This is my explanation of this phenomenon where HIV disappears, you can try and argue with it, we at least need to raise the bar higher.
If you wish to repost this article on any blog or website without changes to the written format you have my permission to do so. Cal Crilly
Originally posted here 17.11.2021
https://mindhealthsoul.blogspot.com/2021/11/what-is-hiv-retrovirus.html
Our own retroviruses are active in pregnancy and go away once pregnancy ends so HIV tests mistake this process as a retroviral infection, I wrote it for some HIV positive pregnant African ladies whose partners are all HIV negative.
In the case of HIV appearing, HIV is a cell fusion retrovirus associated with a gene called HLA-DR which appears on cells in cancers and autoimmune disease to alert immune cells to come and remove the damaged cells.
When HLA-DR appears in pregnancy and HIV with it then it indicates pre-eclampsia or autoimmune disease and not HIV infection.
HIV always resides in HLA-DR genes which will appear with cell death and damage so there never has been an infection, only tests finding the phenomena and virologists presuming HIV is causing cell death when it is part of a cell removal process.
The HIV antibody tests are really a type of cancer test, even 2 months before Gallo said HIV was an infectious retrovirus in gays, he was about to commercialise the p24 antibody test as a test to detect tumours before they appeared and then changed it to use for ‘AIDS’ detection.
The gays with AIDS had lymphomas from snorting poppers and using sexual lubricants containing 5% Benzene, not HIV.
‘According to a report published Monday in the Annals of Internal Medicine, a now 31-year-old woman who was diagnosed with HIV in 2013 only took antiretroviral therapy for six months during pregnancy to prevent transmitting the infection to her baby. Yet multiple sophisticated tests looking for genetic evidence of HIV in the patient’s blood showed no intact virus in her cells, says Dr. Xu Yu, who led the research team reporting on the case. She’s a principal investigator at the Ragon Institute of Massachusetts General Hospital, MIT and Harvard, as well as an associate professor of medicine at Harvard Medical School. The findings suggest that the patient’s immune system was even able to clear the reservoirs of HIV that allow the virus to continue replicating for decades. Current anti-HIV drugs can lower virus levels to undetectable levels but can’t completely rid the body of these lingering reservoirs of the virus.
“There is no way to ever say we have proof that there is not a single virus in this patient,” says Yu. “The only thing we can say is that after analyzing a large number of cells from the patient, with the technology in our lab we cannot reject the hypothesis that the patient probably reached a sterilizing cure by natural immunity.’
A Second HIV Patient Has Cleared the Virus Without Antiviral Drugs
I’ll ramble a bit and talk about what HIV is in relation to pregnancy, HIV can appear in cancers, leukemias, lymphomas and all auto-immune diseases and that can be addressed in another blog with the fixes.
When women get pregnant the placenta becomes highly active with retroviruses, there are 2 types, Syncytin-1 and Syncytin-2 to keep it simple for now. Once pregnancy has stopped HIV also will disappear.
‘Human life begins with sperm and oocyte fusion. After fertilization, various fusion events occur during human embryogenesis and morphogenesis. For example, the fusion of trophoblastic cells constitutes a key process for normal placental development. Fusion in the placenta is facilitated by syncytin-1 and syncytin-2. These syncytins arose from retroviral sequences that entered the primate genome 25 million and more than 40 million years ago respectively. About 8% of the human genome consists of similar human endogenous retroviral (HERVs) sequences. Many are inactive because of mutations or deletions. However, the role of the few that remain transcriptionally active has not been fully elucidated. Syncytin proteins maintain cell–cell fusogenic activity based on env gene-mediated viral cell entry. In this review, we summarize how syncytins and their receptors are involved in fusion events during human reproduction.’ ….
‘Syncytin proteins, syncytin 1 and syncytin 2, belong to the human endogenous retrovirus (HERVs) family and were initially identified in human placenta due to their fusogenic activities. Syncytin A and B, homologous to human syncytins, have also been identified in mice (Dupressoir et al. 2005) and are essential for normal murine placental development (Dupressoir et al. 2009, 2011).
Fertilization requires fusion of sperm and oocyte. Following implantation, the placenta forms and supports development of the embryo/fetus during intrauterine life’
The role of syncytins in human reproduction and reproductive organ cancers https://rep.bioscientifica.com/view/journals/rep/152/5/R167.xml
The war on AIDS and retroviruses is one against cell growth, so when they give people antivirals which are reverse transcriptase inhibitors it is to stop cell growth and the retroviruses which are part of cell growth then disappear. When you take a viral load test you are measuring cell growth.
