The more we research HIV, the less we seem to know about it.
After close to 30 years of research and billions spent, we have no cure, we have no vaccine, no proper prevention. We don't even have a clue about the mechanism HIV supposedly uses to cause degradation of the immune system.
Cal Crilly has gone down the rabbit hole again to put together some of that research. Apparently the 'virus' is found in situations that are part of normal human biology, of our defenses connected with heart disease and perhaps even cancer. Here are Cal's notes, in case you would like to follow this matter of HIV down to its - so far - illogical conclusion.
Caution: It's all speculative, although based on real research from the mainstream of medicine...
This may make some sense ... my brain notes, all speculation
I think I've gone down the rabbit hole far enough now
This is all just speculation but all HIV is just speculation, tuck it away for the brain to process along with all the other thousands and thousands of arguments about what HIV is and how can something so small cause so many deaths etc.
I'm just writing it down.
Regardless I think it points to the fact that if you eat well and avoid toxic things then all these things they measure will go away.
Many people have their negative test results from the doctor to prove it.
My 70 year old HIV+ friend said this about my email on 'what HIV could do' below.
- - -
"Hi Cal- very interesting- why does HAART reduce p24 in blood but not in the GI Tract?
What is the role of Treg cells and the liver?
What is really measured with p24?
Does it measure DNA/RNA?
What if there was a simple test that measured DNA/RNA?
Why does RNA increase with infection?
Why do so many HIV people have CFS and co-infections?
What is the effect of aging?
The role of fat/TG's has been shown with HCV.
More people are now dying from HCV than HIV-1.
Statins reduce HCV.
The latest numbers show people on HAART are dying from liver failure.
I get my new blood numbers Monday-not that I pay a lot of attention to them.
I feel a simple test is needed for all chronic conditions-hopefully the same test, as I believe there is a common cause and it lies in a combination of chromosomal and epigenetic genes which affects methylation, lipids, hormones and immune function, which gets worse with age.
Therefore, aging and chronic disease should have the same cause-definitely lipids are part of it."
There are so many questions because the prevailing version of HIV/AIDS makes no sense.
and I replied... "and basically when it comes down to the simple things enough Vitamin C and Lysine will make your collagen and arteries.
Good fats make the T-cells function as well as lipid walls stay intact.
Oxidised fats wreck T-cells and lipid walls.
And paying attention to B12, Folate, B6, Copper and Vitamin C absorbs Iron and prevents anemia before it ever reaches the bugs creating infections.
Ensuring a balanced pH in the body is needed also to prevent Iron disorders which lead to AIDS, Cancer, Autoimmune and Heart disease.
All infections are a fight to get the iron we eat into hemoglobin so we can breathe before bacteria, fungus and parasites already on us and around us get it.
Proper methylation nutrients B12, Folate, B6, Choline and Selenium ensure genes stay methylated.
This stops retroviruses jumping out of the genome too much but they have purpose.
And adequate Retinoic acid or Vitamin A with Vitamin D or Sunlight ensures our cells get the signals to grow and differentiate.
Vitamin A and estrogen being the natural signalling molecules for both retroviruses and cell growth
That pretty much fixes up most underlying disease."
avoiding poisons too
- - -
So this is what happens when researchers get obsessed with one thing and don't look at other research or at the world around them
We will start out with a description of heart disease.
Not a word about HIV...
"Cardiovascular disease, a leading cause of mortality worldwide, is caused mainly by atherosclerosis, a chronic inflammatory disease of blood vessels. Lesions of atherosclerosis contain macrophages, T cells and other cells of the immune response, together with cholesterol that infiltrates from the blood. Targeted deletion of genes encoding costimulatory factors and proinflammatory cytokines results in less disease in mouse models, whereas interference with regulatory immunity accelerates it. Innate as well as adaptive immune responses have been identified in atherosclerosis, with components of cholesterol-carrying low-density lipoprotein triggering inflammation, T cell activation and antibody production during the course of disease. Studies are now under way to develop new therapies based on these concepts of the involvement of the immune system in atherosclerosis." (2011 from Nature.)
The immune system in atherosclerosis
"Lesions of atherosclerosis contain macrophages, T cells and other cells of the immune response, together with cholesterol that infiltrates from the blood."
