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The Viral Load (AIDS)


Cal Crilly

Reverse Transcriptase is actually a cell growth marker.

The entire war on HIV/AIDS has been a war against reverse transcriptase and with medieval results as AIDS drugs stop cells from growing and people fall apart.

Here's a study that says Nevirapine stopped 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. The endogenous RT was also blocked in murine embryos by microinjection of an anti-RT antibody. Both experimental approaches yielded a dramatic inhibition of proliferation. Murine embryos arrested at pre-implantation stages. Transformed cell lines underwent a significant reduction in the rate of cell growth, concomitant with the induction of differentiation. In addition, RT inhibition induced an extensive reprogramming of the gene expression profile both in cultured cell lines and in preimplantation embryos. From these studies, endogenous RT begins to emerge as a key function with a driving role in normal and pathological developmental processes."

Endogenous reverse transcriptase: a mediator of cell proliferation and differentiation.


2004 not 1984

Nevirapine is a drug touted as a miracle antiretroviral and thrown into pregnant women but causes mutations.

 “In addition, RT inhibition induced an extensive reprogramming of the gene expression profile both in cultured cell lines and in preimplantation embryos.”

 While in AIDS researcher's own words, the prognostic value of gag and env of HIV is to say, somewhat confusing??

“We have studied the antibody responses to Env and Gag antigens of human immunodeficiency virus type 1 (HIV-1) in several cohorts of HIV-1-infected individuals: long-term nonprogressors, progressors to disease, acute seroconvertors, and recipients of HIV-1 protease inhibitors. We conclude that the antibody responses to Env and Gag antigens are differentially regulated and that changes in the plasma viral load in the measurable range (500 to 10(8) RNA copies per ml) do not directly affect the antibody responses to these HIV-1 proteins. We provide quantitative estimates of HIV-1-specific immunoglobulin G concentrations in plasma, which can be in excess of 1 mg/ml for both anti-gp120 and anti-p24 once the immune response to HIV-1 has stabilized after seroconversion. We discuss the apparent paradox that the absence of anti-Gag antibodies (which have, at best, limited antiviral activity) is indicative of disease progression, while the retention of anti-Env antibodies (which do have antiviral activity) is of limited (or no) prognostic value.”

Differential regulation of the antibody responses to Gag and Env proteins of human immunodeficiency virus type 1. 1997

Since reverse transcriptase "is active in early embryos, germ cells, embryo and tumor tissues"

We find env and gag antibodies in normal placentas.

"We previously reported that monoclonal antibodies directed against HIV-1 envelope and gag proteins react with normal human villous trophoblast."

Expression of endogenous HIV-1 crossreactive antigens within normal human extravillous trophoblast cells. 1995

We find the placental HERV-W retrovirus is in all tissues with a closer look so env and gag genes are everywhere where cells grow???

 "We examined the structural genes (gag, pol and env) of the human endogenous retrovirus (HERV-W) family from 12 normal human tissues and 18 human cancer cell lines using RT-PCR. For the gag and pol genes, their expression patterns showed tissue or cell specificity, depending on the samples, whereas the env gene was expressed in all tissues and cancer cells examined."

Expression of the human endogenous retrovirus HERV-W family in various human tissues and cancer cells. 2004


"In addition to the structural proteins Gag and Env and the reverse transcriptase, two regulatory proteins (Rec and Np9) have been described."

Expression of human endogenous retrovirus K in melanomas and melanoma cell lines. 2005

Prostate cancer

Identification of the HERV-K gag antigen in prostate cancer by SEREX using autologous patient serum and its immunogenicity 2008

Germ cell tumours

Specificity of antibodies directed against Env protein of human endogenous retroviruses in patients with germ cell tumors. 1996

 Ovarian cancers.

"PCR with HIV-1 Env-derived primers revealed DNA sequences with over 90% homology to HIV-1 gp41 in syncytia and in ovarian cancer cells but not in normal ovary cells."

Giant Syncytia and Virus-Like Particles in Ovarian Carcinoma Cells Isolated from Ascites Fluid 1999


Expression of multiple human endogenous retrovirus surface envelope proteins in ovarian cancer 2007

Breast cancers

Expression of human endogenous retrovirus k envelope transcripts in human breast cancer. 2001

Cervical cancers

"While investigating whether proteins retrieved by cervicovaginal lavages (CVL) from women with cervical intraepithelial neoplasia (CIN) might correlate with risk of progression to invasive cervical cancer, we unexpectedly identified HIV gag and env glycoprotein in CVL from women with HIV-negative serology."