‘Endogenous, non-telomeric Reverse Transcriptase (RT) is encoded by two classes of repeated genomic elements, retrotransposons and endogenous retroviruses, and is an essential component of the retrotransposition machinery of both types of elements. Expression of RT-coding genes is generally repressed in non-pathological, terminally differentiated cells, but is active in early embryos, germ cells, embryo and tumor tissues, all of which have a high proliferative potential. To clarify whether reverse transcription is functionally implicated in control of cell growth, differentiation and in embryogenesis, recent experiments have been undertaken to inactivate the endogenous RT activity. RT was inhibited in normal and transformed cell lines by exposure to nevirapine, a non-nucleosidic RT inhibitor. ‘
Endogenous reverse transcriptase: a mediator of cell proliferation and differentiation https://www.karger.com/Article/Abstract/78207
This is a child suffering Stevens-Johnson syndrome where the skin can fall off after taking Nevirapine, so cell fusion is important, it holds organs and our bodies together.
Now the give-away for HIV is in this 1991 study on HIV antigens in normal placentae so every pregnant lady can test positive but they dilute the antibody test 400 times so only some women with high levels of HLA-DR antigens test positive
‘Cryostat sections of human normal term placentae were studied for evidence of immunopathology by using antibodies to lymphocytes, macrophages, platelets, and coagulation factors. Areas of so-called chronic villitis of unestablished etiology were identified in all placentae. The same tissues were examined for HIV protein antigens gp120, p17, p24, and gp41. No evidence for gp41 was found. Antigens gp120 and p17 were identified in normal chorionic villi in vimentin-positive fibroblast-like cells and in endothelium, respectively. Antigen p24 was localized to HLA-DR positive cells that morphologically resembled macrophages in areas of villitis. The distribution of gp120 and p17 was similar to that observed for tissue factor. These findings prompted speculation that retroviral proto-oncogenes that are known to encode for certain placental receptors could be involved in the presentation of tissue factor, and that gp120 may be a hitherto unrecognized immunobiological mechanism for the blockade of CD4 on maternal lymphocytes if and when such cells gain entrance to chorionic villi.’
HIV proteins in normal human placentae https://pubmed.ncbi.nlm.nih.gov/1930645/
Monkey mums are also HIV positive, and they have SIV retroviruses to enable the baby to have cells dividing, as well as fusing the placenta to the mum so the placenta does not fall off and fail. SIV is the one these retroviruses that HIV scientists say came from monkeys in Cameroon and somehow became HIV/AIDS in New York etc.
‘Electron microscopic studies have revealed the presence of endogenous retroviral (ERV) particles in normal primate placental tissues. These particles have ultrastructural similarities to type C retroviral particles and are mainly associated with the trophoblast. In normal human placental tissues, they have antigenic similarity with exogenous retroviruses, such as the human immunodeficiency virus (HIV), and may have a role to play in the regulation of cellular gene expression, syncytiotrophoblast formation or pregnancy-related immunosuppression. In this study, a panel of antibodies (polyclonal and monoclonal antibodies) against viral proteins (anti-HIV and anti-SIV) and endogenous retroviral (ERV) proteins were assessed by immunohistochemistry and immunoblotting, for their cross-reactivity with ERV particles isolated from normal baboon placental tissues. The antibodies (anti-HERV-K RT, anti-ERV3 env, anti-HIV-1 p17, anti-HIV-2 gp120) reacted positively with the syncytiotrophoblast and each antibody recognized one or two proteins of molecular weights (MW) 38, 58 or 64 kDa present in the baboon placental villous tissues and SIV-infected molt-4 Cl8 cells, but not in uninfected cells. The results of this study confirm the specific expression of retroviral cross-reactive antigens in normal baboon placental tissues and suggest placental cellular proteins may have antigenic similarity with those recognized by anti-HIV/SIV antibodies. The role of these retroviral-related proteins expressed at the maternal-fetal interface remain unclear.’
Characterization of antigens expressed in normal baboon trophoblast and cross-reactive with HIV/SIV antibodies.
https://europepmc.org/article/MED/10098831
‘Scientists searching for the origin of HIV, the global pandemic infecting more than 40 million people, believe they have finally tracked its original source to two colonies of chimpanzees in a corner of Cameroon.
