The disease manifestations of being 'HIV' positive testing in Africa seem related to Lymphocytosis which appears in cattle exposed to growth hormones and Bovine Leukemia Virus which then appears with the cows as they get cancers and leukemia from the hormones.
Because Bovine Leukemia Virus makes p24 antibodies in humans the HIV antibody test is picking up the Bovine Leukemia Virus presence for a start so any claim that the HIV test picks up HIV is false.
"Using immunoblotting to test the sera of 257 humans for
antibodies of four isotypes (IgG1, IgM, IgA, and IgG4) to the BLV
capsid antigen (p24), we detected at least one antibody isotype
reactive with BLV in 74% of the human sera tested." 2003
Humans Have Antibodies Reactive with Bovine Leukemia Virus
“74% of the human sera tested”
In Africa Lymphocytosis is not being tested because the doctors are paranoid about HIV so the phenomenon is ignored..
"With the high incidence of HIV in our population (South
Africa) it is likely that DILS is under diagnosed probably due to
our ignorance of this disease. Awareness of its various
presentations may bring to light undiscovered patients with
Diffuse Infiltrative Lymphocytosis Syndrome (DILS)
As Africans have a higher prevalence of Diffuse Infiltrative Lymphocytosis Syndrome (DILS) anyway any exposure to hormones will make it worse hence African women who have used the pill or hormone replacement therapy or are pregnant with their own growth hormones need to be aware this could also be making them look HIV+ as well in combination with BLV exposure and antibodies to Bovine Leukemia Virus p24.
"DILS has been reported to occur predominantly in HIV-infected African American middle-aged men. and male-to-male transmission of HIV infection has been consistently reported as a risk factor for the development of DILS. In one of the largest series of patients, Kazi and colleagues reported that the average age of patients with DILS at the time of diagnosis was 36.9 years.
Although the incidence of DILS remains elusive, estimates range
from 0.8% to 7.8% in HIV-infected persons. A study from West
Africa showed that the prevalence of DILS may be as high as 48%
when assessed histologically. DILS is most frequently reported in
the pediatric literature, and many series have noted its
occurrence at an early stage of HIV disease, before the
development of AIDS. For example, in the series reported by
Kazi's group, the average CD4+ T-lymphocyte count was 342/µL,
while the average CD8+ T-lymphocyte count was 1639/µL. Of recent
interest are observations suggesting that this syndrome appears
to be less prevalent as a result of the widespread use of HAART;
this may be explained by the effect of antiretroviral therapy in
decreasing the number of circulating CD8+ lymphocytes"
Diagnosis of Diffuse CD8+ Lymphocytosis Syndrome in HIV-Infected Patients 2002
These are the sort of symptoms BLV creates in cattle, there is evidence that meat workers get leukemias and nervous disorders from exposure to it.
"The occurrence in cattle of a disease called "leukosis" was first reported by Leisering who described as early as in 1871 the presence of yellowish nodules in the enlarged spleen of a cow. In fact, spleen disruption consecutive to tumor formation is one of the most spectacular clinical manifestations of bovine leukemia. These tumors which result from a local accumulation of transformed B cells also infiltrate other tissues such as liver, heart, eye, skin, lung and lymph nodes. Two types of bovine leukemia can be dissociated on the basis of their epidemiology: Enzootic Bovine Leukosis (EBL), a disease caused by a retrovirus called BLV (Bovine Leukemia Virus), and sporadic bovine leukosis which is not transmissible. Besides the lethal form of BLV-induced leukemia, persistent lymphocytosis (PL) is characterized by a permanent and relatively stable increase in the number of B lymphocytes in the peripheral blood. The PL stage, which affects approximately one third of infected animals, is considered to be a benign form of the disease resulting from the accumulation of untransformed B lymphocytes. Finally, viral infection is asymptomatic in the majority of BLV-infected animals; in these settings, fewer than 1 % of peripheral blood cells in animals are found to be infected by virus.
BLV is transmitted horizontally through the transfer of infected cells via direct contact, through milk and possibly by insect bites. However, iatrogenic procedures like dehorning, ear tattooing and, any use of infected needles contribute significantly to viral spread. BLV is nowadays highly prevalent in several regions of the world (e.g. United States) and induces major economical losses in cattle production and export."
It is high in cattle from the USA and South Africa because both these countries use Somatotropin or Bovine Growth Hormone while in Europe BLV is lower because Bovine Growth Hormone is banned.
"BLV is now almost completely eradicated from the European Union after many years of culling infected animals. Since these costly eradication programs are only possible in regions where viral prevalence is low, other strategies have also been considered including isolation of infected animals, passive immunization with colostrum, vaccination with viral proteins or attenuated strains, as well as some other exotic approaches and references therein). None of these latter methods currently achieve the optimal combination of efficiency, economy and safety.
