Symbiont Conversion Theory

Abstract

Symbiont Conversion Theory is a new scientific theory, summarizing and generalizing efforts that have been made by various researchers in the past years; it could even be perceived as a new scientific paradigm. This theory states that microorganisms and cells which are commonly considered to display parasitic behaviour can be "educated" and transformed into symbionts. This is not just a hypothesis but a theory since there is already evidence that proves that this is possible. The primary motivation for developing this theory is the failure of classical approaches to therapy of cancer and infectious diseases that follow the paradigm "destroy and kill". It is common knowledge about medical doctors that chemotherapy and radiation therapy have detrimental side effects on healthy, functional tissue, and also that antibiotics can harm benevolent cells. These negative side effects can possibly be avoided by the new approach of treating parasitic diseases by converting the culprits into symbionts of which the human organism profits. Another motivation for developing this theory is that some researchers have suggested bacteria and other microbes have certain innate rights themselves [Cockell]. Motivation and Goals Symbiont Conversion Theory is the statement that parasites can be converted into symbionts, and it explains by a couple of examples how this can be done. There is both a practical and an ethical motivation for the development of this theory. Some may dismiss the ethical dimension as being unimportant; after all, who empathizes with microorganisms, except perhaps some crazy people? However, even if you dismiss the ethical component, Symbiont Conversion Theory has a practical value: it is just too well-known a matter of fact that chemotherapy, radiation therapy and antibiotics can have harmful side-effects which are better to be avoided. The long-term goal is to create organisms, most of all humanoid organisms, that have an improved immune system. Instead of destroying and killing intruders, the immune system of this post-human species should educate the parasites and convert them into symbionts. This, of course, is only a long-term goal. It requires synthetic biology to reach a level that allows to create artificial immune systems. It also requires artificial life and computational systems biology to be far more developed than now, so that synthetic organisms can be simulated on a computer before the modifications are actually implemented, to avoid mistakes. This may sound more like fiction than science, but it actually is science. Moreover, this is only the long-term goal. The short-term goal is to make new treatments of cancer and infectious diseases possible by means of signalling cascades triggered by hormones and by modification of microorganisms using synthetically engineered bacteriophages that do not kill bacteria but rather alter their behaviour.

Full text

Biomed Sci Clin Res, 2025 Volume 4| Issue 1 | 1
Symbiont Conversion Theory
Short Article
Claus D. Volko*
*Corresponding Author
Claus D. Volko, Austria.
Submitted: 2025, Feb 03; Accepted: 2025, Feb 28; Published: 2025, Mar 05
Citation: Volko, C. D. (2025). Symbiont Conversion Theory. Biomed Sci Clin Res, 4(1), 01-03.
Abstract
Symbiont Conversion Theory is a new scientic theory, summarizing and generalizing eorts that have been made by various
researchers in the past years; it could even be perceived as a new scientic paradigm. This theory states that microorganisms
and cells which are commonly considered to display parasitic behaviour can be "educated" and transformed into symbionts. This
is not just a hypothesis but a theory since there is already evidence that proves that this is possible. The primary motivation for
developing this theory is the failure of classical approaches to therapy of cancer and infectious diseases that follow the paradigm
"destroy and kill". It is common knowledge about medical doctors that chemotherapy and radiation therapy have detrimental side
eects on healthy, functional tissue, and also that antibiotics can harm benevolent cells. These negative side eects can possibly be
avoided by the new approach of treating parasitic diseases by converting the culprits into symbionts of which the human organism
prots. Another motivation for developing this theory is that some researchers have suggested bacteria and other microbes have
certain innate rights themselves [1].
Austria
1. Motivation and Goals
Symbiont Conversion Theory is the statement that parasites
can be converted into symbionts, and it explains by a couple of
examples how this can be done. There is both a practical and an
ethical motivation for the development of this theory. Some may
dismiss the ethical dimension as being unimportant; after all, who
empathizes with microorganisms, except perhaps some crazy
people.
However, even if you dismiss the ethical component, Symbiont
Conversion Theory has a practical value: it is just too well-known a
matter of fact that chemotherapy, radiation therapy and antibiotics
can have harmful side-eects which are better to be avoided.
