Discussion in 'Other Health News and Research' started by acer2000, Dec 1, 2010.
That was really interesting thanks for posting. I wonder what the psychiatrist are going to do in a decade or so when all the "crazy" stuff has been put into the hands of the neurologist and infectious disease doctors?
Perhaps they'll become lawyers or pimps? Or even worse, politicians?
We do seem to be running through politicians like candy these days so in a decade or so we're going to need a new crop. They should fit in quite well. (grins)
They'll have luctrative careers denying any poisons that have acidentally been tipped into the water supply, and calling the symptoms mass hysteria.
Yes they will move on to the next project - and it will be our responsibility to follow them and to campaign for them to be held to account for the mistakes of the past.
Martin J. Walker presents a warning from history:
"If any of these straw men are knocked down, being disproved by proper scientific inquiry and clinical research, The Lobby simply moves on in the hope that no one is tracking their performance. A classic example of this is its early attack on those who suffered from or advocated diagnosis of food intolerance or allergy...
There came a time, however, when the objective clinical evidence began to outstrip the absurdity of the idea that everyone who claimed to have an allergic condition was mentally ill...
The Lobby, naturally, has no reverse gear, nor any desire to make academic amends for its past disinformation and misstatements, so it simply hangs on to the thread of an argument but does not any longer claim allergy and mental illness as one of its central issues. The Lobby moves on, concentrating on other enduring schemes, such as their refutation of multiple chemical sensitivity or environmental causes of cancer. The Lobby is ahistorical, amoral, unscientific and without intellectual integrity. It cares nothing about the damage caused to individuals in the wake of developing science and technology. Rather than address the moral question of what society should do for the individuals damaged by progress, it has chosen to support the cheapest argument for industry: the claim that progress causes no damage. The contemporary trend in the appraisal of adverse reactions, by corporate science, is utter denial."
They will move on as always...but their identities, motives and modus operandi are increasingly exposed thanks to the work of people like LobbyWatch and Martin J. Walker, so our task is to use what we have learnt in a positive way to ensure that what has happened to us can not so easily happen again.
Thanks Acer. This could be incredibly relevant to ME/CFS.
I particularly like this quote from the article:
"The era of writing off endogenous retroviruses and other seemingly inert parts of the genome as genetic fossils is drawing to an end, Perron says. “It’s not completely junk DNA, it’s not dead DNA,” he asserts. “It’s an incredible source of interaction with the environment.” Those interactions may trigger disease in ways that we are only just beginning to imagine."
I am going to see what I can find out about the anti-infective agent Artemisinin mentioned in the article.
Not a Virus - but Streptococcus (Strep) is known to cause personality changes as well
My uncle had Scarlet fever back in the 1930's. Before he got sick with Scarlet Fever, he was a very nice, quiet and bright child. After he recovered there was a major personality change and he became quite a problem. His personality changed dramatically and he caused problems for the rest of his life. My Grandparents saw this change and figured that it was the Strep causing the change (my Grandfather was an eye, ear, nose and throat doctor).
What my Grandparents saw and believed turned out to be quite correct and validated decades later. Strep can cause personality changes in children in addition to a list of other dreadful issues including death.
My Mother's Mother had Rheumatic fever as a child, before antibiotics, and had severe heart valve damage. She died in her late 30's due to the mitral valve being damaged. My mother was only 8 years old at the time. Rheumatic fever is also caused by Strep.
I have long wondered if the Strep infection doesn't somehow enter into one's DNA, change it's character, etc and move down the generations resulting in other diseases, symptoms, etc.
Below is just a grab bag of Strep, Rheumatic Fever, Scarlet Fever and the symptoms.
Because my family is aware of the damage down by a "simple" strep, we are on guard when the young ones get what we think is a strep throat and force the doctors into testing for strep throat. They don't seem to know or remember the damage that Strep can cause. So just be warned. Strep is bacterial, not viral, but the damage is can cause is horrendous.
I have wanted to get in the many risks of Strep into the conversation but there was no real entry. So I am grabbing the Insanity Virus thread to show that not only viruses can damage the brain and change the personality but so to bacterial infections that we believe to be common (they are) but tey are also quite serious.
