The human organism expresses retroviruses.
They are beneficial particles needed for immune defense, growth, and tissue repair.
Since retroviruses were observed in the first AIDS patients, it has been postulated - and it has since become firmly established dogma - that retroviruses "cause" AIDS. Anti-retroviral drugs are the treatment of choice for those who have tested positive to the protein which is a signature for retroviruses.
Of course killing the retrovirus also deprives us of the repair and defense functions they perform. And the drugs' side effects are often deadly for AIDS patients.
Perhaps to re-think our approach in this would be a good idea?
Do White Blood Cells use Retroviruses for Cell fusions?
by Cal Crilly
Alveolar macrophages (white blood cells) produce the Env protein of a human endogenous retrovirus, HERV-E 4-1, in a subgroup of interstitial lung diseases.
Ok I'll try and explain where the research is going and why retroviruses are also likely to appear in white blood cells or macrophages in response to real infections of bacteria and fungi (the retroviruses being functional and already in the macrophage/WBC DNA.)
The white blood cell monocytes or baby white blood cells join together into what they call 'giant cell multinucleated cells', this is in response to large infections, lots of dead cell debris, foreign bodies lodged in the body, anything that needs to be removed etc.
So baby monocyte cells look like they join together into what I call "Giant death star white blood cells" or macrophages made of many immature white blood cell monocytes bound together with retroviruses creating cell fusions.
TB and malaria are prime cases where giant cells are seen as a response to remove quite big bugs.
"Macrophages undergo fusion with other macrophages to form the hallmark multinucleated giant cells of chronic inflammation. However, neither the existence of distinct morphological types of giant cells, the signaling pathways that induce their formation, the molecular mechanism(s) of macrophage fusion, nor the significance of macrophage multinucleation at chronic inflammatory sites are well understood. Our efforts have been focused on these unknowns, particularly as they relate to the foreign body-type giant cells that form on implanted biomaterials and biomedical devices"
Macrophage fusion and multinucleated giant cells of inflammation.
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It is also how bone and bone reformation is done, cell fusion is necessary, this also happens with eyes, muscles and more and we are only beginning to work it out.
Osteoclasts and giant cells: macrophage-macrophage fusion mechanism.
Well it gets more interesting because tumours, leukemias and all autoimmune diseases express retroviruses, especially the very common HERV-K retrovirus which has been found in blood, muscle and more. HERV-K levels rise at the same levels of so called HIV in patients who get ill.
HERV-K also appears in tumours where it is actually releasing env proteins and causing multinucleated cells, so the env in all our retroviruses is the same as the gp120 protein supposedly attributed to being a part of HIV, but all our retroviruses have envelopes or env proteins.
So this is what they do, the retroviruses actually fuse cells together. sometimes that's needed, in the case of cancer it's not a good thing, with babies it's normal part of growing which is why kids have higher levels of retroviruses.
"Our results support the notion that proteins encoded by HERV K can mediate intercellular fusion of melanoma cells, which may generate multinuclear cells and drive the evolution of genetic changes that provide growth and survival advantages." 2013
Human endogenous retroviral K element encodes fusogenic activity in melanoma cells.
In the case of successful pregnancy the HERV-W retrovirus has to work so that the entire remodeling process of the uterus and blood supply and fetal attachment can occur so in experiments where they checked levels of the placental HERV-W retrovirus in pregnant women the lower levels of HERV-W retrovirus were indicative of failed pregnancies.
"Low Syncytin expression in both cultured cytotrophoblasts and primary tissues from pathological placentas supports an intrinsic placenta-specific deregulation of cell-cell fusion in the formation of syncytiotrophoblasts leading to increased apoptosis. These processes could contribute to the development and severity of Preeclampsia (PE), Hemolysis Elevated Liver Enzymes and Low Platelets (HELLP)-syndrome, and intrauterine growth restriction (IUGR)"
Impaired cytotrophoblast cell-cell fusion is associated with reduced Syncytin and increased apoptosis in patients with placental dysfunction.
When a wound happens retroviruses will even appear not only in normal cells but in the T-cells, this was a rather horrid 2013 experiment where they burnt mice and the retroviruses from the mouse genome start doing things at certain times post burning.