The long-term goal is to create organisms, most of all humanoid
organisms, that have an improved immune system. Instead of
destroying and killing intruders, the immune system of this post-
human species should educate the parasites and convert them into
symbionts. This, of course, is only a long- term goal. It requires
synthetic biology to reach a level that allows to create articial
immune systems. It also requires articial life and computational
systems biology to be far more developed than now, so that
synthetic organisms can be simulated on a computer before the
modications are actually implemented, to avoid mistakes. This
may sound more like ction than science, but it actually is science.
Moreover, this is only the long-term goal. The short-term goal is
to make new treatments of cancer and infectious diseases possible
by means of signalling cascades triggered by hormones and by
modication of microorganisms using synthetically engineered
bacteriophages that do not kill bacteria but rather alter their
behaviour.
2. Microorganisms Acting as Pathogens
In the 19th century Robert Koch made the discovery that certain
diseases are caused by infection with microorganisms. Since then,
it has become common knowledge that infectious diseases may
be caused by bacteria or other types of microorganisms, such as
protozoa or fungi.
While symbionts are microorganisms that live in us and from
which we prot, parasites harm us while taking advantage of
our organisms. Bacteria are known to be both parasites and
symbionts, for instance in the intestinal ora there are bacteria that
act as symbionts, while pathogens that cause diseases are to be
considered parasites.
The harmful thing about bacteria is primarily their toxins, which
are chemical compounds synthesized and secreted by them that
interfere with the metabolism of the host organism and thus aect
it in a negative way. However, one must not forget either that the
actual symptoms of bacterial infections are most of all caused by
the way the immune system reacts to them, i.e. by inammation.
We notice pain, see the doctor, and the doctor makes the diagnosis
pharyngitis, laryngitis, pneumonia etc. Then the doctor concludes
that the cause of the inammation is the bacteria and he or she
Biomedical Science and Clinical Research
ISSN: 2835-7914

Biomed Sci Clin Res, 2025 Volume 4| Issue 1 | 2
is most likely to prescribe antibiotics to destroy and kill these
invaders. From a strictly scientic point of view, it is of course
not true to say that the direct cause of the inammation is bacterial
infection; it is just an indirect cause. The actual "culprit", so to
speak, is the human immune system.
We must, however, not make the mistake to believe that the
immune system were a bad thing and that the patient would
prot from disabling the immune system entirely. It is easy to
observe in immune- deciency syndroms such as AIDS what
negative eects on health a heavily suppressed immune system
may have. The actual problem is not the immune system per se
but inammation. Many doctors prescribe cortisone to suppress
inammation and treat some infectious diseases this way, partly
in addition to antibiotics. However, cortisone is a bad thing since
it not only suppresses inammation but also the immune system
as such. What would be more desirable would be suppression of
inammation while sustaining the other mechanisms of immunity
such as phagocytosis and antigen-antibody reactions. According
to my late mentor Uwe Rohr, this can be achieved by means of the
so-called adiols (androstenediol and androstanediol). The adiols
are steroidal hormones just like cortisone. Uwe Rohr proposed
that giving the patient high doses of soy isoavones would lead
to a conversion of other steroidal hormones into adiols and thus
inammation would be suppressed while at the same time the
other functions of the immune system would not be hampered but,
on the contrary, would be boosted [2].
While being a loyal disciple of Uwe Rohr, I would like to go even
beyond that. It is not desirable from an ethical point of view that
the immune system destroys and kills bacteria and other cells that
have a detrimental eect on the host organism. After all, these
pathogens are living things as well, so they should also have a
right to life. That is why I propose a mechanism to "educate" and
convert pathogens to cells that are benecial for the host organism.
3. Cancer
What applies to microorganisms goes for cancer as well, at least to
some extent. Cancer is a potentially deadly disease caused by cells
of the host organism that have undergone mutation and behave
in a manner that harms the host organism. Why should it not be
possible to convert these cancer cells back into normal, functional
tissue?
Uwe Rohr has in particular dealt with cancer. He shared Rudolf
Virchow's view that cancer cells are basically cells that "have lost
the ability to convert themselves into functional epithelial tissue".
He proposed a method to resolve this, for which he adopted the
term "Modify and Repair", which had originally been coined by
researchers from Harvard Medical School and MIT in context of
repair of blood capillaries in a malignant tumor [3]. In Uwe Rohr's
opinion, this process could be undergone by application of steroid
hormones that have previously been blocked. Isoavones such as
daidzein, which share biochemical similarities with a particular
group of steroidal hormones known as adiols, modulate stem cells
in plants where they have been derived from, such as soy and red
clover, and this eect can apparently be obtained in the human
organism as well [4]. In pregnancy, adiol and 2- methoxy-estradiol
stabilize membranes and convert stem cells into dierentiated
functional cells [5-7]. This, according to Uwe Rohr, could be used
to treat cancer în humans eectively without aiming to destroy or
kill the malignant cells.
