Three Big Books

Monday, December 30, 2019

Why is the Washington Post not doing investigative reporting on the damage Truvada is doing and its potential long term effects?

Dear Journalists,

What most journalists do not understand: how deeply the HI virus has sunk into the LGBT culture and how strongly the life of gay men is affected by the HI virus.

However, being gay doesn’t make you an expert in biochemistry and/or HIV. But it makes you afraid.

Being young and being gay means to live a life in fear.

And here comes PreP. The I-solve-all-problems pill. It is from the same substance class, NRTIs, that is used in the antiretroviral therapy (ART) and it is itself also used in ART. And all NRTIs show the same broad range of severe side effects caused by their mitochondrial toxicity.

Every cell in a human being contains mitochondria. They come almost exclusively from the mother and deliver the energy to the cell. They have a DNA of their own which is damaged by NRTIs. That causes the many different symptoms in many different organs and tissues.

The mitochondrial toxicity of NRTIs is undisputed.

Now take away PreP and you take away all hope and all the fears come back.

So, ok, give them PreP, hand it out for free and everybody is fine. No, unfortunately not, as the severe side effects show. These are apart from possible classical infections healthy young men!

There is no such a thing like a wonder pill. The lawyers are right. The consequences should have been named before.

A much broader discussion is needed before young healthy men reduce their life spans by taking this pill, and we sacrifice the lives and the health of these young men because of the putative prophylactic effects of this pill in this highly asymmetric epidemic of a STI.

It is foolish to believe that the severe adverse effects of the TRUVADA substances tenofovir and emtricitabine would only show in HIV+ measured persons and not in HIV-negative persons as the open letter to Facebook by GLAAD alleges, see

One study cited in the open letter did find an increased risk of kidney injury. The other 2 are from the manufacturer (Gilead Science, DISCOVER trial) and compared tablets with 300 mg tenofovir disoproxil fumarate to tablets with 25 mg tenofovir alafenamide which amounts to a dosage reduction of tenofovir of 9 by molecular weight. Cf. on the trial

The dosage is reduced and the kidney values and the bone mineral density improve? You might call that a proof.

The claim is simply not true. Fear is a bad adviser.

Why is the scientific community so silent in this matter? They know that PreP and ART use the same substance class, NRTIs. We are not aware of one life expectancy study that separates the adverse and life threatening effects of ART in the HIV (not AID Syndrome!) epidemic and the changed drug regimes and reduced dosages in the last 2 decades.

Best regards,
Johannes Kreis



“Indeed, increasing evidence demonstrates that the antiretroviral drugs used for HIV treatment have toxic effects resulting in various cellular and tissue pathologies.”

A combination of Tenofovir and Emtricitabine can act as cellular stressors, leading to endothelial cell senescence, as demonstrated by a reduction in proliferation, and an increase in inflammatory markers (Cohen et al. 2018). This results in decreased BBB integrity and impaired endothelial cell functions. Exposure to Efavirenz has been shown to reduce endothelial viability at relatively low concentrations. This effect has been linked to multiple insults, such as a dysregulation of polymerase γ function, imbalance of intracellular calcium levels and depletion of ADP (Bertrand and Toborek 2015; Weiss et al. 2016; Faltz et al. 2017).”

 “Ten percent of HIV-negative MSM had low BMD at baseline. TDF use resulted in a small but statistically significant decline in BMD at the total hip and femoral neck. Larger studies with longer follow-up are needed to determine the trajectory of BMD changes and any association with clinical fractures.”

  • Owino et al., “Neurological syndrome in an HIV-prevention trial participant randomized to daily tenofovir disoproxil fumarate (300 mg) and emtricitabine (200 mg) in Bondo, Kenya”, Int Med Case Rep J. 2013; 6: 91–93,

“After an additional 4 days, she developed a disabling weakness of her upper limbs and tremors in her hands. The study product was discontinued, and within 2 weeks she was free of all symptoms. One month after restarting the drug, she complained of posture-dependent numbness of her upper limbs.”