Cell fusion and macrophage remodeling of collagen is all happening in wound healing, in the case of wounds the white blood cells are literally needed to dissolve old cells and get them out of the way to repair the damage.
So retroviruses may fuse macrophages together and also fuse other cells, we are just learning now.
"Murine leukemia virus-type endogenous retroviruses (MuLV-ERVs) constitute ~10% of the mouse genome and are associated with various pathophysiologic processes. In this study, we examined whether MuLV-ERVs’ response to burn-elicited stressors is specific for certain lymphocyte populations and/or locations of lymphoid organ.”
“MuLV-ERVs’ response to burn-elicited stressors may be differentially controlled depending on lymphocyte type, location of lymphoid organ, MuLV-ERV type, and stress duration.
Injury-elicited stressors alter endogenous retrovirus expression in lymphocytes depending on cell type and source lymphoid organ
In another recent 2013 study the T-cells of people with Lupus were expressing retroviruses with hypomethylation of their DNA as well.
Lupus is a potentially deadly autoimmune disease with symptoms that could easily get labelled as AIDS.
DNA methylation of human endogenous retrovirus in systemic lupus erythematosus.
So the T-cells of people with lupus have dysfunctional DNA and express retroviruses.
'Why' - should be the next question.
Lupus studies have also shown consistently that up to one third of people with Lupus can look HIV+.
So given that their T-cells are activated and showing retroviral activity what is the HIV antibody test actually detecting?
Is it anything meaningful at all?
"22 of 61 systemic lupus erythematosus (SLE) patients produced antibodies to the p24 gag protein of HIV-1 demonstrated by Western blotting." 1990
A conserved idiotype and antibodies to retroviral proteins in systemic lupus erythematosus.
"We have previously demonstrated that about one-third of patients with either Sjögren’s syndrome (SS) or systemic lupus erythematosus (SLE) react to human immunodeficiency virus (HIV) p24 core protein antigen without any evidence of exposure to, or infection with, HIV itself. " 1998
Reactivity of Sera from Systemic Lupus Erythematosus and Sjögren’s Syndrome Patients with Peptides Derived from Human Immunodeficiency Virus p24 Capsid Antigen
If you go back to the beginning and in light of what we know now about cancers fusing together with retroviruses then the symptoms of HTLV-III make more sense, patients had tumours forming and we also see the same phenomena in Multiple Sclerosis.
"It has been postulated that the retrovirus HTLV-III/LAV thought to be the etiologic agent of AIDS also infects the central nervous system and directly causes AIDS encephalopathy. Electron microscopical studies performed on brain sections from three patients with AIDS complicated by progressive encephalopathy revealed structures morphologically consistent with HTLV-III/LAV retrovirus particles. The particles were located principally within multinucleated giant cells but were also present in astrocytes. Many particles were also noted in the extracellular space." 1984
HTLV-III/LAV-like retrovirus particles in the brains of patients with AIDS encephalopathy
Well remember the HERV-W retrovirus that is expressed in the placenta?
It has an envelope and also appears in Multiple Sclerosis and dementia, so this is what HIV viral load tests can detect but they are the envelopes or env proteins of all our retroviruses or 'the gp120 proteins of HIV' as doctors call them.
HERV-W is also expressed highest in the brains of children compared to adults so obviously it is not a pathogenic retrovirus if the placenta and children have the highest levels.
Multiple Sclerosis also has retroviruses like HERV-W causing giant cells and multinucleated cells and is no different to the symptoms detected in 'AIDS' patients by Gallo and co in 1984.
"Endogenous retroviruses in the human DNA probably result from an exogenous infection of germ line cells. ERV-W family has been determined to have entered the mammalian genome after the speciation of old world monkeys, with initial insertion in Catarrhines about 25 million years ago (Voisset et al., 1999). ERV-W copies are present in old world monkeys, superior primates and in humans (then named HERV-W).
