. Apply coverslip to slide and place under
microscope. No further preparation need be made. Blood of
subjects suffering malignancies especially will show a variety of
phenomena, including spores, double spores, bacteria, asci,
yeast and fungus, as well as inclusions in red cells and
sometimes in white cells, as well as budding of bacteria from
red cells. In healthy subjects, the plasma should show large
quantities of motile particles of 0.02 micron diameter, the
microzymas.
Reporting:
Research results can be shared via this thread.
Please indicate your interest in participating in this
collaboration.
Thank you.
--
C. Roy Keys INTERNET: CRK...@APEIRON.CAM.ORG
4405 St. Dominique
Montreal, Quebec
H2W 2B2 Canada
VOX/FAX: 514-842-3667
g1687...@umbsky.cc.umb.edu
john...@GOLD.TC.UMN.EDU ("Jeffrey John") writes:
>....The herpes virus I work with is a herpes viru(Lucke Tumor Herpesvirus) that
>infects north americam leopard frogs.It was the first cancer to be associated
>with a herpes virus and confirmed using Koch postulates.The primary tumor is a
>renal tumor, more specifically the tumor seems to arise from epithelial stem
>cells of the proximal tubules of the kidney.
Any relation to Herpes ateles or H. saimiri? These are extremely fast
acting lymphoma viruses which are harmless in their natural hosts (monkey
species) but quickly kill other monkey species, and rabbits. Fortunately
they are harmless in humans since they were discovered in a monkey house
outbreak similar to, but prior to, Ebola reston.