Originally posted by bsl4doc
...soficrow, sorry. You need to read the titles of the articles again. I can't find any even somewhat related to viral obesity.
Although the titles do not include the word obesity, the articles are related to induced obesity
- as I stated earlier. I did a quick
search on the National Institutes of Health PubMed database, as I also said earlier, and my terms were +virus +induced obesity. No, I did not read the
articles, nor did I claim to have done. I simply shared the first page of the search results.
You need to know a bit more about 'induced obesity' to see how
the articles relate. So here's the poop:
Most infectious obesity does NOT result from a direct cause-and-effect relationship - the disease-causing microbes (pathogens) do NOT head straight
for the fat cells (lipids
cells) when they enter the body.
Instead, induced obesity usually occurs later on in a larger disease process
that affects numerous body systems - sometimes called
"multisystem disease." The systems affected in this disease process include the:
* nerves (neurological);
* hormones (endocrine);
* immune system; and
Many paths lead to obesity, but generally, obesity does not occur unless and until
the multisystem disease reaches the fat or adipose cells.
Once the fat cells are 'infected' one of two things happens: a) individual fat cells grow larger, called
or hypertrophic; or b) fat cells multiply out of control, called
More than one virus is linked to obesity; and in addition, many other pathogens present in food
and the environment also are known to induce
obesity. These other pathogens cause disease by releasing toxins.
 As used herein the term "exposed to a toxin-forming organism" refers to any patient contact with the toxin, such as direct contact with the
toxin-producing organism itself, or by contact with the toxin, produced by the microbial organism. Such contact can occur, for example, by
ingestion, inhalation, or contact through skin or mucosal membrane. Such toxin-forming dinoflagellates include but are not limited to
Pfiesteria, Ciguatera, and Chattonella. Such toxin-forming fungi include but are not limited to Stachybotrys, Penicillium, Aspergillus,
Cladosporium, and Fusarium. Such toxin-forming spirochetes include but are not limited to Borrelia, Treponema, Leptospira, and Denticola. Such
toxin-forming protozoa include, but are not limited to Babesia and Plasmodium. Such toxin-forming cyanobacteria include but are not
limited to Microcystis, Anabaenopsis and Cylindrospermopsis. Such toxin-forming bacteria include but are not limited to Bacillus, Clostridia,
and coagulase-negative Staphylococcus.
United States Patent Application: 0030219400
Sorry, there's no direct link. Go to the US Patent Office website, and search under
applications for #0030219400, or "Methods for treating or inhibiting neurotoxin-mediated syndromes"
* The biphasic change in hypothalamic leptin receptor expression seen during the progression of
obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.
with the obesity-inducing BDV-ob results most likely in neuroendocrine dysregulations leading to the development of an obesity syndrome.
has multiple etiologies
* Viruses can induce progressive neurologic disorders associated with
diverse pathological manifestations
Sometimes these pathogens and toxins cause rapidly progressive acute
disease that ends
quickly, but more often, disease is slowly progressive and occurs as a forme fruste
Traditional western medicine tends to focus on acute disease and ignore the formes fruste. As a result, we now face a worldwide chronic disease
epidemic that's kicking everyone in the butt - individually, nationally, socially and economically.
We "catch" these diseases by eating, drinking, breathing, or touching something that is contaminated - and much of our food is contaminated with one
or another of the "toxin-forming organisms" outlined above. But people react differently to the same exposures.
The disease process is complicated and involves numerous different factors, so it's
. What happens in the individual body results from a complex interplay between pathogen exposure, genetic susceptibility, other
environmental influences, and more. Also, the disease process can take a long time, and makes a lot of stops along the way - affecting various
enzymes, hormones, and other essential body products. Many disease symptoms like obesity result from a domino effect inside the body, called a
The research looks at the whole cascade, all its parts, and all the factors, not just the disease-causing microbe and obesity alone - which is why you
do not see the word obesity in every title.
Damage-control corporate-politicos say obesity is solely a matter of personal responsibility and blame individuals; their goal is to avoid liability
and lawsuits. On the other side, responsible scientists seek the truth, and ways to make the food industry and our world safer. Available research is
either funded by industry and tries to disprove the relationship between common pathogens and the larger multisystem disease process, or alternately,
tries honestly to understand what's really going on.