Domestic cattle are the natural hosts for BLV. The existence of wild reservoirs remains controversial, but convincing evidence indicates that BLV indeed persists in water buffaloes. Experimental transmissions of BLV have been reported in many species including rabbits, rats, chickens, pigs, goats and sheep. However, only sheep consistently develop leukemia whereas rabbits present immune dysfunctions (but no tumors, in a finding different from rabbits inoculated with HTLV). Rare cases of experimental transformation were reported in goats, rats and even chicken. Despite successful infection of a series of cell lines in vitro, BLV does not persistently infects cat, dog, monkey or human although viral-specific seroconversion (p24 antibodies, my note) might occur in these species."
Mechanisms of leukemogenesis induced by bovine leukemia virus:
prospects for novel anti-retroviral therapies in human
The correlation is clear, countries that have banned recombinant bovine somatotropin (rBST) or recombinant bovine growth hormone (rBGH) have lower HIV rates and it was introduced into South Africa in 1994 in time for the exponential rise in HIV rates there.
"rBST has not been allowed on the market in Canada, Australia, New Zealand, Japan, Israel and all European Union countries"
And it's clear there is a link between HIV and Bovine Leukemia Virus...
“a substantial case is presented that HIV-1 is a natural recombinant of Bovine Leukemia Virus (BLV) and Visna Virus (sheep). This natural recombinant may have been inadvertently transferred to humans through the Intensified Smallpox Eradication Program conducted in sub-Saharan Africa in the late 1960s and most of the 1970s.”
The origin of HIV-1, the AIDS virus.
Whether it was smallpox vaccination that started it or not just avoid eating cattle in countries using bovine growth hormones as the hormones and p24 proteins from cancerous cows on hormones will make being tagged as HIV+ look worse and you will never be able to get a HIV negative result on retesting.
Finally HIV sequences or HTLV's and human leukemia retroviruses are not really proven to be isolated, everyone has HERV-K's endogenous retroviruses in our DNA which are all different but barely different from HIV sequences.
They all have GAG, POL and ENV genes.
HTLV's or human leukemia retroviruses are just like HERV-K's in that they mainly appear when cells hypomethylate or turn on genes, so only with damage, new growth, autoimmune disease, leukemia and cancer.
The claim they have defined HTLV sequences as in the types 1, 2 and 3 are false.
Not one of the HTLV sequences are the same from person to person indicating it was always particular to the person's genome
And then the 'HIV' sequences or HTLV-III (the old name for HIV) sequences vary from organ to organ in every single person anyway so HIV is not only different in each and every person 'infected' but in each of their different organs, so HIV in one person's liver is not the same as HIV in another person's liver.
Heart, kidneys, lungs, breast, testes etc. all different.
When they did the human genome project they didn't define all the HERV sequences because there were so many it was commercially impossible to do so they haven't actually worked out all the different retroviruses in the genome yet.
But BLV will make p24 antibodies to make a HIV+ result and the symptoms of drinking hormone filled milk and eating meat from cattle with leukemia creates more growth conditions that make our own retroviruses cross react with viral load tests and women on hormones are likely to look HIV+.
The other indicator is here "All 20 subjects remained HIV seronegative throughout the study. Women with HIV proteins and RNA were comparatively older."
"Women with HIV proteins and RNA were comparatively older" are on Hormone Replacement Therapy these days which is also the main cause of cervical cancer.
So it's the hormones causing the phenoma.
The HIV tests pick up cancers and pre-cancerous conditions and
that's all they do.
"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. HIV antigens were consistently identified by mass spectrometry (MS) in CVL from 4 women but were absent in CVL from the remaining 16 women. HIV serologies of all 20 patients were negative for both HIV-1 and HIV-2 antibodies. To validate the unexpected MS findings we performed Western blot (WB) and immunoaffinity chromatography (IC) analysis of CVL for HIV proteins, viral load assays of paired CVL and blood samples, and immunohistochemical HIV p24 expression in cervical biopsy specimens. WB analysis of CVL for prostate-specific antigen (PSA) was performed to exclude semen contamination as the source of HIV proteins. WB and IC results demonstrated the presence of HIV-1 gp41 and p24 antigens in four CVL that were identified by MS 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. Our findings suggest that CVL HIV proteins in women with CIN could be markers for unrecognized HIV exposure or subclinical infection. Proteomic screening of cervical secretions may be useful in identifying seronegative women exposed to HIV and/or at risk for AIDS."
Human immunodeficiency virus (HIV) antigens and RNA in HIV-seronegative women with cervical intraepithelial neoplasia.