"WB and IC results demonstrated the presence of HIV-1 gp41 and p24 antigens in four CVL that were identified by mass spectrometry to have the HIV proteins. Despite negative serology, HIV RNA in CVL and HIV p24 in cervix biopsies were detected in patients with HIV antigen-positive CVL. HIV p24-positive CVL were PSA negative. All 20 subjects remained HIV seronegative throughout the study. Women with HIV proteins and RNA were comparatively older."

Human immunodeficiency virus (HIV) antigens and RNA in HIV-seronegative women with cervical intraepithelial neoplasia

Lupus and other autoimmune diseases have active retroviral gag and env sequences so the list of Reverse Transcriptase activity in diseases can be made longer with a few hours at a computer.

"Measurement by immunoassay revealed increased frequencies of antiretroviral antibodies against 2 peptides derived from the env gene of the type C-like class, which includes ERV-9 and HERV-H, and against 2 peptides from the gag region of human T lymphotropic virus type I-related endogenous sequence 1, in patients with SLE."

Selective antibody reactivity with peptides from human endogenous retroviruses and nonviral poly(amino acids) in patients with systemic lupus erythematosus. 1996


"Although the etiology of systemic lupus erythematosus (SLE) remains unclear, there is substantial circumstantial evidence that the development of SLE is dependent on environmental, genetic, and retroviral factors. SLE patients produce high titer antibodies to various retroviral proteins, including Gag, Env, and Nef of HIV and HTLV, in the absence of overt retroviral infection. We review the factors linking HERVs to SLE and consider the various processes utilized by endogenous retroviruses in the etiopathogenesis of SLE. In particular, we consider the role of HTLV-1-related endogenous sequence (HRES-1) in SLE."

Endogenous retroviruses in systemic lupus erythematosus: candidate lupus viruses 2002

Then if you look closely the genetic divergence of gag and env of 'HIV' is so varied the claim we are measuring an exogenous transmitted retroviral sequence is just that, a claim.

We can't tell the difference between 'HIV' and our own retroviruses.

Genetic variability of gag and env regions of HIV type 1 strains circulating in Slovenia  +   Genetic diversity of HIV type 1 in rural eastern Cameroon   +   Genetic analysis of HIV-1 strains in rural eastern Cameroon indicates the evolution of second-generation recombinants to circulating recombinant forms etc..

With racist scientific presumptions thrown in...

"HIV-1 strains have diversified extensively through mutation and recombination since their initial transmission to human beings many decades ago in Central Africa in the first part of the 20th Century (between 1915 and 1941)."

Update on HIV-1 diversity in Africa: a decade in review.

To speak in plain English this is why the tests are a form of voodoo, to have a zero viral load you have to stop all your cells from growing, this is called death, to do this you need to use antiretrovirals to stop all cell growth and any retroviral activity.

The CD4 test on the other hand measures arterial inflammation so a high T-cell count happens with inflammation but inflammation is associated with cell growth.

 So a viral load has nothing to do with CD4 T-cell loss.

 Alfred Hassig the immunologist and former Swiss Blood Bank chief pointed out that.

 ""The human immune system was conceived of only in its function against foreign (non-self) structures. The Nobel laureates Burnet, Medawar and Jerne have completely neglected the main function of the human immune system. The human organism dismantles about 1 billion body cells every day. One part of our immune system - the T-cells from the Thymus gland - is in charge of cleaning up this altered-self material. In a healthy organism the immune functions of antibodies produced by B-cells, and of the cytotoxic or cell-clearing T-cells, remain in balance."

In 2011 they wrote..

"It has long been recognised that atherosclerotic plaques contain many of the components of the immune systems such as dendritic cells, T lymphocytes and to a lesser extent the B lymphocytes, immunoglobulins, inflammatory cytokines, and complement, highlighting the involvement of the immune system in modulating atherogenesis.

Immune mechanisms in atherosclerosis and potential for an atherosclerosis vaccine.

On the whole the CD4 T-cells they measure from your blood are involved in arterial repair, the adapative immune system is reacting to the bugs on the skin, in the lungs and the gut.

They only measure 2% of our total T-cells from blood because the other 98% they don't measure are in lymph tissue.

Measuring blood and CD4 cell counts is no guarantee that anything related to infection is being measured, a CD4 blood test measures arterial changes.