Let's take a look at some of the titles in your list...
-1: Shan XC, Goodwin PH. Links
Abstract Silencing an ACC oxidase gene affects the susceptible host response of Nicotiana benthamiana to infection by Colletotrichum orbiculare.
Plant Cell Rep. 2006 Jan 6;:1-7 [Epub ahead of print]
PMID: 16397784 [PubMed - as supplied by publisher]
ACC oxidase is a gene found in plants, not humans or mammals or any other organism other than plants. If you look at the citation entry for that
article, you'll see this phrase "Plant Cell Rep. 2006 Jan 6;:1-7". That means it's found in the journal Plant Cell Reproduction. This has nothing
to do with viral obesity whatsoever.
ACC oxidase is the gene that makes vine-ripened fruits and vegetables ripen. The ACC oxidase gene is silenced in genetically modified (GM) fruit and
vegetables to prevent ripening on the vine, and extend storage life for shipping and sales by delaying ripening off the vine. Ie., see
The cited article shows that silencing the ACC oxidase gene makes GM Nicotiana benthamiana
more susceptible to infection by a fungus called
. Fungi produce poisonous proteins called mycotoxins
Note to hamburglar.
Here it is: The anticipated protein-prion connection.
Just don't ask me to connect all the dots for you.
As outlined above, many mycotoxins are neurotoxins, linked to multisystem disorders that can include obesity and obesity syndromes. For example,
thing neurotoxins do to contribute to the larger disease process is muck up the
So - the article speaks to genetically modified (GM) fruits and vegetables, specifically a transgenic gene affecting ACC oxidase, engineered to
prevent ripening on the vine and delay ripening in shipping and storage. The research is relevant in considering the connection between obesity and
mycotoxins; it suggests that genetically modified (GM) fruits and vegetables play a role in mycotoxin contamination of the food supply.
The researchers show that this particular GM plant is more susceptible to infection by the fungus Colletotrichum orbiculare
NbACO1-silenced plants developed more lesions more quickly
as a result of an accelerated switch from the symptomless, biotrophic phase to the
symptomatic necrotrophic phase of infection compared to inoculated control plants."
Taken further, research also may prove that all
GM fruits and vegetables are more susceptible to all
mycotoxin and neurotoxin producing
pathogens. If so, we will have learned for example that
GM fruits and vegetables cause obesity.
For people unwilling to wait until all the i's are dotted and all the t's are crossed.
The Top-10 MYCO-Toxic Foods
Dietary Strategies to Counteract the Effects of Mycotoxins
2: Yang K, Shi H, Qi R, Sun S, Tang Y, Zhang B, Wang C. Links
Free Full Text Hsp90 Regulates Activation of IRF-3 and TBK-1 Stabilization in Sendai Virus-infected Cells.
Mol Biol Cell. 2006 Jan 4; [Epub ahead of print]
PMID: 16394098 [PubMed - as supplied by publisher]
This article is about the immune responses phosphorylation of IRF-3 and TBK-1, intracellular signal molecules, in response to laboratory controlled
sendai virus infection. It focuses on the ability of IRF-3 to control dsRNA regulation. Nothing at all about obesity.
The immune system in general is involved in multisystem disease processes that lead to obesity, sometimes by mucking up metabolism. There are many
paths to the same place, but IRF3 specifically is involved in metabolism regulation; it causes inflammation, which in turn contributes to causing
obesity. This article looks at one way IRF3 gets activated on exposure to viruses: "Our study uncovers an essential role of Hsp90 in the
virus-induced activation of IRF3."
Here are a few other articles that mention IRF3. They might help you to understand the very complicated links between viruses, IRF3, inflammation and
obesity, and the many different ways IRF3 can be activated:
Obesity, diabetes, and cardiovascular disease are the leading causes of morbidity and mortality in industrialized societies. The common thread
that links these disorders is dysregulation of lipid metabolism. With the discovery of nuclear receptors that are activated by lipids, a new
paradigm has emerged for the transcriptional regulation of metabolic pathways. Included in this group of receptors are the peroxisome
proliferator-activated receptors (PPARa, -g, and -d) and the liver X receptors (LXRa and -b). ...PPAR and LXR Mediate Oxidized Lipid Signaling in
Macrophages. ...LXRs Link Metabolic and Immune Functions in Macrophages. ...These observations identify the LXR pathway as a common regulator of
lipid metabolic and immune functions in macrophages and suggest that LXR ligands may have utility in the treatment of inflammatory diseases.