HERV-W encodes and may express an envelope protein (ENV), which activates a pro-inflammatory and autoimmune cascade through interaction with Toll-Like receptor 4 (TLR4) on antigen-presenting cells. The specific association of HERV-W RNA with circulating virion particles (previously named ''Multiple Sclerosis associated Retroviral element'', MSRV) with Multiple Sclerosis disease, its evolution and prognosis has been repeatedly reported.
The role of certain viral infections as triggers for HERV-W expression has also been characterised. This ENV protein was evidenced by several independent RT-PCR and immunohistological studies in MS brain lesions post-mortem.
Using a specific ELISA for HERV-W ENV protein, we report a significant clustering of ENV antigenaemia in about 75% of MS sera ex-vivo. Large cohorts of blood donors revealed positive antigenaemia in few healthy individuals only (p less than 0,001).
Moreover, HERV-W ENV protein is shown to reproduce the ''Experimental Encephalomyelitis'' MS animal model (EAE) with important inflammatory demyelination evidenced by MRI and histology, as well as anti-myelin autoimmunity. In this MS model, selected anti-ENV monoclonal antibody (mAb) significantly inhibited clinical symptoms compared to untreated controls. Untreated ''ENV EAE'' mice all died while treated animal survived.
These results now pave the way to the first clinical assessment of a therapeutic agent targeting a human endogenous retroviral protein in a human disease. This anti-ENV mAb has now been humanised and is subjected to pre-clinical studies."
HERV-W envelope is significantly expressed in Multiple Sclerosis and causes neuroinflammation in animal models with specific antibody inhibition
Now here's the messed up catch 22 in which everyone arguing about HIV and the immune system have to face, the monocytes themselves express retroviruses and so do the macrophages, the immune system itself is often the cause of problems in Multiple Sclerosis because macrophages are attacking the nervous system's myelin sheath, no different from the symptoms where HTLV-III or HIV as it was later renamed were detected in 1984.
B cells and monocytes from patients with active multiple sclerosis exhibit increased surface expression of both HERV-H Env and HERV-W Env, accompanied by increased seroreactivity
There is no difference, HIV and the other endogenous retroviruses appear together with same symptoms and in monocytes or baby white blood cells.
"Compared with controls, HERV-W and HERV-K expression was increased in brain tissue from patients with multiple sclerosis or human immunodeficiency virus infection or AIDS, with concomitant elevated tumor necrosis factor-alpha levels. Similarly, elevated HERV-W levels were detected in patients with Alzheimer's dementia only when tumor necrosis factor-alpha expression was also evident (2 of 6 cases). The detection of several HERVs in inflammatory brain diseases and the capacity to augment HERV expression in monocytes with compounds that influence cellular activity suggest that increased expression of these viruses is a consequence of increased immune activity rather than causative of distinct diseases.”
Monocyte activation and differentiation augment human endogenous retrovirus expression: implications for inflammatory brain diseases.
The way the research is heading indicates retroviruses will be part of the cell fusion process in macrophages and hence when infected with TB for instance the monocytes bind together to form giant cells, it's an immune response to make white blood cells bigger and tougher.
"Multinucleated giant cells (MGC), a characteristic feature of tuberculous granulomas, form by fusion of monocytes or macrophages, but little is known about the mechanism of the fusion process itself."
Generation of Multinucleated Giant Cells In Vitro by Culture of Human Monocytes with Mycobacterium bovis BCG in Combination with Cytokine-Containing Supernatants
In the case of cancer, the immune system can be reversed and macrophages can fuse to the cancer cells and then act to degrade any collagen in the way, so the immune system itself often spreads cancer when macrophages actually bind to tumour cells and then act by removing obstacles for the cancer cells.
You can see where it's all going in regards to HIV, Robert Gallo was a cancer virus doctor looking for the 'viral' infection when the Catch 22 is that both cancer cells fuse with retroviruses and so do immune macrophage cells. So Gallo detected retroviruses in patients with cancers or leukemia while the activated immune system itself in these patients also had active retroviruses creating cell fusions and giant cell immune cells.