HIV appears in "Lesions of atherosclerosis, macrophages and T cells" as everyone knows but it also synthesizes LDL cholesterol and transports it to the sites of lesions. So when they mutated "Nef became unable to transport newly synthesized cholesterol into lipid rafts"
"HIV buds from lipid rafts and requires cholesterol for its egress from and entry into cells. Viral accessory protein Nef plays a major role in this process. In this study, it not only increased the biosynthesis of lipid rafts and viral particles with newly synthesized cholesterol, but also enriched them. Furthermore, via the consensus cholesterol recognition motif at its C terminus, Nef bound cholesterol. When this sequence was mutated, Nef became unable to transport newly synthesized cholesterol into lipid rafts and viral particles. Interestingly, although its levels in lipid rafts were not affected, this mutant Nef protein was poorly incorporated into viral particles, and viral infectivity decreased dramatically. Thus, Nef also transports newly synthesized cholesterol to the site of viral budding. As such, it provides essential building blocks for the formation of viruses that replicate optimally in the host. 2003
Nef increases the synthesis of and transports cholesterol to lipid rafts and HIV-1 progeny virions
Nef induces multiple genes involved in cholesterol synthesis and uptake in human immunodeficiency virus type 1-infected T cells. 2005
But using Protease inhibitors just makes heart disease worse so why would stopping a retrovirus from working make a person sicker?
"The currently available data strongly suggest that HIV protease inhibitors negatively impact the cardiovascular system. As is often the case with complex diseases like atherosclerosis it appears that HIV protease inhibitors affect the cardiovascular system through several distinct mechanisms by affecting various components of the arterial wall directly or indirectly by influencing lipoprotein and glucose metabolism of the body." 2007
How HIV protease inhibitors promote atherosclerotic lesion formation. 2007
And why is HIV dumping synthesizing LDL cholesterol and leaving fat around the place???
"Macrophages play a central role in the pathogenesis of atherosclerosis and are also a host for a number of viruses, most importantly, HIV. Many viruses, including HIV, require cholesterol for their replication and as a structural element. Cholesterol also plays a pivotal role in innate antiviral immune responses. Although impairing innate immune response by increasing cell cholesterol content may be a deliberate strategy used by a pathogen to improve its infectivity, enhancing the risk of atherosclerosis is likely a byproduct. Consistent association between HIV infection and elevated risk of atherosclerosis suggested a connection between virus-induced changes in cholesterol metabolism and atherogenesis, but the mechanisms of such connection have not been identified." 2006
Human immunodeficiency virus infection and macrophage cholesterol metabolism
I'll say HIV is possibly binding the fat together at the sites of wounds and also synthesizing and pumping LDL cholesterol into a wound to start repair.
And without the right type of good cholesterol that is not oxidised the entire arterial system goes wrong.
And AIDS scientists measure it with their machines while Heart disease scientists measure with different machines.
"We have shown that HIV budding occurs at cholesterol-rich membrane microdomains called lipid rafts. This observation prompted us to examine the role in HIV entry of cholesterol in the membrane of cells. We recently reported that host cell cholesterol is required for HIV infection."
"Our results show that removal of cholesterol from the membrane of HIV-infected cells dramatically lowered virus release and that virions released from cholesterol-depleted cells are minimally infectious. Exposure of infectious HIV particles to beta-cyclodextrin resulted in a dose-dependent inactivation of the virus. In both cases, the effect was attributable to loss of cholesterol and could be reversed by replenishing cholesterol."
"The results indicate that cholesterol in HIV particles is strictly required for fusion and infectivity. These observations in combination with those of past studies indicate beta-cyclodextrin to be an excellent candidate for use as a chemical barrier for AIDS prophylaxis." 2006
Lipid rafts and HIV pathogenesis: virion-associated cholesterol is required for fusion and infection of susceptible cells.
I wouldn't use beta-cyclodextrin, it will dissolve your fat and cause bleeding.
So HIV may be just a form of RNA to transport LDL cholesterol around via vesicle budding using lipid rafts.
Lipid rafts being a whole new bunch of cell transport discoveries this last decade or so.
They didn't have pictures of lipid rafts until recently, bear in mind HIV is attached to lipid rafts via caveolin in studies.
HIV even binds in particular via gp41 to caveolin which is attached to lipid rafts.