...Dissection of the TLR3/4 signaling pathway revealed that inhibition of LXR is mediated by the viral response transcription factor IRF3.
Lipid Signaling Pathways in Physiology and Disease
An effective immune system requires rapid and appropriate activation of inflammatory mechanisms but equally rapid and effective resolution of the
inflammatory state. A review of the canonical host response to gram-negative bacteria, the lipopolysaccharide-Toll-like receptor 4 signaling
cascade, highlights the induction of repressors that act at each step of the activation process. These inflammation suppressor genes are characterized
by their induction in response to pathogen, typically late in the macrophage activation program, and include an expanding class of dominant-negative
proteins derived from alternate splicing of common signaling components. Despite the expanse of anti-inflammatory mechanisms available to an
activated macrophage, the frailty of this system is apparent in the large numbers of genes implicated in chronic inflammatory diseases. This
apparent lack of redundancy between inflammation suppressor genes is discussed with regard to evolutionary benefits in generating a heterogeneous
population of immune cells and consequential robustness in defense against new and evolving pathogens.
Inflammation suppressor genes: please
switch out all the lights. J Leukoc Biol. 2005 Jul;78(1):9-13. Wells CA, Ravasi T, Hume DA. Griffith University, Queensland, Australia. PMID:
Mammalian cells respond to virus infections by eliciting both innate and adaptive immune responses. One of the most effective innate antiviral
responses is the production of alpha/beta interferon and the subsequent induction of interferon-stimulated genes (ISGs), whose products collectively
limit virus replication and spread. Following viral infection, interferon is produced in a biphasic fashion that involves a number of transcription
factors, including the interferon regulatory factors (IRFs) 1, 3, 7, and 9. In addition, virus infection has been shown to directly induce ISGs in
the absence of prior interferon production through the activation of IRF3. This process is believed to require virus replication and results in
IRF3 hyperphosphorylation, nuclear localization, and proteasome-mediated degradation. Previously, we and others demonstrated that herpes simplex virus
type 1 (HSV-1) induces ISGs and an antiviral response in fibroblasts in the absence of both interferon production and virus replication. In this
report, we show that the entry of enveloped virus particles from diverse virus families elicits a similar innate response. This process requires IRF3,
but not IRF1, IRF7, or IRF9. Following virus replication, the large DNA viruses HSV-1 and vaccinia virus effectively inhibit ISG mRNA accumulation,
whereas the small RNA viruses Newcastle disease virus, Sendai virus, and vesicular stomatitis virus do not. In addition, we found that IRF3
hyperphosphorylation and degradation do not correlate with ISG and antiviral state induction but instead serve as a hallmark of productive virus
replication, particularly following a high-multiplicity infection. Collectively, these data suggest that virus entry triggers an innate antiviral
response mediated by IRF3 and that subsequent virus replication results in posttranslational modification of IRF3, such as hyperphosphorylation,
depending on the nature of the incoming virus.
Innate cellular response to virus particle
entry requires IRF3 but not virus replication. J Virol. 2004 Feb;78(4):1706-17. Collins SE, Noyce RS, Mossman KL. Department of Pathology and
Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5. PMID: 14747536
Chen and his colleagues were seeking a regulatory molecule that would provide a missing link in the activation of two important triggers of the
innate immune system -- NF-eB and IRF3. Somehow, these molecules are activated in response to a receptor molecule, called RIG-I, which detects
viral genetic material. RIG-I binds to the RNA of viruses such as the influenza virus, hepatitis C virus, West Nile virus and SARS virus. ...The
researchers knew the molecule they were seeking was present in a biochemical pathway somewhere between RIG-I and other "downstream" regulatory
molecules. They initiated a search for this missing molecule by searching for proteins in the cell that contain a characteristic molecular domain,
called a CARD domain, which mediates interactions between different regulatory proteins. Their search yielded a protein, which they called MAVS for
mitochondrial antiviral signaling. ...Their experiments revealed that MAVS activated NF-eB and IRF3 in cell cultures.
