The HIV assault on women and children

“HIV” tests do not detect an infectious agent (section 3.1 in The Case against HIV).

Innumerable conditions cause “false positives” (section 3.2 in The Case against HIV), notably pregnancy.
Transmission of “HIV” from mother to child, dogmatically accepted in mainstream practice, has never been proven actually to occur (section 3.3.4 in The Case against HIV).

Despite these facts, pregnant women are routinely subjected to “HIV” tests, and if “HIV-positive” they and their babies are then forced to take highly toxic antiretroviral drugs whose “side” effects are legion and highly damaging (section 5.3 in The Case against HIV); babies, even if drugged for only a short period, are likely to suffer permanently because antiretroviral drugs cause irreparable damage to mitochondria (section 5.3.3.1 in The Case against HIV).

In most places, laws and social workers and health-care workers make it impossible for women to fend off these damaging assaults on themselves and their children. Sometimes the children are even taken away from their parents if the latter try to resist having their children poisoned.

Graphic personal stories of several such women are presented in the recent documentary, I won’t go quietly. Short  and  long trailers can be viewed on YouTube.

Fanatical ideologies and willful ignorance
are WMDs — weapons of mass destruction
that are politically and socially countenanced and wielded.

HIV/AIDS theory is a fanatical ideology,
and willful ignorance is exemplified
by the dogmatic acceptance of “HIV-positive”
as indicating infection by a fatal retrovirus
and the refusal to recognize healthy pregnancy
as a risk factor for testing “HIV-positive”.

“HIV” testing constitutes a WMD directed at everyone,
but affecting prominently all women and children.

“HIV” is NOT sexually transmitted — yet more clear evidence

Recent Nobelist in biology, Randy Schekman, launched a venture to improve publication of valuable research (Science rewards hucksters and spin artists, not soundly tested science): the Open Access on-line eLIFE.

Straightforward evidence that “HIV” is not sexually transmitted — in particular, not by heterosexual intercourse in Africa — is present in “Earlier menarche is associated with a higher prevalence of Herpes simplex type-2 (HSV-2) in young women in rural Malawi”, Glynn et al., eLife 2014;3:e01604, 28 January 2014.

The article’s main point is less than surprising: “girls with earlier menarche tend to have earlier sexual debut and school drop-out, so an association might be expected” with being more likely to contract sexually transmitted infections (STIs or STDs).
That expectation was confirmed by a close-to-linear relationship between age at menarche and prevalence of herpes (HSV-2) infection:

By contrast, there was no correlation at all between “HIV-positive” and age at menarche.

Furthermore, prevalence of “HIV” was much lower than that of HSV-2, contrary to yet another shibboleth of HIV/AIDS theory, namely, that infections by an STD like HSV-2 makes “HIV-positive” more likely:

In an earlier article (Glynn et al., “Assessing the validity of sexual behaviour reports in a whole population survey in rural Malawi”, PLoSONE, 27 July 2011) the ratio of “HIV-positive” to HSV-2 infection had been reported as 4/31 for females and 2/52 for males, again confirming that “HIV-positive” is much less prevalent than HSV-2.

Not, of course, that this further evidence that “HIV” isn’t an STD will make any difference, more-than-ample evidence has been around for many years.

Cervical cancer — An update to “HPV Insanity”

After posting “HPV insanity”, I had asked some technically competent people for comments on the press release touting lopinavir as a cure for “HPV infection”. That brought a highly informative albeit also highly technical article (McCormack et al., Individual karyotypes at the origins of cervical carcinoma”,  Molecular Cytogenetics, 6 [2013 ] 44.) in which actual cases of cervical cancer were successfully classified — independently of HPV infection or non-infection — by degree of disturbance of the cell’s chromosomes (aneuploidy, as opposed to the normal diploid state of paired chromosomes).

Peter Duesberg was one of the leaders of the erstwhile and unsuccessful search for human-cancer-causing viruses, and of the subsequent switch to considering activation of “oncogenes” as responsible for cancer. He has more recently been studying the possible role of aneuploidy, a condition in which cells acquire an abnormal complement of chromosomes: “Chromosomal chaos and cancer”, Scientific American, May 2007, 53-9.