Sorry to steal your thread. And thank you for posting this information on this Insanity virus. I agree with all the comments made before me. I do think that at some point we won't really need the shrinks. I hope so anyway.
When I was first sick with CFS/FM I really believed that the neurologists and the infectious disease doctors would be my primary care doctors. NOPE! Neither group of doctors had a clue about CFC/FM nor did they want any involvement in it at all. I believe the main reason was that they knew they would be labeled as NUTS and QUACKS because the CDC did such a great number in damning us CFS sick as crazy and thus, those doctors that treated us would also be nuts and quacks.
So again, Great Job CDC!!! The damage you have caused millions and millions worldwide is part of the reason that no one will ever trust the CDC and anything that comes out of it.
Anyone notice that no one is lining up for the Flu Shots? I have seen FREE FLU SHOTS given at CVS, Walgreens and Walmart. NO ONE is in line and the poor nurse is just sitting there doing nothing. Few people are bothering to get the Flu shot esp. when they find out that the Swine Flu vaccine is in this years Flu shot. Want Swine Flu? Then get the vaccine like my sister's poor boyfriend did and was so sick for 2 weeks he and my sister thought he might need to be hospitalized. The next two weeks he was terribly ill and it took about another month for the coughing, sick feeling, etc to finally go away. In his case, the doctor just gave him the vaccine before he had a chance to say NO!
I guess that doctor was trying to get rid of his stock of Flu/Swine Flu vaccines and so he would hit people without asking. Needless to say, my sister and her boyfriend will not be going back to that doctor.
Streptococcus pyogenes and Streptococcal Disease (page 1)
2008 Kenneth Todar, PhD
Streptococcus pyogenes (Group A streptococcus) is a Gram-positive, nonmotile, nonsporeforming coccus that occurs in chains or in pairs of cells. Individual cells are round-to-ovoid cocci, 0.6-1.0 micrometer in diameter (Figure 1). Streptococci divide in one plane and thus occur in pairs or (especially in liquid media or clinical material) in chains of varying lengths. The metabolism of S. pyogenes is fermentative; the organism is a catalase-negative aerotolerant anaerobe (facultative anaerobe), and requires enriched medium containing blood in order to grow. Group A streptococci typically have a capsule composed of hyaluronic acid and exhibit beta (clear) hemolysis on blood agar.
Figure 1. Streptococcus pyogenes. Left. Gram stain of Streptococcus pyogenes in a clinical specimen. Right. Colonies of Streptococcus pyogenes on blood agar exhibiting beta (clear) hemolysis.
Streptococcus pyogenes is one of the most frequent pathogens of humans. It is estimated that between 5-15% of normal individuals harbor the bacterium, usually in the respiratory tract, without signs of disease. As normal flora, S. pyogenes can infect when defenses are compromised or when the organisms are able to penetrate the constitutive defenses. When the bacteria are introduced or transmitted to vulnerable tissues, a variety of types of suppurative infections can occur.
In the last century, infections by S. pyogenes claimed many lives especially since the organism was the most important cause of puerperal fever (sepsis after childbirth). Scarlet fever was formerly a severe complication of streptococcal infection, but now, because of antibiotic therapy, it is little more than streptococcal pharyngitis accompanied by rash. Similarly, erysipelas (a form of cellulitis accompanied by fever and systemic toxicity) is less common today. However, there has been a recent increase in variety, severity and sequelae of Streptococcus pyogenes infections, and a resurgence of severe invasive infections, prompting descriptions of "flesh eating bacteria" in the news media. A complete explanation for the decline and resurgence is not known. Today, the pathogen is of major concern because of the occasional cases of rapidly progressive disease and because of the small risk of serious sequelae in untreated infections. These diseases remain a major worldwide health concern, and effort is being directed toward clarifying the risk and mechanisms of these sequelae and identifying rheumatogenic and nephritogenic strains of streptococci.