"Specifically, how cancer cells evade immune surveillance and gain the ability to navigate the circulatory system remains a focus. One possible mechanism underlying metastatic conversion is fusion between blood-derived immune cells and cancer cells. While this notion is a century old, in vivo evidence that cell fusion occurs within tumors and imparts genetic or physiologic changes remains controversial. We have previously demonstrated in vivo cell fusion between blood cells and intestinal epithelial cells in an injury setting. Here, we hypothesize that immune cells, such as macrophages, fuse with tumor cells imparting metastatic capabilities by transferring their cellular identity."
Fusion between Intestinal epithelial cells and macrophages in a cancer context results in nuclear reprogramming.
The HIV antibody tests don't detect retroviruses, they measure immune response to some antigens, mostly random, and the claim is the immune system response to these antigens is to HIV???
But p24 proteins attributed to 'HIV' are a normal part of cell trafficking in mammals and yeast so they are common.
The viral load tests pick up actual retroviral pieces but since the envelope of retroviruses are involved in so many of the body's cell fusion processes it's not a surprise that if macrophages themselves bind together using retroviral envelopes then this is what HIV env bits do as well so we are still at square one.
In this study 'HIV' env just fused macrophages together, this is not a big deal, that happens all the time in cells using our retroviruses.
This is just the process of making 'giant multinucleated cells'.
"Our results suggest that primary macrophages are sensitive to cell-to-cell but not to virion-to-cell fusion induced by the envelope glycoproteins of several T-cell tropic HIV-1 strains."
Cell-to-cell fusion, but not virus entry in macrophages by T-cell line tropic HIV-1 strains: a V3 loop-determined restriction.
If the 'HIV' viral load tests are picking up env and gag proteins of retroviruses and the symptoms of 'AIDS' dementia compared to multiple sclerosis or dementia are no different there is no cause at all in saying a patient is HIV+ due to the presence of unrelated antibodies.
The same retroviral pieces appear in AIDS, dementia, MS, Cancer, leukemia, arthritis, psoriasis and so on, in fact anyone who is sick will have extra retroviruses active.
2005 "Antigen expression of a human endogenous retrovirus family, HERV-W, in normal human brain and multiple sclerosis lesions was studied by immunohistochemistry by three independent groups. The HERV-W multicopy family was identified in human DNA from the previously characterized multiple sclerosis-associated retroviral element (MSRV). A panel of antibodies against envelope (ENV) and capsid (GAG) antigens was tested. A physiological expression of GAG proteins in neuronal cells was observed in normal brain, whereas there was a striking accumulation of GAG antigen in axonal structures in demyelinated white matter from patients with MS. Prominent HERV-W GAG expression was also detected in endothelial cells of MS lesions from acute or actively demyelinating cases, a pattern not found in any control. A physiological expression of ENV proteins was detected in microglia in normal brain; however,a specific expression in macrophages was apparently restricted to early MS lesions. Thus, converging results from three groups confirm that GAG and ENV proteins encoded by the HERV-W multicopy gene family are expressed in cells of the central nervous system under normal conditions. Similar to HERV-W7q ENV (Syncitin), which is expressed in placenta and has been shown to have a physiological function in syncytio-trophoblast fusion, HERV-W GAG may thus also have a physiological function in human brain."
Human endogenous retrovirus (HERV)-W ENV and GAG proteins: physiological expression in human brain and pathophysiological modulation in multiple sclerosis lesions.
Here they are talking about multinucleated cells and the role of retroviruses...
2011. "The overall focus of this review is the characterization and functional role of cell–cell fusions in connection with human endogenous retroviruses (HERV ) in cancer. Examples of multinucleated cells presented include placental syncytiotrophoblasts, muscle myotubes, bone osteoclasts involved in normal human development and cell–cell fusions detected in tumors. Examples of multinucleated cells in various cancers include germ cell tumors, glioblastoma, melanoma, lung, breast, ovarian and endometrial carcinomas. The role of different HERV-envelope proteins mediating fusion or regulation of cells in tumors is highlighted. Although multinucleated cells are detected in various tumors, their origin, functional role and overall cellular fate are ambiguous. The effect of multiple cancer cells fusing and in contrast cancer cells fusing with somatic cells is also discussed. Understanding tumorigenesis has to ultimately link the knowledge between the function and action of multinucleated cells, cell fusion, HERVs, retroviruses and cell signalling pathways."