Updates to The Case against HIV

The following additions have been made to The Case against HIV

1.1.6.1 Co-factors in addition to HIV required to bring on AIDS have been postulated on a number of occasions: mycoplasma (refs. 26-31); HTLVs (p. 248 in ref. 257); cell surface protein CD26 (Callebaut et al., “T-cell activation antigen CD26, as a cofactor for entry of HIV into CD4+ cells”, Science, 262 [1993] 2045; Jon Cohen, “HIV ‘cofactor’ comes in for heavy fire”, Science, 262 [1993] 1971); the protein fusin (Jon Cohen, “Likely HIV cofactor found, Science, 272 [1996] 809-10)

2.3.1.3 Malnutrition is widespread in Africa and is a known cause of lack of resistance to infection. It can be responsible for any infection incurred within 1 month of the end of food deprivation.
”Acquired Immunodeficiency Syndrome (AIDS) — WHO/CDC case definition for AIDS”, Weekly Epidemiological Record, 7 March 1986, 69-73

3.2.2.9 Fever is very non-specific. “HIV-positive” is often associated with fever.
Celia Farber, “Positively Flawed: Welcome to the Machine”, Impression, June 1999; http://www.virusmyth.com/aids/hiv/cfposflaw.htm
AND ALSO ADD THIS REFERENCE TO 3.2.2.5 FOR PREGNANCY

3.3.1.1 In Africa, more than two thirds of couples are serodiscordant: one is “HIV-positive”, the other is not
UNAIDS 2008 Report on the Global AIDS Epidemic, p. 118

3.3.18 add ref 465

4.1.5.1 In 1995, Peter Godwin, head of the Regional HIV Project, United Nations Development Program: “by the year 1997 the annual number of new HIV infections in Asia will exceed those in Africa, and its share of worldwide cumulative infections will increase to nearly 25% by the year 2000”
J. C., “Thailand points the way”, Science, 270 (1995) 30
but by 2007, Asia had only 5 out of a global 33 million “HIV-positives” while sub-Saharan Africa had 19 million
UNAIDS 2008 Report on the Global AIDS Epidemic

4.1.8.1 Trojan Horse inhibitors
National Institute of Allergy and Infectious Diseases, “Trojan Horse Virus controls HIV infection”, 4 September 1997; http://aidsinfo.nih.gov/news/385/trojan-horse-virus-controls-hiv-infection
Tom Nurre, “Radical research”, Angelo State University Magazine, Summer 2011, 16-9
Buckley et al., “HIV protease-mediated activation of sterically capped proteasome inhibitors and substrates”, Journal of the American Chemical Society, 133 (2011) 698-700

4.1.8.2 Killing “HIV” by shaking it with tuned laser
Orli Van Mourik, “Good vibrations vs. bad viruses”, Discover, June 2008, p. 16

4.2.6 Add Cavrois, Neidleman & Greene, “The Achilles Heel of the Trojan Horse Model of HIV-1 trans-infection”, PLoS Pathogen, 4(#6, 2008): e1000051

4.3.2.10 Cardiovascular disease
refs 34, 120-5, 131-2 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232

4.3.4.8 Bone disease, osteopenia, osteoporosis
refs. 35-43, 103 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232

4.7.6 add another reference: UNAIDS 2008 Report on the Global AIDS Epidemic, p. 89

5.3.3.15 Vitamin D deficiency
Refs 74, 76, 77, 84, 89, 93-100, 102 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232

5.3.3.10
Add Refs. 35, 38, 39, 41, 104-6, 111-6 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232

6.1.3 Add “and from other experimental treatments”.

6.1.3.2 Chemotherapy to kill the immune system to avoid rejection of transplanted baboon bone-marrow cells because baboons couldn’t be infected with “HIV”. (Rick Weiss, “Doctor hopes to repeat baboon cell transplant”, Washington Post, 11 February 1996, p. A9) The first attempt involved “an unidentified 56-year-old man who was dying of AIDS. . . . The experiment was not a success. The baboon cells failed to grow, and the man died two months later. But Dr. Ricordi said his team had been encouraged because the man did not suffer any adverse reactions from the transplant” [emphasis added].
Lawrence K. Altman, “The Doctor’s World; Baboon cells might repair AIDS-ravaged immune systems”, New York Times, 19 July 1994