Acute Streptococcus pyogenes infections may present as pharyngitis (strep throat), scarlet fever (rash), impetigo (infection of the superficial layers of the skin) or cellulitis (infection of the deep layers of the skin). Invasive, toxigenic infections can result in necrotizing fasciitis, myositis and streptococcal toxic shock syndrome. Patients may also develop immune-mediated post-streptococcal sequelae, such as acute rheumatic fever and acute glomerulonephritis, following acute infections caused by Streptococcus pyogenes.
Streptococcus pyogenes produces a wide array of virulence factors and a very large number of diseases. Virulence factors of Group A streptococci include: (1) M protein, fibronectin-binding protein (Protein F) and lipoteichoic acid for adherence; (2) hyaluronic acid capsule as an immunological disguise and to inhibit phagocytosis; M-protein to inhibit phagocytosis (3) invasins such as streptokinase, streptodornase (DNase B), hyaluronidase, and streptolysins; (4) exotoxins, such as pyrogenic (erythrogenic) toxin which causes the rash of scarlet fever and systemic toxic shock syndrome.
Classification of Streptococci
Hemolysis on blood agar
The type of hemolytic reaction displayed on blood agar has long been used to classify the streptococci. Beta -hemolysis is associated with complete lysis of red cells surrounding the colony, whereas alpha-hemolysis is a partial or "green" hemolysis associated with reduction of red cell hemoglobin. Nonhemolytic colonies have been termed gamma-hemolytic. Hemolysis is affected by the species and age of red cells, as well as by other properties of the base medium. Group A streptococci are nearly always beta-hemolytic; related Group B can manifest alpha, beta or gamma hemolysis. Most strains of S. pneumoniae are alpha-hemolytic but can cause -hemolysis during anaerobic incubation. Most of the oral streptococci and enterococci are non hemolytic. The property of hemolysis is not very reliable for the absolute identification of streptococci, but it is widely used in rapid screens for identification of S. pyogenes and S. pneumoniae.
The cell surface structure of Group A streptococci is among the most studied of any bacteria (Figure 2). The cell wall is composed of repeating units of N-acetylglucosamine and N-acetylmuramic acid, the standard peptidoglycan. Historically, the definitive identification of streptococci has rested on the serologic reactivity of "cell wall" polysaccharide antigens as originally described by Rebecca Lancefield. Eighteen group-specific antigens (Lancefield groups) were established. The Group A polysaccharide is a polymer of N-acetylglucosamine and rhamnose. Some group antigens are shared by more than one species. This polysaccharide is also called the C substance or group carbohydrate antigen.
Rheumatic fever is an inflammatory disease that may develop as a complication of a streptococcus infection, such as strep throat or scarlet fever (caused by Streptococcus pyogenes or group A beta-hemolytic streptococcus). If it does develop, it will usually do so two to three weeks after the Group A streptococcal infection.
Rheumatic fever mainly affects children aged between 5 and 15 years; however, it can affect adults and younger children. Boys and girls have the same risk of developing the disease; girls and women tend to have more severe symptoms. The disease may cause long term effects on the skin, heart, brain and joints. Rheumatic fever may cause permanent damage to the heart valves (rheumatic heart disease). Rheumatic fever has the potential to cause heart failure, stroke and even death.Even though there is no current cure for rheumatic fever, antibiotics, anti-inflammatory drugs and anticonvulsants may be used to relieve symptoms and prevent recurrences.
The disease is fairly rare in most developed nations, but is still common in many other parts of the world, particularly in sub-Saharan Africa, south central Asia, and the indigenous population of Australia and New Zealand. Before the widespread introduction of antibiotics and increased levels of public sanitation and living standards, rheumatic fever used to be one of the leading causes of acquired heart disease in developed nations.
The National Health Service (NHS), UK, estimates that approximately 1 in every 100,000 people is affected by rheumatic fever in England annually.
Patients aged between 25 and 35 years may have recurring episodes of rheumatic fever.
According to Medilexicons medical dictionary:
Rheumatic Fever is a subacute febrile syndrome occurring after group A β-hemolytic streptococcal infection (usually pharyngitis) and mediated by an immune response to the organism; most often seen in children and young adults; features include fever, myocarditis (causing tachycardia and sometimes acute cardiac failure), endocarditis (with valvular incompetence, followed after healing by scarring), and migratory polyarthritis; less often, subcutaneous nodules, erythema marginatum, and Sydenham chorea; relapses can occur after reinfection with streptococci.