"Caveolin-1 is a scaffolding protein that organizes and concentrates specific ligands (sort of lock and key signal molecules) within the caveolae membranes."
"Caveolin 1 (Cav-1) is a major protein of a specific membrane lipid raft known as caveolae. Cav-1 interacts with the gp41 of the human immunodeficiency virus (HIV) envelope, but the role of Cav-1 in HIV replication and pathogenesis is not known. In this report, we demonstrate that HIV infection in primary human monocyte-derived macrophages...and CD4 cells results in a dramatic upregulation of Cav-1 expression mediated by HIV Tat." 2010
HIV Infection Upregulates Caveolin 1 Expression To Restrict Virus Production 2010
Once you put more caveolin in to the mix though, HIV binds to it and stops replicating??? Why?
"Caveolin 1 (Cav-1), the scaffold protein of a specific membrane lipid raft called caveolae, has been reported to suppress HIV-1 replication." 2011
Caveolin 1 Inhibits HIV Replication by Transcriptional Repression Mediated through NF-κB
Membrane lipids and vesicular traffic
All new - remember, they have just worked out that fat is needed for moving things around, what does this do for the anti-cholesterol campaign?
"the contribution of lipids to membrane trafficking has been neglected for too long. "In our model, the membrane lipids themselves are functionally involved in the sorting process. There are a few thousand genes involved in lipid synthesis, metabolism, and regulation in mammalian cells. The diversity of lipid species is there for a reason." 2009
Lipid rafts inflate at the trans-Golgi
And for the nervous system to work.
"Historically, the lion's share of the attention has been focused on the proteins that are involved in this cycle; but, in recent years, it has become clear that the previously unheralded plasma membrane and vesicle lipids are also key regulators of this cycle. This article reviews recent insights into the roles of lipid-modifying enzymes and lipids in the acute modulation of neurotransmission." 2005
Lipid regulation of the synaptic vesicle cycle
Vesicles are basically a description of what HIV does.
"The formation of vesicles by budding from cell membranes is essential to a variety of biological functions. Small vesicles are extruded from membranes to transport cargo from one compartment to another. Notable examples of this interplay between proteins and lipid membranes1 include exocytosis of enveloped viruses,2 transport in the Golgi apparatus and endoplasmic reticulum,3 and signaling in neuron synapses.4" 2009
Vesicle Budding Induced by a Pore-Forming Peptide
HIV can get across cells.
"Cell-penetrating peptides (CPPs), such as the HIV TAT peptide, are able to translocate across cellular membranes efficiently."
It's bendy like a vesicle.
A vesicle being a bubble of fat that transports a protein or anything chemical required out of the cell.
"A plethora of mechanisms of action have been proposed for exogenous Tat to explain the pleiotropic, and sometimes controversial, extracellular effects reported for this molecule." 1998
HIV-1 Tat: a polypeptide for all seasons
Buds from a cell like a vesicle.
"The transactivator protein of human immunodeficiency virus type 1 Tat has the unique property of mediating the delivery of large protein cargoes into the cells when present in the extracellular milieu. Here we show that Tat fusion proteins are internalized by the cells through a temperature-dependent endocytic pathway that originates from cell membrane lipid rafts and follows caveolar endocytosis." 2003
Cell membrane lipid rafts mediate caveolar endocytosis of HIV-1 Tat fusion proteins.
HIV appears in the same Golgi and Endoplasmic reticulum cell factories that vesicles do.
The assembly of HIV within the Golgi apparatus and Golgi-derived vesicles of JM cell syncytia 1991
Macrophage bridging conduit trafficking of HIV-1 through the endoplasmic reticulum and Golgi network. 2011
And protease inhibitors supposedly great for stopping HIV just wreck the Endoplasmic Reticulum so are terrible for cells.
HIV protease inhibitors induce endoplasmic reticulum stress and disrupt barrier integrity in intestinal epithelial cells.
Has anyone ever wondered whether HIV budding from cells are just plain vesicles from the Endoplasmic Reticulum and Golgi Apparatus factories sending out a cholesterol 'retrovirus carrying packages'?
Or Vesicles of RNA?
Because that is where p24 proteins turn up too.
Is the HIV core p24 antigen that defines being 'infected with AIDS' a HIV p24 or vesicle p24????