6.4 Hegemony of HIV/AIDS theory and practices means that some central questions cannot be answered
6.4.1 When “HIV-positive” individuals become ill, all too often the real cause of illness is not looked for
6.4.2 When “HIV-positive” individuals using antiretroviral drugs die, no autopsy inquires into whether death may have been owing to the drugs
”42-yr-old Glen Elder, dead of heart attack at 42”, Chronicle of Higher Education, 12 June 2009, A33
” Jeff Getty, 49, AIDS activist who received baboon cells, is dead”, New York Times, 16 October 2006; http://www.nytimes.com/2006/10/16/health/16getty.html?_r=0
AND ADD THIS LAST REF. TO 6.1.3.2

7.1.4.9 That many hemophiliacs were infected by tainted blood products
”Two thirds of our hemophiliacs have received infected blood”
Jonathan Kellerman, Devil’s Waltz, Bantam 1993, p. 336

7.2.1.3 The mistaken belief that “HIV” is transmitted sexually (see Section 3.3 for disproof) is incessantly repeated, for example that prostitutes contract and spread “HIV”
Colin Thubron, “Believers’ bazaar”, review of In Search of the Sacred in Modern India by William Dalrymple, New York Times Book Review, 18 July 2010, p. 19
Gurav & Blanchard, “Disease, Death and Dhandha: Gharwali’s Perspectives on the Impact of AIDS on Devadasi System and the Sex Work in South India”, World Journal of AIDS, 3 (2013) 26-32

8.3 Add “; see also Sections 7.1, 7.2, 7.4, 7.7”

HPV insanity

Number of Americans living with HPV: 79,100,000 (M and F about equally)
Number of new HPV infections annually: 14,100,000
(for 2008, cited in CDC Fact Sheet “Incidence, Prevalence, and Cost of Sexually Transmitted Infections in the United States”, February 2013)

In 2010 (the most recent year numbers are available) —
11,818 women in the United States were diagnosed with cervical cancer.

So the risk of developing cervical cancer if infected with HPV is roughly 12,000 out of ~40 million (only women get cervical cancer)
In what sense can it be said meaningfully that HPV causes cervical cancer, if that happens to one HPV-infected woman in every 3000?

* * * * * * * *

Not only is the incidence of cervical cancer low compared to most other cancers, it has also declined steadily for many decades: from 14.79 per 100,000 in 1975 to 6.71 in 2010 (SEER Cancer Statistics Review 1975-2010). Between 2001 and 2010, incidence decreased steadily at 1.9% per year (Gynecologic Cancers).

Despite the steady decrease in incidence of cervical cancer, official recommendations are that pre-puberty girls be vaccinated — a practice that carries more risks of harm than possible benefit:
CDC mongers fear and hawks deadly vaccine; Gardasil and Cervarix: Vaccination insanity

* * * * * * * *

“HIV” may be a role model for wrong inferences based on mistaken confusion of correlation with causation. (Refresher: Correlation never proves causation.)
Because “HIV-positive” is found in a great variety of conditions, “HIV” is being blamed for an increasing range of ailments, many of which are actually caused by antiretroviral drugs, for example heart failure — see The Case against HIV,  sections 3.2, 4.3, 5, 6.1
So HPV too is being credited with causing more and more things.
First there was a campaign to treat boys as well as girls with anti-HPV vaccine so that they would be less likely to suffer from genital warts, a practice whose risk/benefit ratio is even less desirable than for women and cervical cancer. Bear in mind that, once again, all that’s known is that there appears to be a correlation between some strains of HPV and genital warts.
Then “studies” have found that “HPV also has been associated with . . . vaginal, vulvar, penile, anal, and some head and neck cancers” (The Link Between HPV and Non-Cervical Cancers).

Here’s another pertinent fact about statistics and correlations. The typical criterion of significance used by sociologists and medical researchers is p < 0.05, meaning that there is a 5% chance or less that the apparent correlation has no significance. Very roughly speaking, that means 5 of every 100 apparent correlations are purely random, chance occurrences.
Look at that another way. Assume there are a number of variables, and each is tested against each of the others to see whether there is a correlation. Purely by chance, 5% of all the tests will appear to show a correlation that is, however, spurious.
In other words: If a study tests 100 possible correlations and finds 5 statistically significant correlations, then all 5 are most probably spurious.
One trouble is that research articles report their “statistically significant” correlations, but don’t alert the reader to how many possible correlations were considered.