  • Chan et al., “Potential kidney toxicity from the antiviral drug tenofovir: new indications, new formulations, and a new prodrug”, Curr Opin Nephrol Hypertens. 2018 Mar;27(2):102-112,

“Nephrologists should be aware of the potential kidney and bone toxicity of TDF, as well as unique situations in which the newer prodrug TAF may contribute to kidney injury.”

  • Kasonde et al., “Bone mineral density changes among HIV-uninfected young adults in a randomised trial of pre-exposure prophylaxis with tenofovir-emtricitabine or placebo in Botswana.”, PLoS One. 2014 Mar 13;9(3):e90111,

“Use of TDF-FTC was associated with a small but statistically significant decrease in BMD at the forearm, hip and lumbar spine. A high percentage (6.8%) of healthy Batswana young adults had abnormal baseline BMD  Further evaluation is needed of the longer-term use of TDF in HIV-uninfected persons.”

“Despite the triumph of highly active antiretroviral therapy (HAART) in anti-HIV infection, more than half of the HIV infection individuals receiving antiretroviral therapy acquire HIV-associated neurocognitive disorder (HAND). Previously researches had reported that the HAART neurotoxicity is implicated in HAND-related morbidity.”

TDF has neural toxicity effect that is relevant to the cell apoptosis, which may be related to the increasing prevalence of HAND.”

“Although the initial results of the clinical trials supported the renal safety of Tenofovir, clinical use of it has caused a low, albeit a significant, risk of renal damage either in the form of AKI or CKD. The pathophysiology has been linked to the effect of this medication on the proximal tubular cell. Although the exact mechanism is unknown, studies have suggested that Tenofovir accumulates in proximal tubular cells which are rich in mitochondria.”

“Here we present a case where Tenofovir treatment resulted in severe hypophosphatemia requiring hospitalization for parentral phosphate repletion.”

  • Suzuki et al., “Effect of Tenofovir Disoproxil Fumarate on Incidence of Chronic Kidney Disease and Rate of Estimated Glomerular Filtration Rate Decrement in HIV-1-Infected Treatment-Naïve Asian Patients: Results from 12-Year Observational Cohort.”, AIDS Patient Care STDS. 2017 Mar;31(3):105-112,

TDF use was associated with CKD [odds ratio (OR), 1.8 …]. The cumulative mean loss in the TDF group, relative to the control, increased over time after 1, 4, and 8 years of TDF exposure (-3.8, -5.5, and -9.0 mL/min/1.73 m2, respectively; p < 0.0001).

The eGFR rapidly declined during the first 3 months of cART, particularly in the TDF group (-26.4 vs. -7.4 mL/min/1.73 m2/year in the control).

In the TDF group, cART introduction was significantly associated with a faster rate of eGFR decline (from -0.44 to -2.11 mL/min/1.73 m2/year; p = 0.010), whereas in the control, the difference was not significant.

For HIV-1-infected Asian patients with low body weight, TDF-containing cART is associated with CKD and faster eGFR decline.”

“Sexually active women who were HIV negative were randomly assigned (3:1) to a tenofovir disoproxil fumarate ring or placebo ring.”

 “…; eight were asked to discontinue ring use early because of ulcerations (grade 1) near the ring; in the remaining two women, rings were electively removed by study staff on day 20 and day 23.”

 “…, all ulcers resolved after ring removal. No participants in the placebo group developed ulcers.

“Concentrations of multiple inflammatory cytokines and chemokines were significantly higher at days 14 and 28 compared with baseline in the tenofovir disoproxil fumarate ring group but not the placebo group.”

“In 1988, the suggestion that the first antiretroviral drug, zidovudine, was the potential cause of muscle pathology in HIV-infected persons resulted in structural and biochemical patient studies demonstrating acquired mitochondrial dysfunction. Assessment of subsequent nucleoside analog reverse transcriptase inhibitor (NRTI) antiretroviral drugs has indicated that mitochondria are a common target of NRTI toxicity in multiple tissues, leading to a wide variety of pathology ranging from lipodystrophy to neuropathy. Overwhelmingly, these complications have emerged during post-licensing human studies.”

“Millions of patients have been treated with mitochondrially toxic NRTIs and these drugs remain the backbone of antiretroviral rollout in much of sub-Saharan Africa.”