4. Reprogramming of B Cell Leukemia Cells
A paper that takes the same line as Uwe Rohr has recently been
published by James Scott McClellan and his team [8]. It states that
BCR-ABL1+ precursor B-cell acute lymphoblastic leukemia is
"characterized by a block in dierentiation due in part to the somatic
loss of transcription factors required for B-cell development" and
that the authors "hypothesized that overcoming this dierentiation
block by forcing cells to reprogram to the myeloid lineage would
reduce the leukemogenicity of these cells". This could be achieved
"by exposure to myeloid dierentiation- promoting cytokines in
vitro or by transient expression of the myeloid transcription factor
C/EBP alpha or PU.1". According to the authors, "[t]he resultant
cells were clonally related to the primary leukemic blasts but
resembled normal macrophages in appearance, immunophenotype,
gene expression, and function".
The paper also refers to a publication by Nowak which gives an
overview of several other hypotheses regarding the possibility to
treat leukemia by stimulating the dierentiation of the malignant
cells [Nowak], but it also states that "[t]o date, [...] dierentiation
therapy has only been used routinely in a subtype of acute myeloid
leukemia, namely, acute promyelocytic leukemia (APL)".
Furthermore, the authors refer to work by Graf and coworkers, which
"has demonstrated that immature B cells can be reprogrammed to
apparently normal macrophages although enforced expression of
C/EBP alpha" and has "also demonstrated that a human B-ALL cell
line can be induced to reprogram into macrophages" [9]. In contrast
to these older publications, McClellan and his co-authors "report
here the rst example to our knowledge of myeloid reprogramming
of primary human BCR- ABL1+ B-ALL cells occurring in samples
from multiple dierent patients" and "demonstrate that myeloid
reprogramming can be accomplished through the action of soluble
cytokines without genetic manipulation of leukemic cells".
However, there is still an unsolved problem: "Even after a second
round of sorting and culturing B- ALL blasts in reprogramming
conditions, a population of residual blasts remains." The authors
"speculate that our culture methods are not yet optimized for
maximal reprogramming".
Another recent publication on the reprogramming of cancer cells
has been authored by Akihiro Fujikawa [10]. This paper states
that targeting a receptor-type protein tyrosine phosphatase called
PTPRZ "inhibits stem cell-like properties and tumorigenicity in
glioblastoma cells".
Moreover, an Israeli group around Anna Shteinfer-Kuzmine has
published a paper that deals with selective induction of apoptosis

Biomed Sci Clin Res, 2025 Volume 4| Issue 1 | 3
in cancer cells [11]. Although apoptosis is generally considered to
be a form of cell death, according to Uwe Rohr the same processes
that initiate apoptosis may also lead to dierentiation of stem cells
into functional tissue.
5. Reprogramming Bacteria
In a recent study by Liao et al., it was found that adding an acetyl
tag to the histone HU modied both "the thermal stability and DNA
binding kinetics of HU" [12]. "Accordingly, this modication likely
destabilizes the chromosome structure and regulates bacterial
gene transcription. This work indicates that acetyllysine plays an
important role in bacterial epigenetics." In their conclusions, the
authors point out that "[i]ntroducing two mutations into E. coli
HU alpha converts a commensal strain into an invasive form, so
it is likely that post-translational modication of HU may exert
similar eect" [13]. Moreover, "[s]uch molecules may modulate
the transcription- activation prole of pathogen and eliminate
the virulence without killing the bacteria, thereby preventing the
emergence of drug resistance" [14,15].
6. Summary and Conclusions
This paper marks only the beginning of the new scientic
paradigm of Symbiont Conversion Theory. In this paper, several
publications have been cited which demonstrate that it is possible
to "transform", "convert" or "reprogram" malignant cells as well
as intruders (i.e., bacteria) into dierentiated, functional cells that
actually have a benecial eect for the host organism. Thus, it has
been shown that parasites can be "educated" to become symbionts.
This makes Symbiont Conversion Theory not just a hypothesis,
but a theory. My own contribution is that I have generalized several
novel attempts at treating various forms of disease and pointed out
what they have in common, i. e. that their mechanism is to convert
parasites into symbionts.