“HPV is a group of more than 100 related viruses” but only 2 — HPV 16 and 18 — are said to cause cervical cancer, or rather “about 70 percent of all cervical cancers”.
If just 40 strains of HPV had been tested for possible correlation with cervical cancer, purely by chance there would appear to be 2 correlations, spurious correlations.

Once an unwarranted theory has become mainstream, further research will turn up any number of intriguing things — intriguing because they make no sense. With HPV, for example, because there are so many strains one can come up with really mind-boggling results clearly demanding further research and research grants (HPV vaccines may be less effective in African American women, researchers find):
“Among women with mild cervical dysplasia, or early precancerous cells:
African American women: HPV types 33, 35, 58, 68
White women: HPV 16, 18, 56, 39, 66
Among women with moderate to severe cervical dysplasia, or advanced precancerous cells:
African American women: HPV types 31, 35, 45, 56, 58, 66, 68
White women: HPV 16, 18, 33, 39, 59”.

Since the presumption is that “mild cervical dysplasia, or early precancerous cells” lead to “moderate to severe cervical dysplasia, or advanced precancerous cells” on the way to actual cervical cancer, isn’t it intriguing (= makes no sense) that not the same sets of strains are “associated” with the first conditions as with the second?

What are the odds that these findings will be repeatable?
More likely, later studies will find equally spurious correlations with other strains.

And by the way: What inspiration was behind the hypothesis that cervical cancers would be caused by different strains of HPV in white women and in African-American women?

* * * * * * * *

I had been stimulated into this sidetrack into HPV and associated vaccines by something that popped up on my Goggle HIV Alert:

HIV drug used to reverse effects of virus that causes cervical cancer

This seemed so bizarre that I followed the suggestion that “For further information, please contact Alison Barbuti, Media Relations Officer | Faculty of Medical and Human Sciences | The University of Manchester Tel: +44(0)161 275 8383 Email: alison.barbuti@manchester.ac.uk”

An immediate response came that since I was not a journalist, my request had been forwarded to the authors. One of them e-mailed immediately that the material would be sent as soon as they were back home. That was a month ago. My paranoia is showing again: maybe they looked at my website and didn’t like my attitude toward HIV and antiretroviral drugs?
After all, for lopinavir (LPV) — the “HIV drug” of the title of the press release —one finds in the literature that all protease inhibitors have the following “side” effects (Table 13 in Treatment Guidelines, updated 12 February 2013):
Bleeding events
Cardiovascular disease
(Associated with MI and stroke in some cohort studies. . . .) . . . LPV/r: PR interval prolongation. Risks include structural heart disease, conduction system abnormalities, cardiomyopathy, ischemic heart disease, and coadministration with drugs that prolong PR interval.
Gastrointestinal (GI) effects
GI intolerance (e.g., diarrhea, nausea, vomiting); Diarrhea: . . . LPV/r > DRV/r and ATV/r
Hepatic effects
All PIs: Drug-induced hepatitis and hepatic decompensation (and rare cases of fatalities) have been reported with all PIs to varying degrees
Lipodystrophy
Trunk fat increase . . . ; however, causal relationship has not been established.
Stevens-Johnson syndrome (SJS)/ toxic epidermal necrosis (TEN)
. . . LPV/r . . . : Reported cases

For LPV specifically (Lopinavir + Ritonavir LPV/r)/Kaletra:
“GI intolerance, nausea, vomiting, diarrhea; Pancreatitis; Asthenia [weakness]; Hyperlipidemia (especially hypertriglyceridemia); Serum transaminase elevation; Hyperglycemia; Insulin resistance/diabetes mellitus; Fat maldistribution; Possible increased bleeding episodes in patients with hemophilia; PR interval prolongation; QT interval prolongation and torsades de pointes have been reported; however, causality could not be established”.

Again with “HIV” as role model, the idea appears to be to administer dangerous drugs in absence of any substantial and proven risk.