EU data base of adverse effects with 5400+ cases of severe side effects of TRUVADA (access 4.12.2019),

Could new antibody tests be used to test American pork for African Swine Fever?

Creative Diagnostics Launches New ASFV Antigens & Antibodies for Research

Read more:

African Swine Fever is a big story already because, when and if it spreads to all of Western Europe, all of Asia and the USA (where it may already be in pigs), it will cause the collapse of a major portion of the agricultural export economies of the affected countries. We're talking about many billions of dollars of losses. And the problem is not temporary because those countries will be suspected of harboring the disease in their wild boar and ticks for decades to come. The disease could easily become endemic. 

But the issue is so much more important because of the disturbing body of evidence that shows that African Swine Fever Virus can infect humans (despite what authorities currently insist). Thus far, Europe and America's leading publications and journalists have failed to warn the public of the impending ASFV risk to their health. Here are the biggest African Swine Fever stories they have missed.

1. The African Swine Fever Vaccine for humans.

"African Swine fever is an endemic disease in sub-Saharan Africa and many other parts of the developing world. It is caused by the African Swine virus that primarily replicates in macrophages and monocytes leading to the impairment of the structure and function of the immune system of the infected organisms. Until now the African Swine epidemic continues to spread despite all efforts to contain it. Thus, there is an objective need for effective, safe and affordable preventive and therapeutic approaches, in particular for effective vaccines, to control and eventually eradicate this disease. Since the characteristic feature of the African Swine virus is to impair the immune system and to cause immune deficiencies in its hosts the development of vaccines and other therapeutic approaches against the African Swine virus has implications for other immune deficiencies or diseases. Several other viruses are also known to cause immunodeficiency-like syndromes in humans, including cytomegalovirus, Epstein Barr Virus and others. Moreover, a series of cases of so-called "idiopathic" immunodeficiencies have been documented that display CD4+T-lymphocytopenia with opportunistic infections, but show no evidence of HIV infection. Since antibodies for the African Swine virus have been detected in humans, the possibility of human infection with the African Swine virus exists and may thus far have escaped any systematic screening. Thus, any preventive and therapeutic approach to African Swine fever can have far-reaching implications to control immune deficiency conditions in humans."

2. Evidence of African Swine Fever found in people with fevers.

Virus Identification in Unknown Tropical Febrile Illness Cases Using Deep Sequencing

Dengue virus is an emerging infectious agent that infects an estimated 50–100 million people annually worldwide, yet current diagnostic practices cannot detect an etiologic pathogen in ∼40% of dengue-like illnesses. Metagenomic approaches to pathogen detection, such as viral microarrays and deep sequencing, are promising tools to address emerging and non-diagnosable disease challenges. In this study, we used the Virochip microarray and deep sequencing to characterize the spectrum of viruses present in human sera from 123 Nicaraguan patients presenting with dengue-like symptoms but testing negative for dengue virus. We utilized a barcoding strategy to simultaneously deep sequence multiple serum specimens, generating on average over 1 million reads per sample. We then implemented a stepwise bioinformatic filtering pipeline to remove the majority of human and low-quality sequences to improve the speed and accuracy of subsequent unbiased database searches. By deep sequencing, we were able to detect virus sequence in 37% (45/123) of previously negative cases. These included 13 cases with Human Herpesvirus 6 sequences. Other samples contained sequences with similarity to sequences from viruses in the Herpesviridae, Flaviviridae, Circoviridae, Anelloviridae, Asfarviridae, and Parvoviridae families. In some cases, the putative viral sequences were virtually identical to known viruses, and in others they diverged, suggesting that they may derive from novel viruses. These results demonstrate the utility of unbiased metagenomic approaches in the detection of known and divergent viruses in the study of tropical febrile illness.

3. A Russian Scientist warns that African Swine Fever could infect humans.

Russian Scientist: ASF could become a human health risk

"The African swine fever (ASF) virus, may in the future become dangerous for humans, according to the head of the Russian Epidemiology Service, Chief State Sanitary Doctor Gennady Onishchenko, at the press-conference in St. Petersburg. According to him almost all viruses from time to time go through mutation processes which can give them some additional functions."