"Please explain" is the term required here.
"The trafficking of proteins in the secretory pathway is mediated by vesicles. Proteins of the p24 family are present on the membranes of secretory pathway organelles (ER, Golgi, COPI and COPII vesicles). Evidence exists showing that p24 proteins play a role in the development of Alzheimer disease, making them an interesting research subject. Their presence in the secretory pathway and their tissue-dependent expression levels suggest that p24 proteins are involved in secretion. However, their molecular function is not clear. Several potential functions have been proposed for p24 proteins: (1) that they function as receptors for selected cargo; (2) that they regulate vesicle biogenesis; (3) that they perform structural and morphogenetic functions in the secretory pathway; (4) that they are responsible for quality control of transported proteins. In this article, we provide a critical review of the postulated functions of p24 proteins. 2010
The p24 family proteins--regulators of vesicular trafficking
So onto CD4 T-cells and heart disease. Does Oxidized LDL cause the T-cell and arterial cell death that HIV is blamed for???
End stage kidney patients: Here, yes, Oxidized LDL may kill CD4 T-cells.
"Oxidized LDL (oxLDL) are cytotoxic to vascular cells, but their possible toxic action on T cells from patients with ESRD has not been evaluated" 2006
Oxidized Low-Density Lipoproteins Activate CD4+ T Cell Apoptosis in Patients with End-Stage Renal Disease through Fas Engagement
Yes 'Oxidized LDL are cytotoxic to T-cells' again...
"Oxidized low density lipoproteins (oxLDLs) and activated T lymphocytes are present in early atherosclerotic plaques.
It has been shown that oxLDLs are cytotoxic to cultured vascular cells but their possible toxic action on T lymphocytes
has not been described.
Peripheral blood lymphocytes from healthy individuals were stimulated in vitro with the polyclonal activator phytohemagglutinin and treated
with various doses of native and mildly oxidized LDLs.
Lowdoses of oxLDLs inhibited cell growth and DNA synthesis after 48 h culture..." 1999
Oxidized low density lipoproteins induce apoptosis in PHA-activated peripheral blood mononuclear cells and in the Jurkat T-cell line
When trophoblast cells which guide new blood vessels and attach the fetus to the placenta in pregnancy were exposed to oxidized LDLs instead of good LDL they couldn't work.
"We demonstrated using this invasion assay that oxLDL, but not native LDL, inhibited cell invasion in a concentration-dependent manner."
Oxidized low-density lipoproteins inhibit trophoblastic cell invasion.
The cell invasion in trophoblasts has a placental retrovirus called HERV-W involved.
As I wrote here:
"Retroviruses kick into action when pregnant and are involved in creating the blood supply to the fetus so if they are not working properly the blood flow is less and the fetus can starve from lack of nutrients.
Around the year 2000 a few studies came online about a so called retrovirus called HERV-W.
HERV-W or Syncytin was found to be a part of the trophoblast cells that surround fetal cells in pregnancy. The trophoblast cells do amazing things where they remodel arterial walls and divert blood from the mother's spinal artery and feed the baby with the blood supply."
What Retoviruses Do When Pregnant?
So in my book, 'oxidized LDLs' or damaged rusting cholesterol are causing cell death - not retroviruses.
This is what happens with 'HIV' infection.
"A critical event in the early stages of atherosclerosis is the focal accumulation of lipid-laden foam cells derived from macrophages." 2001
Role of oxidized LDL in atherosclerosis.
"HIV-infected and Nef-transfected macrophages accumulated substantial amounts of lipids, thus resembling foam cells."
Human Immunodeficiency Virus Impairs Reverse Cholesterol Transport from Macrophages
So is HIV just there because heart disease is there?
HIV emerges from activated HLA-DR genes and in lesions as I first wrote down here and it is all speculation.
All of HIV/AIDS has been speculation for 28 years as it was never peer reviewed and no argument was allowed in public.
So I can speculate.
Aids and Arteries - The smooth muscle CD4 connection
"This study demonstrates that DR expressed on CD4+ T cells dramatically increases HIV-1 expression. Virus production in DR+ cells was > 10-fold higher than in DR- cells as measured by p24 production. Moreover, two T cell lines that were derived from the same parental cell, one DR+ and the other DR-, differentially expressed HIV-1 following transfection with full-length HIV-1 clone as determined by luciferase.