What are the signs and symptoms of rheumatic fever?
A symptom is something the patient feels and reports, while a sign is something other people, such as the doctor detect. For example, pain may be a symptom while a rash may be a sign.
Largest morbidity mortality study in chronic heart failure According to The Mayo Clinic (USA), rheumatic fever signs and symptoms generally develop 2 to 4 weeks after a streptococcal throat infection (1 to 5 weeks according to the National Health Service, UK).
As you can see below, there are many possible signs and symptoms linked to rheumatic fever a patient will not necessarily have them all:
Arthritis (joint pain and swelling) generally starts in the knees and ankles, and then works its way to other joints in the body
Bumps and lumps (nodules) under the skin
Chorea uncontrollable jerking of knees, elbows, wrists and ankles
High fever above 39C (102F)
Inappropriate crying or laughing
Pain in one joint that migrates to another joint
Pain in the abdomen
Palpitations sensation that the heart is fluttering or pounding hard
Panting (shortness of breath)
Red blotchy skin rash
Short attention span
What are the risk factors for rheumatic fever?
A risk factor is something which increases the likelihood of developing a condition or disease. For example, obesity significantly raises the risk of developing diabetes type 2. Therefore, obesity is a risk factor for diabetes type 2.
Genetics some individuals possibly carry genes (or a gene) that make them more susceptible to developing rheumatic fever. A person with a family history of rheumatic fever has a higher risk of developing it himself/herself.
Type of strep bacteria some strep bacteria strains are more likely to lead to rheumatic fever than others. Environment such factors are overcrowding, poor sanitation and poor access to healthcare increase the risk of rheumatic fever.
What are the causes of rheumatic fever?
Rheumatic fever may develop as a complication after a throat infection with Streptococcus pyogenes, or group A streptococcus (a bacterium). Strep throat, and less commonly scarlet fever are infections caused by Group A streptococcus infections. Group A streptococcus skin infections, as well as infections in other parts of the body may lead to rheumatic fever (much less common).
Although experts are not completely sure what the link between strep infection and rheumatic fever is, they believe that the bacterium upsets the patients immune system. Strep bacteria have a protein which is similar to one found in some tissues in our body. Immune system cells that would usually target the bacterium may subsequently start attacking the bodys own tissues, as if they were toxins or infectious agents; especially tissues of the heart, joints, CNS (central nervous system) and skin, resulting in inflammation.
Inflammation can cause the following symptoms:
Inflammation of the heart chest pain, fatigue, shortness of breath
Inflammation of the joints arthritis symptoms
Inflammation of the skin skin rashes and nodules
Inflammation of the CNS (central nervous system) chorea (jerking), personality changes
If the patient who is infected with strep bacteria takes the complete antibiotic treatment, the chances of rheumatic fever developing are negligible (zero or tiny). However, if the patient has at least one episode of untreated strep throat or scarlet fever, his/her risk of developing rheumatic fever increases significantly.
Diagnosis of rheumatic fever
According to the National Health Service (NHS), UK, there are so many different rheumatic fever symptoms that a checklist is needed to help in the diagnosis process this checklist is called the Jones Criteria. The Jones Criteria involves checking whether the patient has specific signs and symptoms strongly linked to rheumatic fevers. These signs and symptoms are collectively known as criteria.
There are two types of criteria:
Major criteria signs and symptoms are strongly linked to rheumatic fever. They include:
Inflammation of the heart (carditis)
Several joints have become swollen, painful and stiff (polyarthritis)
The patient has jerky involuntary movements (chorea)
There is a red or pink skin rash (erythema marginatum)
There are small nodules (lumps and bumps) under the skin, especially on the elbows, ankles, knees and knuckles (subcutaneous nodules)
Minor criteria signs and symptoms are moderately linked to rheumatic fever:
The patient has joint pain, but it is not as severe as arthritis joint pain (arthralgia)
Elevated body temperature usually over 102F (39C)
Elevated erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) types of blood tests that detect inflammatory conditions
Irregular heart rhythm
A confident rheumatic fever diagnosis can be made if:
Two or more major criteria are detected
One major and two minor criteria are detected
Some of the signs and symptoms may be detected just by examining and interviewing the patient. Others will require testing. Testing may include:
ECG (electrocardiogram) up to 12 adhesive electrodes are attached to the skin on certain parts of the body, usually the arms, legs and chest. The ECG (a device) measures the electrical activity of the patients heart, revealing any possible abnormalities in heart rhythms. Abnormal heart rhythms usually occur when there is inflammation of the heart a common complication of rheumatic fever. Early detection with subsequent prompt treatment is important.