A nal note: Originally I wanted to call Symbiont Conversion
Theory simply Symbiosis Theory. But then I realized that there is
another theory, namely Serial Endosymbiotic Theory, coined by
Lynn Margulis, which would also deserve to be called Symbiosis
Theory. I therefore propose that the term Symbiosis Theory should
be used as an umbrella term for the two of these theories.
References
1. Cockell, C. S. (2011). Microbial rights?. EMBO reports,
12(3), 181-181.
2. Dickey, S. W., Cheung, G. Y., & Otto, M. (2017). Dierent
drugs for bad bugs: antivirulence strategies in the age of
antibiotic resistance. Nature Reviews Drug Discovery, 16(7),
457-471.
3. Fujikawa, A., Sugawara, H., Tanaka, T., Matsumoto, M.,
Kuboyama, K., Suzuki, R., ... & Noda, M. (2017). Targeting
PTPRZ inhibits stem cell-like properties and tumorigenicity
in glioblastoma cells. Scientic reports, 7(1), 5609.
4. Jain, R. K. (2008). Taming vessels to treat cancer. Scientic
American, 298(1), 56-63.
5. Kobayashi, S., Sugiura, H., Ando, Y., Shiraki, N., Yanagi, T.,
Yamashita, H., & Toyama, T. (2012). Reproductive history
and breast cancer risk. Breast cancer, 19, 302-308.
6. Koli, P., Sudan, S., Fitzgerald, D., Adhya, S., & Kar, S.
(2011). Conversion of commensal Escherichia coli K-12 to an
invasive form via expression of a mutant histone-like protein.
MBio, 2(5), 10-1128.
7. Liao, J. H., Tsai, C. H., Patel, S. G., Yang, J. T., Tu, I. F., Lo
Cicero, M., ... & Wu, S. H. (2017). Acetylome of Acinetobacter
baumannii SK17 reveals a highly-conserved modication of
histone-like protein HU. Frontiers in molecular biosciences,
4, 77.
8. McClellan, J. S., Dove, C., Gentles, A. J., Ryan, C. E.,
& Majeti, R. (2015). Reprogramming of primary human
Philadelphia chromosome-positive B cell acute lymphoblastic
leukemia cells into nonleukemic macrophages. Proceedings
of the National Academy of Sciences, 112(13), 4074-4079.
9. Nowak, D., Stewart, D., & Koeer, H. P. (2009). Dierentiation
therapy of leukemia: 3 decades of development. Blood, The
Journal of the American Society of Hematology, 113(16),
3655-3665.
10. Rapino, F., Robles, E. F., Richter-Larrea, J. A., Kallin, E.
M., Martinez-Climent, J. A., & Graf, T. (2013). C/EBPα
induces highly ecient macrophage transdierentiation
of B lymphoma and leukemia cell lines and impairs their
tumorigenicity. Cell reports, 3(4), 1153-1163.
11. Rohr, U. D., Gocan, A. G., Bachg, D., & Schindler, A. E.
(2010). Cancer protection of soy resembles cancer protection
during pregnancy. Hormone Molecular Biology and Clinical
Investigation, 3(2), 391-409.
12. Schilling, T., Ebert, R., Raaijmakers, N., Schütze, N., & Jakob,
F. (2014). Eects of phytoestrogens and other plant-derived
compounds on mesenchymal stem cells, bone maintenance
and regeneration. The Journal of steroid biochemistry and
molecular biology, 139, 252-261.
13. Shteinfer‐Kuzmine, A., Amsalem, Z., Arif, T., Zooravlov, A.,
& Shoshan‐Barmatz, V. (2018). Selective induction of cancer
cell death by VDAC 1‐based peptides and their potential use
in cancer therapy. Molecular oncology, 12(7), 1077-1103.
14. Tagawa, N., Hidaka, Y., Takano, T., Shimaoka, Y.,
Kobayashi, Y., & Amino, N. (2004). Serum concentrations of
androstenediol and androstenediol sulfate, and their relation
to cytokine production during and after normal pregnancy.
Steroids, 69(10), 675-680.
15. Xie, H., Ye, M., Feng, R., & Graf, T. (2004). Stepwise
reprogramming of B cells into macrophages. Cell, 117(5),
663-676.
Copyright: ©2025 Claus D. Volko. This is an open-access
article distributed under the terms of the Creative Commons
Attribution License, which permits unrestricted use, distribution,
and reproduction in any medium, provided the original author
and source are credited.
https://opastpublishers.com/