4. Detection of Novel Sequences Related to African Swine Fever Virus in Human Serum and Sewage.
Loh J, Zhao G, Presti RM, Holtz LR, Finkbeiner SR, Droit L, Villasana Z, Todd C, Pipas JM, Calgua B, Girones R, Wang D, Virgin HW.

Departments of Pathology & Immunology and Molecular Microbiology, Department of Medicine and Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Microbiology, Faculty of Biology, University of Barcelona, Barcelona, Spain.

"The family Asfarviridae contains only a single virus species, African swine fever virus (ASFV). ASFV is a viral agent with significant economic impact due to its devastating effects on populations of domesticated pigs during outbreaks, but has not been reported to infect humans. We report here the discovery of novel viral sequences in human serum and sewage which are clearly related to the Asfarvirus family, but highly divergent from ASFV. Detection of these sequences suggests that greater genetic diversity may exist among Asfarviruses than previously thought, and raises the possibility that human infection by Asfarviruses may occur."

5. How the American science Robert Gallo may have stolen the African Swine Fever research of a Boston University scientist and may have given African swine Fever the fraudulent new name of "HHV-6."

"In August, 1986, John Beldekas was invited to go to the NCI and present his findings on the link between ASFV [African Swine Fever virus] and AIDS, which he did. Beldekas gave samples of all his lab work to Gallo. Later, the government asked Beldekas to turn over all his reagents and lab work to the government, which he did. Beldekas had found ASFV presence in nine of 21 AIDS patients using two standard procedures. At the meeting, Gallo was reported saying: “we know it is not ASFV.” How could Gallo know this as he hadn’t done any of his own tests to look for ASFV?
Two months later, Gallo published an article in Science (Oct 31, 1986) that he discovered a new possible co-factor in AIDS, a virus he called Human B Cell Lymphotropic Virus which he named HBLV. Like ASFV, HBLV infected B cells and also lived in macrophages. Did Gallo steal Beldekas’s ASF virus he found in AIDS patients and rename it HBLV? Later on, when Gallo found that HBLV could also infect other immune cells, he changed the name of HBLV to HHV-6. Eventually, Gallo identified his HBLV as the variant A strain of HHV-6 and called it a human herpesvirus."
--Mark Konlee

6. The epidemiology that suggests that African Swine Fever in people in Sardinia is misidentified as HHV-8.

The world's highest incidence of Kaposi's sarcoma occurs in Sardinia (Reference) Is it possible that it is due to the fact that African Swine Fever Virus is endemic on the island? (Reference) One study suggests that the incidence of K.S. in northern Sardinia is highest in a countryside area where people have contact with animals. (Reference) Given the high prevalence of HHV-8,--the so-called K.S. herpes virus--in Sardinia (Reference) is it at all possible that HHV-8 may have been misclassified and actually is a human-adapted form of African Swine Fever Virus? (ASFV has been at least visually mistaken for another herpes virus, CMV, in the past.)

A number of experiments could be conducted to explore this hypothesis. In addition to a direct comparison of ASFV and HHV-8, pigs with African Swine Fever Virus could be tested for sequences of HHV-8. People with Kaposi's sarcoma could be tested for sequences of African Swine Fever, including new Asfaviridae sequences recently discovered. (Reference) 

A comparison of the K.S. lesions in humans and ASFV lesions in pigs might be in order.Given that African Swine Fever is currently spreading in Russia and is now threatening Europe and China, (Reference) it would be useful to know whether people who are exposed to pigs with ASFV are at increased risk for HHV-8, Kaposi's sarcoma and the other pathologies associated with HHV-8. A study in sub-Saharan Africa where ASFV is endemic and HHV-8 is also endemic (Reference) might be useful. And areas of Russia where ASFV is spreading could be monitored closely for any signs of an increase of K.S. or HHV-8 infection and HHV-8 related pathologies.HHV-8 is an emerging health problem. HHV-8-associated K.S. is a significant problem in AIDS patients. It may also be the key to Chronic Fatigue Syndrome. HHV-8 has been found in the cerebrospinal fluid of 50% of Chronic Fatigue Syndrome patients. (Reference) HHV-8 has been linked to type 2 diabetes. (Reference) HHV-8 has been detected in B-cells in Castleman's disease and primary effusion lymphoma. (Reference).