The finding represents the culmination of a 10-year hunt for the source of the pandemic and provides a crucial link between HIV, which causes Aids in humans, and the simian immunodeficiency virus (SIV), a strikingly similar virus that infects monkeys and chimpanzees. Researchers believe that south-east Cameroon is where the virus first jumped from chimpanzees to humans before HIV infection began spreading among people as far back as the 1930s.
At the time, HIV, which destroys the immune system leaving those infected vulnerable to myriad diseases, was difficult to diagnose. Carried by people travelling along the rivers, it spread unnoticed to Kinshasa, where the first human epidemic began to grow.’
Hunt for origin of HIV pandemic ends at chimpanzee colony in Cameroon https://www.theguardian.com/world/2006/may/26/aids.topstories3
This was Gallo the inventor of the HIV antibody test in his own childish way talking about the origins of HIV.
“The subject turns to Africa, where AIDS is most prevalent and probably began. Gallo and nearly all others in the field believe the virus began around the rural areas near Lake Victoria.
The virus probably passed from African green monkeys into man when hunters ate the animals or, less likely, when monkeys bit their human predators. “Who really knows?” Gallo says blithely. “Maybe there’s some ritual with monkey blood — who knows? They do a lot of funny things in Africa, like when they make the lower lip stick out or when they put things through their noses.”
According to Gallo, Belgian missionaries reported illnesses resembling AIDS as many as 25 years ago, but those reports soon passed. Tribes were more isolated from one another then, and such a disease was unlikely to go far. The virus began its spread with the change in African demographics and sexual habits.
“Tribes began to be less isolated,” Gallo says. “There was more social and sexual contact between tribes, and people began moving more into the cities. There’s been a rise of prostitution and promiscuity. The infection rate in places like Zaire and Kenya is astronomical.
“The ancient Romans had a saying: ‘Anything new . . . Africa.’ “
I say HIV is a racist theory that claims Africans eating monkeys infected with a monkey retrovirus called Simian Immunodeficiency Virus or SIV then contracted HIV and passed it to cities in the West.
Rosalind Harrison-Chirimuuta & Richard Chirimuuta did a great article outlining this in detail back in 1997 and it well worth a read to see through the ‘scientific’ claims of HIV/AIDS.
‘To explain how a disease originating in one continent was yet disseminated to the rest of the world from another, the scientists have argued that there was a remote central African “lost tribe” in whom the virus had been present for centuries, or alternatively who acquired the infection from monkeys 30 or so years ago. Haitians (but no-one else) working in central Africa then became infected (presumably heterosexually) and, on returning home, spread the disease to homosexual American tourists. By this circuitous route the virus reached the United States and from there spread to the rest of the world.’
AIDS AND AFRICA: A CASE OF RACISM VS SCIENCE?
http://www.virusmyth.com/aids/hiv/rcafrica.htm
In the 1980’s they also extracted blood from sick people with ‘AIDS’ symptoms and injected chimpanzees to try and kill them. This was a complete failure and most of those chimps survived into old age and were moved to a retirement zoo about 12 years ago, sort of putting paid to the deadly virus theory, but you will only hear about this from me.
‘During the 1970s and 1980s, animal research laboratories relied heavily on chimpanzees. After the AIDS epidemic, there was an upsurge in demand for chimps.
Monkey catchers swarmed around the African rainforest to trap baby chimps for Research. Adult chimps are difficult to catch, they are highly intelligent, and also seven times stronger than humans. The catchers wasted no time. They used brutal methods to trap the young chimps. The mother–child relationship is as intense for chimps as for humans. Infants cling to their mother’s belly for three years, and ride piggyback for four more years. Shooting their mothers was the only way to catch the infants.
Most of our Chimpanzees came from Sierra Leone and were intended for the IMMUNO lab in Orth – then, located in Vienna. After 1997, due to a company takeover, they were released from animal experimentation. Their new owners (Baxter) conduct no experiments with primates. In 2002 the chimps were transferred to a safari park. After the Safari Park went bankrupt in 2004, the chimpanzees became in 2009 ‘Aiderbichler’! The construction of their future home began.’
Former Lab-Chimps
http://www.gut-aiderbichl.eu/page.headline.php?cid=2580&redir=
The other thing that syncytins or the retroviruses do is bind to white blood cells on the outside of the placenta, and then the white blood cells dissolve collagen to then burrow new arteries to feed the baby.
2021 article here, they are finally working it out nicely, real science.