Cellular power plants also fend off viruses
IKK-i(epsilon) overexpression promotes dimerization and nuclear translocation of interferon regulatory factor 3 (IRF3), induces activation of
the DNA-binding protein C/EBPdelta and enhances proinflammatory gene induction by transforming growth factor-beta (TGF-beta).
Meeting on the biology and pathology of NF-kappaB
Also see: Mitofusin-2 determines mitochondrial network architecture and mitochondrial metabolism.
A novel regulatory mechanism altered in
Cell-line-induced mutation of the rotavirus
genome alters expression of an IRF3-interacting protein.
4: Gern JE, Brooks GD, Meyer P, Chang A, Shen K, Evans MD, Tisler C, Dasilva D, Roberg KA, Mikus LD, Rosenthal LA, Kirk CJ, Shult PA, Bhattacharya A,
Li Z, Gangnon R, Lemanske RF Jr. Links
Abstract Bidirectional interactions between viral respiratory illnesses and cytokine responses in the first year of life.
J Allergy Clin Immunol. 2006 Jan;117(1):72-8. Epub 2005 Nov 28.
PMID: 16387587 [PubMed - in process]
This article is about the development of allergies as a response to cytokines (cellular signal molecules of the immune system) as a result of early
life repiratory infections. Nothing mentioned in the journal article in reference to obesity or viral linked obesity.
Viruses cause immune responses that involve inflammation, which involve cytokines. Some allergies develop in response to cytokines and some cause a
cytokine response - the article basically says it's a two-way street, and potentially part of a larger cascade.
Elevated levels of pro-inflammatory cytokines cause deficiencies in the
-stimulating hormone called MSH - and
of MSH deficiency include obesity.
 We have seen that deficiencies in MSH are commonly seen in patients with elevated levels of pro-inflammatory cytokines associated with
exposure to environmental sources of biotoxin production, including indoor toxin forming fungi leading to SBS. The pro-opiomelanocortoid pathway
(POMC) generates MSH in the hypothalamus. Leptin is an agonist of cytokine receptors that initiate activity of the POMC. Serum leptin can be measured
looking for evidence of reduced receptor activity for the leptin agonist, and thus an elevated level of leptin is a marker of impaired MSH production.
The inability of the POMC pathway to make MSH is marked by refractory symptoms, such as obesity and leptin resistance.
United States Patent Application: 0030219400
Sorry, there's no direct link. Go to the US Patent Office website, and search under
applications for #0030219400, or "Methods for treating or inhibiting neurotoxin-mediated syndromes"
11: Morrison TE, Whitmore AC, Shabman RS, Lidbury BA, Mahalingam S, Heise MT. Related Articles, Links
Abstract Characterization of ross river virus tropism and virus-induced inflammation in a mouse model of viral arthritis and myositis.
J Virol. 2006 Jan;80(2):737-49.
PMID: 16378976 [PubMed - in process]
This article is about the possible link between viruses and myositis (a swelling of muscles at the joints) and arthritis (a swelling of the joints due
to rubbing or wear of cartilage, among other causes). No mention of obesity or viral linked obesity.
This research shows that viruses can cause myositis and arthritis by causing inflammation in the infected tissues: "...histological analyses
demonstrated that RRV infection resulted in severe inflammation of these tissues." Other research shows that physical trauma like rubbing only causes
arthritis or myositis when infection already is present. These researchers say, "...we found that the primary targets of RRV infection are bone,
joint, and skeletal muscle tissues," and "Characterization of the inflammatory infiltrate within the skeletal muscle tissue identified inflammatory
macrophages, NK cells, and CD4+ and CD8+ T lymphocytes."
Again, as explained above, the disease process involves inflammation and cytokines implicated in a larger, longer disease process that can cause
obesity. Here is an article from Arthritis Research and Therapy
that might help explain some of the connections:
...both IL-2 and IL-15 act as chemoattractants for T cells. The two cytokines stimulate the proliferation of NK cells and can synergize with IL-12 to
facilitate their synthesis of IFN-γ and TNF-α . Both cytokines induce the proliferation and immunoglobulin synthesis by human B cells stimulated
with anti-IgM or CD40 ligand . ...mice made JAK3-deficient by homologous recombination manifest an absence of NK cells and abnormalities of T and
B cells but do not have disorders in nonimmunological systems . ...our emerging understanding of the IL-15/ IL-15R system, including the
definition of the actions that this cytokine manifests – both those that are shared with IL-2 and those that are distinct – is opening new
possibilities for the development of more rational immune interventions directed toward IL-15 and IL-15 receptors that may be of value in the
treatment of cancer, the prevention of allograft rejection, the therapy of diseases associated with the retrovirus HTLV-I, and the treatment of
autoimmune diseases such as RA.