If HHV-8 is a form of ASFV, it is possible that pigs might constitute a useful animal model for the study of possible treatments for K.S. and other pathologies associated with HHV-8. And if there is any relationship between ASFV and HHV-8, people may have to be warned to take special precautions around pigs in areas where there are ASFV outbreaks. And countries where undercooked pork is consumed (like Ukraine where salo is a staple) may need to alert the public to cook all pork products thoroughly during ASFV epidemics.

7. ASF virus, adapted to grow in VERO cells, produces a strong cytopathic effect in human macrophages leading to cell destruction.

8. A sick child tests positive for African Swine Fever virus.

9. Newspaper publisher writes The Chronic Fatigue Syndrome Epidemic Cover-up, a memoir about uncovering the African Swine Fever cover-up in America.

The Chronic Fatigue Syndrome Epidemic Cover-up details the investigative reporting of a New York Native that reveals the Centers for Disease Control and the United States Department of Agriculture lied about the presence of African Swine Fever in pigs and people.

10. Journalist pens The African Swine Fever Novel, an Orwellian novel warning about the consequences of an African Swine Fever Virus epidemic in humans.

The African Swine Fever Novel is available here

11. Prisoners fed meat infected with African Swine Fever

12. African Swine Fever seems to be in the USA already.!

13. African Swine Fever has its evolutionary origins in marine environments.

H. Ogata, K. Toyoda, Y. Tomaru, N. Nakayama, Y. Shirai, J.-M. Claverie, K. NagasakiRemarkable sequence similarity between the dinoflagellate-infecting marine girus and the terrestrial pathogen African swine fever virus
Virol. J., 6 (2009), p. 178, 10.1186/1743-422X-6-178

Heterocapsa circularisquama DNA virus (HcDNAV; previously designated as HcV) is a giant virus (girus) with a approximately 356-kbp double-stranded DNA (dsDNA) genome. HcDNAV lytically infects the bivalve-killing marine dinoflagellate H. circularisquama, and currently represents the sole DNA virus isolated from dinoflagellates, one of the most abundant protists in marine ecosystems. Its morphological features, genome type, and host range previously suggested that HcDNAV might be a member of the family Phycodnaviridae of Nucleo-Cytoplasmic Large DNA Viruses (NCLDVs), though no supporting sequence data was available. NCLDVs currently include two families found in aquatic environments (Phycodnaviridae, Mimiviridae), one mostly infecting terrestrial animals (Poxviridae), another isolated from fish, amphibians and insects (Iridoviridae), and the last one (Asfarviridae) exclusively represented by the animal pathogen African swine fever virus (ASFV), the agent of a fatal hemorrhagic disease in domestic swine. In this study, we determined the complete sequence of the type B DNA polymerase (PolB) gene of HcDNAV. The viral PolB was transcribed at least from 6 h post inoculation (hpi), suggesting its crucial function for viral replication. Most unexpectedly, the HcDNAV PolB sequence was found to be closely related to the PolB sequence of ASFV. In addition, the amino acid sequence of HcDNAV PolB showed a rare amino acid substitution within a motif containing highly conserved motif: YSDTDS was found in HcDNAV PolB instead of YGDTDS in most dsDNA viruses. Together with the previous observation of ASFV-like sequences in the Sorcerer II Global Ocean Sampling metagenomic datasets, our results further reinforce the ideas that the terrestrial ASFV has its evolutionary origin in marine environments.

books on kindle

Two books on amazon

Everyone needs to know what the CDC is hiding about CFS and HHV-6. NEW YORK NATIVE contains both volumes of THE CHRONIC FATIGUE SYNDROME EPIDEMIC COVER-UP. The print version is $23. Only $7.98 in Kindle.

Popular Posts in the Last 7 Days

Our books on Amazon that are changing the way the world looks at CFS, HHV-6, and AIDS

Blog Archive

Closing Argument Audible

African Swine Fever Novel Audible

Stonewall Audible