‘Multinucleate syncytialized trophoblast is found in three forms in the human placenta. In the earliest stages of pregnancy, it is seen at the invasive leading edge of the implanting embryo and has been called primitive trophoblast. In later pregnancy, it is represented by the immense, multinucleated layer covering the surface of placental villi and by the trophoblast giant cells found deep within the uterine decidua and myometrium. These syncytia interact with local and/or systemic maternal immune effector cells in a fine balance that allows for invasion and persistence of allogeneic cells in a mother who must retain immunocompetence for 40 weeks of pregnancy. Maternal immune interactions with syncytialized trophoblast require tightly regulated mechanisms that may differ depending on the location of fetal cells and their invasiveness, the nature of the surrounding immune effector cells and the gestational age of the pregnancy. Some specifically reflect the unique mechanisms involved in trophoblast cell–cell fusion (aka syncytialization) settings.’
The Immunology of Syncytialized Trophoblast
https://www.mdpi.com/1422-0067/22/4/1767/htm
Retroviruses appear as cell fusion molecules from our HLA antigens which are molecules on our cells that tell immune cells like t-cells or white blood cells what to do in the cell area. ‘The human leukocyte antigen (HLA) system or complex is a complex of genes on chromosome 6 in humans which encode cell-surface proteins responsible for the regulation of the immune system.’
So when someone is pregnant, HLA-G is the marker for the white blood cells to see ‘this area is a new baby or new cell growth’.
‘The human leukocyte antigen G (HLA-G) is expressed on the fetal-maternal interface and plays a role in protecting fetal-derived trophoblasts from the maternal immune response, allowing trophoblasts to invade the uterus. However, HLA-G also possesses immune suppressing-independent functions.’
The immune suppression is so the immune system does not attack the baby and kill it.
The human leukocyte antigen G promotes trophoblast fusion and β-hCG production through the Erk1/2 pathway in human choriocarcinoma cell lines https://pubmed.ncbi.nlm.nih.gov/23583402/
HIV is a cell fusion retrovirus for the HLA-DR antigen which is a marker for an inflamed or dying cell so for years the HIV crowd have seen HIV in cells which express HLA-DR and are sick or in trouble, so they stupidly blamed HIV as being the cause when HIV is just a cell fusion retrovirus that is binding the white blood cells to the HLA-DR markers to remove the cells. They scratch their heads over why HIV never goes away and that is because it is part of HLA-DR and always will be there.
‘To date, most assays for measuring the human immunodeficiency virus (HIV-1) reservoir do not include memory CD4+ T-cells expressing the activation marker, human leukocyte antigen-antigen D related (HLA-DR). However, little is known concerning the role these cells play in maintaining persistent HIV-1 during effective antiretroviral therapy (ART).’
Memory CD4 + T-Cells Expressing HLA-DR Contribute to HIV Persistence During Prolonged Antiretroviral Therapy https://www.frontiersin.org/articles/10.3389/fmicb.2019.02214/full
This is an old study gone offline, key points are that HLA-DR4 markers are very HIV positive. HTLV-III is the early term for HIV.
‘However, of 310 HLA-DR antisera 10 gave positive HTLV-III antibody results.’ …. ‘Since an antigenic relation between HLA-DR4 and HTLV-III or the probability that all 9 donors of the different DR4 antisera were HTLV-III infected is unlikely, the recognition of DR4 antibodies in the sera of homosexuals (immunized by sperm and white blood cells), hemophiliacs, and patients on hemodialysis is important in the interpretation of positive HTLV-III antibody ELISA results.”
Preeclampsia is a condition where these cell fusion retroviruses are muddled up with arthritic retroviruses from inflamed cells showing HLA-DR markers and therefore many African mums test HIV+ because of the high levels of preeclampsia there which could just be from diet.
In South Africa they have a rate of around 18% of pre-eclampsia, which also features HLA-DR4.
Pre-eclampsia is associated with HLA-DR4 sharing between mother and fetus http://www.ncbi.nlm.nih.gov/pubmed/2371715?dopt=Abstract
Association between susceptibility to pre-eclampsia within families and HLA DR4. http://www.ncbi.nlm.nih.gov/pubmed/2572795
And all Africans with autoimmune diseases like arthritis and psoriasis will also appear ‘HIV’ positive because of their HLA-DR4 genes.