Electrocardiography this device uses sound waves that produce images of the heart. The test enables the doctor to see whether there is any inflammation of the heart. Heart valve damage, if present, may also be revealed in this test (much less likely early on in the disease).
CRP rates blood tests can detect higher-than-normal levels of CRP (C reactive protein), which is produced by the liver. High CRP blood levels means there is inflammation.
Erythrocyte sedimentation rate (ESR) a sample of red blood cells are placed in a test tube of liquid, their rate of descent is measured. If the cells descend faster than normal it could mean the patient has an inflammatory condition.
Test for strep infection if the patient has already been diagnosed with a strep infection the doctor may not order additional tests.
What are the treatment options for rheumatic fever?
The medical teams aims are to destroy the bacteria, relieve symptoms, control inflammation and prevent recurrences of rheumatic fever.
Antibiotics the patient, usually a child, will probably be prescribed penicillin or some other antibiotic to destroy any remaining strep bacteria in the body.
Preventing recurrence after completing the full course of antibiotics, the patient will be prescribed another course of antibiotics to prevent recurrence. This preventive treatment will generally continue until the patient is about 20 years old. If the patient is older, for example a teenager when rheumatic fever develops for the first time, preventive treatments may continue beyond the age of 20 years.
Heart inflammation some patients may be advised to continue taking preventive antibiotic treatment for much longer, in some cases for the rest of their lives.
It is important to get rid any streptococcocal bacteria. If any is left inside the body and the patient has another throat infection, there is a serious risk of a recurrence of rheumatic fever. Repeated occurrences of rheumatic fever significantly raise the risk of heart damage (sometimes permanent).
Anti-inflammatory treatment an anti-inflammatory drug, such as or naproxen (Anaprox, Naprosyn, etc.) may be prescribed. These medications reduce pain, inflammation and fever. A corticosteroid, such as prednisone may be prescribed if the patient does not respond to anti-inflammatory medications or there is inflammation of the heart.
Aspirin is not usually recommended for children aged less than 16 years because there is a risk of developing Reyes syndrome, which can cause liver and brain damage, and even death. However, an exception is usually made when the child has rheumatic fever because the dose is small and the results are very good in other words, the benefits are far greater than the risks.
Anti-convulsant medications if chorea symptoms are severe an anticonvulsant, such as valproic acid (Depakene, Stavzor) or carbamazepine (Carbatrol, Equetro) may be prescribed.
Long term care any child who had rheumatic fever will need to know later on that he/she once had rheumatic fever. As an adult the individual should discuss this with his/her doctor. Heart damage from rheumatic fever may not appear for many years after the illness.
What are the possible complications of rheumatic fever?
Rheumatic fever symptoms, specifically inflammation, may persist for several weeks, months, and in some cases much longer, causing long-term problems.
Rheumatic heart disease the most common and most serious complication. According to the National Health Service (NHS), UK, an estimated 9% to 34% of rheumatic fever cases have this complication. Rheumatic heart disease means permanent damage to the heart caused by the inflammation of rheumatic fever. The most common complication occurs with the mitral valve the valve between the two left chambers of the heart. Sometimes other valves may also be affected. The following conditions may result:
Valve stenosis the valve narrows, causing a drop in blood flow.
Valve regurgitation blood flows in the wrong direction because of a leak.
Heart muscle damage inflammation can weaken the heart muscle, leading to improper pumping function of the heart.