Viral expression in DR+ transfectants were up to 20-fold higher than the DR- counterparts."
HLA-DR on T cells enhances HIV-1 expression. (this study from NIH is now offline)
This study below just indicates lesions happen in sick people and so HLA-DR will be around in the lesions until the lesions either fix or get worse, of course AIDS drugs keep the lesions open so don't work, they just lower HIV measurements.
Incorporation of HLA-DR into the Envelope of Human Immunodeficiency Virus Type 1 In Vivo: Correlation with Stage of Disease and Presence of Opportunistic Infection
But studies are everywhere showing this that HIV can be coming out of our MHC antigens or the HLA-DR ones in particular and mostly when HLA-DR is activated in lesions.
More from me on this subject.
Retroviral Talk: Is HIV Just in Lesions?
So this could be what happens below, without the (MHC antigens or HLA-DR on Monocytes) working with 'HIV' in them "oxidised low density lipoproteins (oxLDL) induced a state of apoptosis in T lymphocytes cultured in the absence of monocytes."
T-cell death from rusting cholesterol to simplify.
And "The expression of the HLA-DR marker and the B7.2 protein were up-regulated in monocytes exposed to oxLDL" means HLA-DR activates monocytes with 'HIV' possibly appearing in them actually respond to the oxidised fat.
In other words 'HIV' has nothing to do with the T-cells dying, it's just bad fats and HIV or HERV-K or any of our retroviral bits may be binding via HLA-DR to let monocytes clear up the bad fat or even preparing new cell growth via cell to cell fusion.
We still don't know obviously and to me it all looks like it is about structural changes in blood vessels and lesions. Which can't be fixed with drugs or vaccines.
"Atherosclerosis has been implicated in myocardial infarction, stroke and a host of cardiovascular diseases. The presence of activated T lymphocytes and macrophages, and the increased expression of HLA-DR antigen are consistent with the notion of immune activity in the atherosclerotic plaque. The nature of the causative antigen has not been established although oxidised low density lipoproteins (oxLDL) that accumulate in atherosclerotic plaques could fulfil this role. Here, we report that monocytes play a key role in influencing the fate of purified peripheral human T lymphocytes from healthy donors when the cells are exposed to LDL oxidised under the controlled conditions of water radiolysis. Our data showed that oxLDL generated under these conditions were chemoattractants for T cells. However, they induced a state of apoptosis in T lymphocytes cultured in the absence of monocytes. The extent of apoptosis was related to the degree of oxidation of LDL and the time of T cell exposure to oxLDL. OxLDL-dependent apoptosis did not involve a scavenger-like receptor. CD4(+) cells were more sensitive to the apoptotic effect of oxLDL than CD8(+) cells."
"The expression of the HLA-DR marker and the B7.2 protein were up-regulated in monocytes exposed to oxLDL but not to natLDL. The levels of B7.1 were unchanged. Our data are consistent with the notion that monocytes are critical for T cell survival in the presence of oxLDL and MHC-restricted T cell proliferative response to oxLDL."
Monocytes influence the fate of T cells challenged with oxidised low density lipoproteins towards apoptosis or MHC-restricted proliferation.
But when HLA-DR genes didn't activate in dying patients they died so if HIV comes out of HLA-DR+ activated genes it is also needed for wound repair which is why AIDS drugs stop HIV but the lesions keep open.
Basically in the end HIV/AIDS is either about heart disease or cancer.
Plus Anemia and/or Iron overload leading to infections and inflammatory diseases.
The basic causes of heart disease, cancer or AIDS are Iron overload and inflammation and they can't be fixed with allopathic drugs.
And doctors are not always educated in the nutrients for treating Anemia and/or Iron overload.
Or balancing methylation of DNA which can be chapters worth to describe.
Or fixing collagen and our structure.
We know now how to guide all of these diseases to a better outcome and the studies are all being done so the fixes can be common knowledge and will be in the future.
There is just a monopoly on belief at the moment and for alternative health it's a case of picking up the pieces after chemo.
This will change.
So once you get past the long words, AIDS is all the diseases we die of - complicated by bizarre drugs.
Any thoughts welcome but you'll have to think about it yourselves.
I just describe what something looks like.