“There was a significant association of HLA-DR4 with Rheumatoid Arthritis. The frequency of DR4 in RA was 44% in comparison with 10% in controls’
HLA associations with rheumatoid arthritis in African blacks.
http://www.ncbi.nlm.nih.gov/pubmed/2810257
1997 study here showing HLA-DR is a positive cell surface marker or the real source of so called HIV as I am saying
“During preliminary experiments to establish the proportion of virus-coded p24 protein to virus membrane-associated HLA-DR in gradient-enriched HIV-1 preparations, we became aware of a large variability between experiments. In order to determine whether HLA-DR-containing cellular material was contaminating the virus preparations, we carried out enrichment by gradient centrifugation of clarified supernatants from noninfected cells and tested this material for HLA-DR content. We found that, independently of the cell type used, gradient enrichment resulted in the isolation of large quantities of HLA-DR-containing material which banded at a density overlapping that of infectious HIV.”
Cell Membrane Vesicles Are a Major Contaminant of Gradient-Enriched Human Immunodeficiency Virus Type-1 Preparations http://www.sciencedirect.com/science/article/pii/S0042682297984531
So, if you are a healthy mother with no odd genetic issues the HLA-G markers will allow the foetus to stay stuck to you, and also allow normal arterial remodelling as it gets called to bring blood to the child, but HLA-DR markers which appear in arthritis or autoimmune disease will confuse the t-cells and white blood cells and things get messy.
The HIV scientists see the cell death and chaos of HLA-DR as AIDS but that is all old rubbish, literally rubbish cell debris to get removed.
‘HLA-DR-dependent induction of Endothelial cell death is primarily mediated via a pathway that involves reorganization of the actin cytoskeleton, lysosomal membrane permeabilization (LMP), and mitochondrial stress with generation of reactive oxygen species (ROS).’
HLA class II antibodies induce necrotic cell death in human endothelial cells via a lysosomal membrane permeabilization-mediated pathway
https://www.nature.com/articles/s41419-019-1319-5
And p24 also is a marker for HLA-DR so Gallo just stuffed up years ago and thought he was onto a cancer-causing retrovirus when the HLA-DR was just a cell marker to say to the immune system ‘I’m stuffed, get me out of here’ and HIV was coming out of the HLA-DR marker….
‘The evaluation of the presence of p24 antigen on the membrane of peripheral blood mononuclear cells from 31 HIV infected individuals is presented.’ … ‘Cases showing p24 Ag on peripheral blood mononuclear cells also presented percentages of CD3, HLA-DR positive cells significantly higher than p24 negative ones.’
Detection of the HIV p24 antigen on lymphocyte membranes using flow cytometry https://pubmed.ncbi.nlm.nih.gov/1363372/
This is Gallo’s study in February of 1984 about finding p24 in cancer patients. In their own words they were about to commercialise the p24 antigen test as a measure of how big a tumour was.
But any detection of retroviruses in tumours is irrelevant as they are full of retroviruses anyway as was found out later in research from this century.
“Circulating immune complexes from two patients with human T-cell leukaemia/ lymphoma virus (HTLV)-related lymphoma were shown to contain the major internal antigen of the virus, p24.
The amount of complex-bound p24 in sequential serum samples correlated roughly with tumour cell mass.
Small amounts of complex-bound p24 were detected in samples before a relapse became clinically manifest.
Measurement of complex-bound p24 in patients with HTLV-associated lymphomas and leukaemias might thus be helpful in management of malignancies and offer the possibility of detecting imminent relapse and preventing it by intensification of treatment.”
DEMONSTRATION OF VIRAL ANTIGEN p24 IN CIRCULATING IMMUNE COMPLEXES OF TWO PATIENTS WITH HUMAN T-CELL LEUKAEMIA/LYMPHOMA VIRUS (HTLV) POSITIVE LYMPHOMA …Feb 1984
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2884%2990358-1/abstract
So, within 2 months you must ask how did a p24 antigen to detect tumour size suddenly become a deadly sex virus in gays? And this was all claimed as the cause of AIDS at a press conference without any reference to other researchers.
When those gays involved had lymphomas from popper use and other party drugs anyway?
‘The amount of complex-bound p24 in sequential serum samples correlated roughly with tumour cell mass.’ (This means the size of a tumour can affect the HIV test measure levels… or there are more HLA-DR markers and therefore HIV on a tumour as the cell is damaged.)
‘Small amounts of complex-bound p24 were detected in samples before a relapse became clinically manifest.’ (This means they found p24 was a measure of a tumour coming back before it was found.)