Cell–Cell Fusions and Human Endogenous Retroviruses in Cancer
So this is what they saw back in 1984 and claimed was sexually transmitted retrovirus HTLV-III being HIV, the usual cell fusions with retroviruses that are occurring in cancer or MS.
1987 "In an autopsied case of a 37-year-old man with acquired immune deficiency syndrome (AIDS), multinucleated giant cell encephalopathy was noted in close proximity to multiple nodules of primary lymphoma of the brain. Some multinucleated giant cells and macrophages contained HTLV-III-like viral particles."
Nuclear bridges in multinucleated giant cells associated with primary lymphoma of the brain in acquired immune deficiency syndrome (AIDS)
Remember - many of these poor people were tagged HIV+ on the basis of the HIV antibody tests which is another whole story of fraudulence.
1986 "Examination of the brains of these children at autopsy revealed a unique constellation of findings, including varying degrees of diminished brain weight in all cases, inflammatory cell infiltrates in nine brains, multinucleated cells in eight, three of which also contained multinucleated giant cells, vascular calcification in ten, vascular and perivascular inflammation in five, and white matter changes in nine. Inflammatory and vascular lesions were most prominent in basal ganglia and pons. LAV/HTLV-III retroviral particles, associated with multinucleated giant cells, were observed in two brains on electron microscopic examination."
Pathologic features of AIDS encephalopathy in children: evidence for LAV/HTLV-III infection of brain.
So all they were seeing in 1983/84 were retroviral particles.
30 years of claims about retroviruses have now muddled science to the point where it has got so lost we are all in trouble, careers have been built on sand, an estimated 50 billion dollars could be spent a year on blaming our own retroviruses for normal disease while the world is becoming more toxic, water supplies becoming contaminated and good healthy food supplies are running out.
Virology can never fix toxicology but this is where we are in the 21st century, facing a very bleak toxic future with a health profession that has literally lost its marbles.
1983 "It has been postulated that the retrovirus HTLV-III/LAV thought to be the etiologic agent of AIDS also infects the central nervous system and directly causes AIDS encephalopathy. Electron microscopical studies performed on brain sections from three patients with AIDS complicated by progressive encephalopathy revealed structures morphologically consistent with HTLV-III/LAV retrovirus particles. The particles were located principally within multinucleated giant cells but were also present in astrocytes. Many particles were also noted in the extracellular space.”
HTLV-III/LAV-LIKE RETROVIRUS PARTICLES IN THE BRAINS OF PATIENTS WITH AIDS ENCEPHALOPATHY
And this is where it's finally hitting the light of day while the rest hits the fan.
This 2013 study is mumbling about sperm to egg cell fusions.
If you catch the line towards the end it says "Secondly, there are similarities between the generation of retroviruses in the host cells and the formation of small cellular vesicles, termed exosomes, in mammalian cells."
Which means sperm have active retroviruses needed for the cell fusions to occur with the egg.
"In mammals, two integral membrane proteins, sperm IZUMO1 and egg CD9, regulate sperm–egg fusion, and their roles are critical, but yet unclear. Recent studies, however, indicate interesting connections between the sperm–egg fusion and virus-induced cell–cell fusion. First, CD9-containing exosome-like vesicles, which are released from wild-type eggs, can induce the fusion between sperm and CD9-deficient egg, even though CD9-deficient eggs are highly refractory to the fusion with sperm. This finding provides strong evidence for the involvement of CD9-containing, fusion-facilitating vesicles in the sperm–egg fusion. Secondly, there are similarities between the generation of retroviruses in the host cells and the formation of small cellular vesicles, termed exosomes, in mammalian cells. The exosomes are involved in intercellular communication through transfer of proteins and ribonucleic acids (RNAs) including mRNAs and microRNAs. These collective studies provide an insight into the molecular mechanism of membrane fusion events."
Critical role of exosomes in sperm–egg fusion and virus-induced cell–cell fusion
CD9 is also a 24kDa protein involved in "cell fusion, migration and cancer progression" in tumours.
Everything claimed as infectious by modern science has already been there for millions of years.
Keep thinking about it and ask 'Can toxic drugs fix this problem??"