These conditions may also develop if there is damage to heart tissue, and/or damage to the mitral valve or other heart valves:
Heart failure even though it may sound like it, heart failure does not necessarily mean that the heart has failed. Heart failure is a serious condition in which the heart is not pumping blood around the body efficiently. The patients left side, right side, or even both sides of the body can be affected.
Atrial fibrillation the human heart has two upper chambers and two lower chambers. The upper chambers are called the left atrium and the right atrium the plural of atrium is atria. The two lower chambers are the the left ventricle and the right ventricle. When the two upper chambers the atria contract at an excessively high rate, and in an irregular way, the patient has atrial fibrillation.
Muffin's post about Streptococcus reminded me of this paper, which I read recently:
Observations on the Epidemic of Polio-Encephalitis in Los Angeles, 1934:
I wrote about it in #35 here:
The researchers who wrote that report - on what now looks fairly likely to be the first ever XAND/ME/CFS outbreak, since it occurred at just the right time and place where P/X XMRV evolved - seem to have found a very strong association with the streptococcus they recovered from nasal swabs. They found that this streptococcus was "pleomorphic" - ie, shape-changing - which caused great controversy, and eventually it was generally accepted that this "pleomorphism" was a myth. Recently, however, shape-changing bacteria have been observed, so it turns out they might have been right all along.
Here's part of what I wrote about pleomorphism in #35 on the thread mentioned above:
The observations place a great deal of evidence on the "pleomorphic streptococci" found consistently in nasopharyngeal swabs, findings "obtained in Rochester and reproduced and greatly extended in Los Angeles". Intriguingly, the paper states:
I had to look up "pleomorphism" and the wiki entry is also intriguing:
I find this a really fascinating subject...
I always take note of research into HERV's in relation to schizophrenia etc, and this research is far more advanced than I knew it was. One company are already developing some treatments... http://www.geneuro.com/index2.php?rubID=5
I've highlighted a couple of passages that really struck me because what they describe has striking similarities to our own disease:
Not xmrv but herv??
The insanity virus revisited
I feel its an opportune time to revive this thread that some of you may remember posited basically that schizophrenia may be due to the following chain of events :
a common seasonal viral infection (e.g. mono) at or near birth;
reactivates a HERV (HERV-W) in some people with a genetic predisposition or whose immune system reacts in a certain way (explaining why not everyone exposed has reactivated HERVs);
who may then appear relatively normal until exposed to another virus or other stressor at which point clear symptoms of schizophrenia emerge.
I'm reposting some excerpts as a little aide memoire.
Its worth re-reading the whole article in the context or recent research on Rituximab; EBV in Rheumatoid arthritis and of course Brigette Huber's ongoing work on ME/CFS and HERV-K.
Post XMRV (until someone produces evidence of an HGRV that isn't XMRV I consider the exogenous retrovirus theory to be speculative) we can now uncontroversially reopen discussion on a multi-hit scenario and (I believe importantly) prodromal symptoms
Nice thread - thanks everyone - strawmen to become a bad dream only at last ?
Great article! very interessting.
"Scribbled onto the marker board in Yolkens office is a list of infections that are now known to awaken HERV-Wincluding herpes, toxoplasma, cytomegalovirus, and a dozen others."
MS has been linked to EBV in a few papers, but the evidence is not yet convincing enough. I think if EBV is just one of the virusses that activates HERV-W, this could be an explaination.
The problem with much of this work is that we have associations rather than causal links. I've pondered the problem off and on for years, while checking on research on genetic etiology for mental illness. One very interesting discovery in that line was a Scottish family in which every member over three generations who got a particular variant of a gene had a serious mental illness. They did not always have the same diagnosis. Schizophrenia was there, but so were major depressive disorder and bipolar illness.
The gene, dubbed DISC1, has been researched considerably since then. There are even mice with a parallel genetic defect available. Exactly what the gene does would take us far afield, though it has a lot to do with brain development. What interested me was that the defective version has a truncated open reading frame, which implies it was created by a deletion event.
We now know of other lineages with the same defect. They are not only in Scotland, England and the U.S. They are also found in Japan and China. The puzzle is that these are isolated lineages with no recent common ancestor, but apparently with the same gene defect.