So antiretrovirals create inflammation by poisoning the arterial walls and T-cells then gather at the lesions and damage caused by AIDS drugs but because the Antiretrovirals have stopped all cell growth nothing can heal again.

This is how they confuse people and so many people get in trouble on alternative therapies which are generally anti-inflammatory and reduce T-cells, so getting healthier arteries can reduce T-cells.

A very low T-cell count either means a very low fat diet as T-cells increase with good cholesterol or it means arterial blood flow slowing and clogging, too much exercise can even cause a drop, using corticosteroids for too long is still the biggest risk for T-cell failure.

Commonly a person turns up to a clinic with some sort of inflammation symptoms, the T-cell count is often too high indicating leukemia, cancer or autoimmune disease which are all diseases that can cross react with the HIV antibody test and the doctor will tell them that the 'HIV' is causing a fever.

The person goes away and changes their lifestyle and diet and taking antioxidants like vitamin C that reduce inflammation and the T-cells go down, people avoid a high fat diet and the T-cells go down because T-cells needs lipids to exist.

An oxidised fat diet also makes T-cells go lower so don't eat rancid fats.

Then the doctor sees the lowered T-cell count and says you're under attack from a retrovirus, if your viral load is up it means cells are growing and replacing themselves so there is a healing process under way which may be perfectly normal if you had toxins coming out from eating too well.

The patient takes AIDS drugs and the viral load goes down but because the poison is freaking out the body and causing lesions the T-cells go up for a period until the AIDS drugs destroy the bone marrow and T-cells can't be made anymore.

So to fix yourself you just avoid drugs, eat all the antioxidant foods needed to lower inflammation but make sure you have enough good fats to raise the T-cells and keep the doctors happy with the numbers.

My Note.

Women have more reproductive tissue and this is where our retroviruses are most active so women are at even more risk from AIDS drugs.

They also give women 3 times the dose of AZT as men get when pregnant.

If you imagine the cells that anti-retrovirals can damage in women compared to men you can see why women die even quicker on AIDS drugs and suffer more organ damage because the reproductive tissue includes breasts and all of the uterine area as compared to men which is testicles.

The main cause of CD4 loss has been from Corticosteroid use.

The cause of Kaposi's Sarcoma was originally in men who had used poppers and then were given high doses of corticosteroids for inflammation, the reason for the entire immune failure seen in AIDS can be traced back to corticosteroids.

The Hemophiliacs were already being treated with corticosteroids for Factor VIII allergies so have always had immune problems.

Factor VIII needed heat treatment to remove any pooled retroviruses from donors so a media panic ensued but the population is already chock full of retroviruses so we donate them all the time but inactivate them with heat treatment..

Once AZT was given to hemophiliacs misdiagnosed by the HIV antibody test it destroyed their bone marrow and they were poisoned.

Kaposi Sarcoma after Corticosteroid Therapy for Idiopathic Thrombocytopenic Purpura

Kaposi's sarcoma in two patients following low?dose corticosteroid treatment for rheumatological disease

Kaposi Sarcoma Associated With Systemic Corticosteroid Therapy

Iron imbalances causing anemia or iron overload infections are a major a cause for opportunistic infections, HAART cannot fix anemia.

Only the people with cancers or leukemia or autoimmune disease can have any temporary benefit from stopping all their cells.

ARV's then simply become cytotoxic medication but not against a retrovirus but against cell growth.

As Alfred Hassig said in 1997 the claim that 'HIV' antigens were exclusive to 'HIV' is a lie or that anything was infectious is also a lie.

"In your opinion where were the gravest mistakes made in the handling of AIDS?

Dr Gallo himself described his mistakes best in great detail in his book The Virus Hunters. He falsely interpreted the cell envelope structure actin, containing glycoproteins like p40, gp120 and gp160, as exclusively foreign to the body, or exogenous, and thus due to retroviral infection. Even though it is, as had been demonstrated earlier, endogenous and existent in all of us to a certain extent. This false assessment led to the deadly treatment with virucides like AZT. That AZT actually was an already failed cancer drug highlights the helplessness and lack of overview with which this virological cancer researcher approached AIDS from the start."

Immunologist Prof. Alfred Hässig was on the Board of Trustees of the International Society of Blood Transfusion from 1980 to 1986, as its President from 1982 to 1984

He said "If the cause of the illness is cytotoxic damage by so-called antiviral treatments, I consider this a legal matter for litigation, which should be discussed with a lawyer."






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