The contrasting roles of IL-2 and IL-15 in the life and death of lymphocytes: implications for
the immunotherapy of rheumatological diseases
17: Haller O, Kochs G, Weber F. Related Articles, Links
Abstract The interferon response circuit: Induction and suppression by pathogenic viruses.
Virology. 2006 Jan 5;344(1):119-30.
PMID: 16364743 [PubMed - in process]
This article is about the role of inteferons (cellular signal molecules specific for certain cells) and their ability to destabilize viral molecules.
No mention of obesity or viral linked obesity.
Again, this article came up on a search for "induced obesity" because the interferon response circuit is part of the immune system - and is involved
in multisystem disease processes and cascades leading to obesity.
The research reported here looks at how one part of the immune system works - and why it doesn't
work - to fight viruses and block
viral-related disease cascades. As the researchers say, "Viruses, ...have evolved multiple strategies to counter the IFN system which would otherwise
stop virus growth early in infection." And again, the focus is on inflammation and cytokines, both implicated in larger disease cascades that can
lead to obesity.
This kind of research is geared towards developing vaccines to prevent chronic disease like obesity. Here is an earlier article that outlines the
problem a bit more clearly:
Viruses need to multiply extensively in the infected host in order to ensure transmission to new hosts and survival as a population. This
is a formidable task, given the powerful innate and adaptive immune responses of the host. In particular, the interferon (IFN) system plays an
important role in limiting virus spread at an early stage of infection. It has become increasingly clear that viruses have evolved multiple strategies
to escape the IFN system. They either inhibit IFN synthesis, bind and inactivate secreted IFN molecules, block IFN-activated signaling, or disturb the
action of IFN-induced antiviral proteins. The molecular mechanisms involved range from a broad shut-off of the host cell metabolism to fine-tuned
elimination of key components of the IFN system. Type I (alpha/beta) IFNs are produced in direct response to virus infection and double-stranded
RNA (dsRNA) molecules that are sensed as a danger signal by infected cells. IFNs induce the expression of a number of antiviral proteins, some of
which are again activated by dsRNA. Therefore, many viruses produce dsRNA-binding proteins to sequester the danger signal or express virulence genes
that target specific components of the IFN system, such as members of the IFN regulatory factor (IRF) family or components of the JAK-STAT signaling
pathway. Finally, some viruses have adopted means to directly suppress the very antiviral effector proteins of the IFN-induced antiviral state
directed against them. Evidently, viruses and their host's innate immune responses have coevolved, leading to a subtle balance between
virus-promoting and virus-inhibiting factors. A better understanding of virus-host interactions is now emerging with great implications for vaccine
development and drug design.
interference: how viruses fight the interferon system. Viral Immunol. 2004;17(4):498-515. Weber F, Kochs G, Haller O. Abteilung Virologie,
Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg, Freiburg, Germany. PMID: 15671747
So, basically, your list is a wash.
Not at all. Quite illuminating, IMO.
I went through and picked a few I thought would be the most interesting reads for me, personally.
If you'd be so kind, could you show me which ones you feel have anything whatsoever to do with obesity in any way?
Done. And I hope it helps. But pulling this stuff together and writing simple explanations is time-consuming hard work. So when I say, "Done," I
mean it. I have other interests. Honest. You have to do your own research now.
If you're really interested in the very many pathogens in our food, air and water that can cause obesity, and how all the different factors work
together - here are a few search terms that will help:
Obesity Pathogenesis Brown Fat/metabolism Membrane Transport Proteins/biosynthesis Energy Metabolism/physiology Fatty Acids, Nonesterified/blood
Hypothalamus/metabolism Hypothalamus/physiopathology Neuropeptides/metabolism Neuropeptides/physiology Obesity/physiopathology Mycotoxins/pathogenesis