‘Measurement of complex-bound p24 in patients with HTLV-associated lymphomas and leukaemias might thus be helpful in management of malignancies…’ (Means they were about to commercialise the p24 test as a measure for detecting tumours before they appeared.)
Not a sexually transmitted deadly immune damaging virus as claimed two months later at this press conference.
Margaret Heckler & Robert Gallo – 1984 Press Conference
These are further examples of where p24 was found before claiming it was always an indicator of HIV infection.
p24: A HUMAN LEUKEMIA-ASSOCIA TED AND LYMPHOHEMOPOIETI C PROGENITOR CELL SURFACE STRUCTURE IDENTIFIED WITH MONOCLONAL ANTIBODY 1981
‘A monoclonal antibody (SJ-9A4) to P24 present on common alls, neuroblastomas and platelets – I. Characterization and development of a unique radioimmunometric assay 1983
https://pubmed.ncbi.nlm.nih.gov/6578390/
‘The release of the P24 antigen into the culture medium by a C-ALL cell line maintained at 37 degrees C could be detected; however, no P24 antigen was present in the culture medium when the cells were maintained at 4 degrees C. Sequential analysis of the culture medium for soluble P24 antigen revealed that release of the P24 antigen associated with cell growth. Molecular sieve chromatography of concentrated culture medium indicated that shed P24 antigen was eluted in the macromolecule fraction. P24 antigen was detected in the cerebrospinal fluid (CSF) of four patients with P24 positive ALL at the time of relapse of the central nervous system (CNS) and was undetectable while in complete remission. The CSF from three patients with P24 negative ALL and three patients with aseptic meningitis had no detectable activity.’
Shedding of leukemia-associated P24 antigen by lymphoblastoid cell lines 1987
https://pubmed.ncbi.nlm.nih.gov/2447310/
HIV-1 propagates in human neuroblastoma cells 1988
https://pubmed.ncbi.nlm.nih.gov/1704060/
HLA-DR expression on myeloid cells is a potential prognostic factor in patients with high-risk neuroblastoma 2013
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857328/
I will use one more updated example of HLA-DR on breast cancer cells.
‘However, only breast cancer patients without axillary lymph node metastasis and Neoadjuvant Chemotherapy (NACT) responders have HLA-DRhi cytotoxic T lymphocytes (CTLs).’
Which means the cells with HLA-DR on them were recognised as cancer and the t-cells took them out.
‘Moreover, the level of HLA-DR in cytotoxic T lymphocytes (CTLs). is negatively correlated with the level of HLA-DR in T regulatory lymphocytes and with immunosuppressive and pro-tumor molecules in the tumor microenvironment.’
Meaning if HLA-DR didn’t appear on the cancer the immune cells did not bother to do anything, and the cancer spread.’
With HIV the general public probably think t-cells just die and disappear but AIDS as a syndrome is like the immune system is on fire and then at the end it flumps, and people die. In the first stages the doctors say that HIV (HLA-DR) is out of control in the t-cells before they die off.
This is a normal disease process, for example in diabetes where inflammation is rampant at first and then later blood flow stops, and then gangrene and sepsis begin when t-cells and white blood cells fail.
I will write about these things later.
If you want to read further then I wrote this piece on retroviruses, pregnancy, and cancer back in 2012, wow, still not noticed. (:
The Pregnancy Cancer Connection
https://calcrillycancerinfo.blogspot.com/2020/02/the-pregnancy-cancer-connection.html
This is more specific to what retroviruses do in white blood cells.
Macrophage Polarization and IDO Enzymes, Immunity, Cancer and Depression
https://calcrillycancerinfo.blogspot.com/2020/02/macrophage-polarization-and-ido-enzymes.html
And these are historical pieces on AIDS.
The Muddled Beginnings of The AIDS ‘Pandemic’ 1981
https://mindhealthsoul.blogspot.com/2021/11/the-muddled-beginnings-of-aids-pandemic.html
This follows from the previous story and tells what Michael Gottleib and Liz Taylor did to Rock Hudson.
How Rock Hudson’s Liver Failure Conned 325 Million Out Of Congress
https://mindhealthsoul.blogspot.com/2020/05/how-rock-hudsons-liver-failure-conned.html
The AIDS Experiments on Black and Hispanic Children from New York
https://mindhealthsoul.blogspot.com/2021/11/the-aids-experiments-on-black-and.html
HTLV-1 Alert for Aboriginal Communities in Australia
https://mindhealthsoul.blogspot.com/2021/07/htlv-1-alert-for-aboriginal-communities.html