A second problem came when large numbers of carefully diagnosed schizophrenics were tested for the abnormal variant. In one study over 600 were tested without finding a single example. Yes, they might have more subtle defects in that gene, or in interacting genes. However, the naive hypothesis had failed.
At this point, I went looking for research answering a specific question about those mouse lineages with the parallel defect. How did multiple lineages get the same deletion without recent common ancestors? The answer involves short-hairpin RNA, which begs another question: how does a common defect in RNA get inherited via DNA? The answer was a retrovirus.
This resolves several problems, but to get any activity in RNA you need activated genes, not simply passive ERVs. Now, all the proposed viruses which are not retroviruses might independently activate ERVs, but the parsimonious hypothesis is that a single exogenous retrovirus, not necessarily identical to an ERV, started the process of activating ERV sequences, which then converged on an optimum sequence for that host. The high copy numbers for ERVs passed by inheritance would give such sequences a heavy advantage over many others in the quasispecies.
Associations with other viruses would naturally result if the retrovirus caused limited immune impairment in order to protect itself. In this case those viral infections or reactivations would follow, not precede, retroviral infection. These coinfections might cooperate, or they might be opportunistic parasites on the original infection. I propose that they provide a smoke screen which allows the retrovirus to hide while the others fight with the host immune response.
An infectious origin would explain the limited (25%) concordance between homozygotic twins with one having schizophrenia. On the downside, an active retrovirus would invalidate a large number of studies of genetics which assumed inheritance of genes was always vertical.
For some reason you reminded me of a time way back as a psych undergrad during a computational vision tutorial when we were discussing the problem of how a visual system deals with the fact that objects change shape as they rotate or as the observer moves around them. The perennial problem being do we infer form from motion or motion from a prior knowledge of form (and how does the latter cope with novel objects). The associated problem being how the visual system determines 'slant'. Having recently moved from an engineering background I naively suggested interferometry as a possible mechanism at which point our tutor went apeshit spluttering that we don't have an interferometer built into our brains. Of course I wasn't suggesting this literally but couldn't see any good reason why, given that we know that there are neurons or neural nets dedicated to detecting colours; greyscale; lines and edges etc that it wasn't inconceivable that other neural networks might be dedicated to detecting interference patterns resulting from incident light reflecting off objects.
Anyway, the lesson was learned that we were only to discuss what was 'known' and to stay away from speculation.
Regarding a human gammaretrovirus, as I understand the current situation (leaving aside the issue of potential false negatives that might have masked other sequences) there is strong evidence that XMRV was a lab created contaminant and that it was the XMRV sequence that Silverman sequenced and uploaded to Genbank. Which of course doesn't rule out the possibility of a HGRV existing but until a sequence is published it unfortunately must be considered speculative.
Getting back to the subject in hand, I agree that associations do not imply causality. I don't think researchers (in the schizophrenia field specifically) have ruled out the possibility of an exogenous retrovirus as it does seem to still figure in discussions. If it was simply a matter of detecting increased reverse transcriptase activity or overexpression of HERV activity then an exogenous retrovirus as a trigger remains a possibility. However there is recent research that goes beyond associations to describe a putative mechanism by which HERV-W causes the pathology seen in schizophrenia :
Implication of the env Gene of the Human Endogenous Retrovirus W Family in the Expression of BDNF and DRD3 and Development of Recent-Onset Schizophrenia
Of course another (exogenous) retrovirus could be 'hiding in the open' but the parsimonious interpretation is that HERV-W activation is sufficient to cause the pathology and that common viruses or other environmental triggers, rather than just being opportunistic, can explain the epidemiological findings.
As a further digression, I've been interested in schizophrenia; bipolar disorder; autism; Alzheimer's; OCD; Huntington's and similar neurological diseases recently after noticing that all (plus fibromyalgia) have been shown to involve a neurological sensory processing deficit. The failure to properly filter 'signal from noise' can readily explain auditory hallucinations in schizophrenia and diffuse pain in fibromyalgia. I would suggest it can also explain pain; fatigue; IBS; brain fog and PEM etc in ME/CFS.
As far as I'm aware the relatively simple test for a sensory processing deficit has never been applied to a ME/CFS cohort.
I learned a lot from the article. So, thanks for bringing it up. I have been thinking in the line of endogenous retroviruses for a while now. I think it makes just as good sense as exogenous RVs.
I have also had some past connection with computational vision. My immediate response to any idea about interferometry is that human visual perception has never been shown to be sensitive to phase information in light. Radically different visual systems might have this ability, but I don't see a physical basis in our own. Without this I can't give neurons any information to work on, no matter how sophisticated the processing.
My point about endogenous and exogenous viruses is that all known human endogenous sequences are seriously defective. It is not enough to say that somehow they became activated. Without a helper virus they shouldn't be able to form the virions which have turned up repeatedly in the past. Without active selection, those latent sequences have very little chance to mutate into functional sequences. The process must start with an active viral infection. If that virus resembles the endogenous sequence, activation and subsequent selection is plausible. Inferring a possible undetected retrovirus in these circumstances is much easier than inferring the existence of, say, a neutrino.
To rephrase my argument, I'm saying that those lineages with a particular defect in a particular gene do not have a recent common ancestor, yet they have very similar molecular characteristics. The molecular explanation for the defect is natural if the change takes place in RNA. This should not result in a heritable change in DNA without reverse transcription. In mice such a thing has been discovered in connection with a retrovirus. In humans there is evidence of reverse transcription, but a retrovirus has not been identified. All assumptions about the sequence of events surrounding onset of the illness remain speculative because we are still unable to predict who will develop the illness, except in the peculiar case of a few lineages. Most cases are outside of those identified lineages.
A second point I'm getting at is that assumptions common to work in genetics do not allow for horizontal transfer of genetic information. If you find a gene active in someone you tend to assume they must have inherited that gene, even if it was not actively expressed. If there are undetected human retroviruses, much of the vast confusion in genetic studies becomes understandable.
Finally, the insight that diagnostic categories may reflect nothing more than the particular nerves which happen to have been infected seems worth pursuing. If the doctor can see something like intentional tremor, the diagnosis veers toward MS. If the patient perceives things the doctor does not, the diagnosis heads toward schizophrenia. We may find a single pathogen causing not only mental disorders as different as schizophrenia, MDD and bipolar illness, but also traditionally neurological diseases like MS. I already know that significant percentages of MS sufferers do become either depressive or bipolar.
I think you're going to have to help me out a little anciendaze. A number of studies that implicate HERV's in human disease report increased reverse transcription activity and also state environmental factors that can reactivate HERVs (including Brigette Huber's work implicating herpesvirus). I'm not sure how settled the science is here but for example amongst the enviromental factors are :
So, is it the case that proposed reactivation of HERVs via means other than a retrovirus may cause diseases either directly through deregulation of physiological processes or via an autoimmune response but that this reactivation does not involve replication and the elevated reverse transcription activity is ignored?
If on the other hand HERvs require the presence of an exogenous retrovirus to replicate (via the exogenous virus inserting or changing sequences in the HERV) but it can be shown that it is the HERV sequences that cause pathology then what do we consider the pathogen? Is it the exogenous retrovirus that may be benign or the now replication competent HERV?
As for looking at other diseases; I've complained in the past that differential diagnosis has the unfortunate side effect of elevating signs or symptoms that allow you to discriminate between diseases (or labels based on a collection of signs or symptoms) while downplaying signs or symptoms that overlap. The presence of an identified neurological deficit such as a sensory gating deficit in a range of conditions suggests to me at least the possibility that the same or similar processes (which may be downstream consequences but still treatable) and possibly pathogens may underlie them.
If a similar sensory gating deficit was found in ME/CFS there might be a great deal to learn from other diseases that also show a similar deficit and where research is better funded and advanced.
While not the ideal design to examine this, I'm still pleased to see this upcoming research :
Assessment of visual function in ME/CFS
While a sensory gating deficit may seem a little obscure compared to all our other symptoms, its interesting, in the context of the various methylation/glutathione deficiency/mitochondrial deficiency/high oxidative stress findings that sensory gating deficits may be ameliorated or reversed as brain glutathione levels are raised :
You can also try a Google Site Search
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