“When you get an idea into your head you find it in everything.”
“There are plenty who regard a wall behind which something is happening as a very curious thing.”
Quasimodo to the To the Gargoyle: “Why was I not made of stone like thee?”
― Victor Hugo, The Hunchback of Notre-Dame
The heart is deceitful above all things and beyond cure— And desperately wicked; Who can know it? Jeremiah 17:9
“…Israel, which shall know every man the plague of his own heart, and spread forth his hands toward this house: Then hear thou in heaven thy dwelling place, and forgive, and do, and give to every man according to his ways…”
1 Kings 8:35-40, KJV
“Heads rule hearts in most its true, for hearts are tender and need strong protection. Heads keep order and still the pain, explain our being, and make things plain. Everything ordered, shaped, and transformed, into ideas that fit the norm. Who wants to step out, take a risk and live ruled by the heart…” Wisdom is in the Heart 8-10-98
Published April 19, 2020
So I have absolutely no business speculating about Covid-19-HIV. I have no medical training, no research credentials and absolutely no good manners. However, people are dying and people’s reproductive health is possibly being impacted by an infectious disease for which there is little understanding and confusion in the medical community. The scientific community is biased against, intuitive, right brained, whole to parts thinkers. How dare a poet speak about science? Right brained thinkers have the incredible gift, or curse depending on how you view it, of being able to synthesize large data sets into a manageable core. If this musing should by some incredible stroke of luck be true, maybe it’s time for poets to rule over science, so the hubris of the scientists who have brought us to the brink can be reined in. And when the true intent of this elegantly designed evil is uncovered, the whole world may gasp at the wickedness of the minds that created it.
First, I should discuss my “genesis bias.” It is the vision of how we perceive something when we are first introduced to it. Unfortunately, our genesis biases often continue to follow us and color our beliefs long after they should be discarded. My first impression of Covid-19-HIV was it was little more than the ordinary flu and being totally overblown for political purposes. In spite of this view, I had this nagging worry caused by the fear that I saw in faces of those in positions of authority around the world.
PART I: The Weapon
Most people are aware of the much discredited and discounted theory that Covid-19-HIV was developed in a lab. There are two different takes on this. The first is that it was developed as a biological weapon. The second is that Covid-19-HIV was being developed as a vaccine for HIV. It doesn’t really matter which of these is correct, (or if neither are correct) because the effect on the general population after release is exactly the same. That being the case, it is hard not to speculate about what an effective weapon, Covid-19-HIV would be if it did indeed have HIV inserted into it.
While this all could be true, I also feel that there might be another source for Covid-19 that has been unleashed on the world. It could have come from the American Military Industrial Complex. It also may of been launched by the elite who are trying to bring about a New World Order. The Davos crowd and the people funded by the Rockefeller Foundation. I have no profound bias toward a Chinese source. Covid-19 is accomplishing many long standing goals of the elites in one package:
- It is destroying the world economy. This will also weaken America and the dollar. This allows for the long standing goal of bringing into being a world, digital currency.
- It is destroying the middle class all over the world. Their are huge divides forming among the American population. When the middle class is destroyed fascism always follows.
- Everyone will become poor and lose their political power accept for the elites.
- There will be calls for a world government so this never happens again.
- The vaccination will include tracking technology to keep us safe but which can also be used to track all of our movements.
- It will probably bring down President Donald Trump who was pursuing a nationalistic agenda for America which is at odds with the globalist goals.
- Its training “citizens” to be snitches, useful proles.
- And…if there were a population control mechanism inserted in the virus, that would meet long standing goals to cull the population to prevent global warming.
Wow! So many goals accomplished, in days, with one little virus, after spending decades trying to bring about these same goals with global warming. Bill Gates and Henry Kissinger have both crawled out of their hidey-holes to give their vaunted opinions.
Some have convincingly made the case that this is a U.S. defense research is actually the basis of the entry of the virus into the general population. Whitney Webb at thelastamericanvagabond.com makes the case with detailed links that: “Though most English-language media outlets to date have not examined such a possibility, there is considerable supporting evidence that deserves to be examined. For instance, not only was the U.S. military, including its controversial research arm — the Defense Advanced Research Projects Agency (DARPA), recently funding studies in and near China that discovered new, mutant coronaviruses originating from bats, but the Pentagon also became recently concerned about the potential use of bats as bioweapons.”
“Two years ago, media reports began discussing the Pentagon’s sudden concern that bats could be used as biological weapons, particularly in spreading coronaviruses and other deadly diseases. The Washington Post asserted that the Pentagon’s interest in investigating the potential use of bats to spread weaponized and deadly diseases was because of alleged Russian efforts to do the same. However, those claims regarding this Russian interest in using bats as bioweapons date back to the 1980s when the Soviet Union engaged in covert research involving the Marburg virus, research that did not even involve bats and which ended with the Soviet Union’s collapse in 1991.”
“Like much of the Pentagon’s controversial research programs, the bats as bioweapons research has been framed as defensive, despite the fact that no imminent threat involving bat-propagated bioweapons has been acknowledged. However, independent scientists have recently accused the Pentagon, particularly its research arm DARPA, of claiming to be engaged in research it says is ‘defensive’ but is actually ‘offensive.'”
“The most recent example of this involved DARPA’s “Insect Allies” program, which officially “aims to protect the U.S. agricultural food supply by delivering protective genes to plants via insects, which are responsible for the transmission of most plant viruses” and to ensure “food security in the event of a major threat,” according to both DARPA and media reports. “
“However, a group of well-respected, independent scientists revealed in a scathing analysis of the program that, far from a “defensive” research project, the Insect Allies program was aimed at creating and delivering “new class of biological weapon.’ The scientists, writing in the journal Science and led by Richard Guy Reeves, from the Max Planck Institute for Evolutionary Biology in Germany, warned that DARPA’s program — which uses insects as the vehicle for as horizontal environmental genetic alteration agents (HEGAAS) — revealed ‘an intention to develop a means of delivery of HEGAAs for offensive purposes (emphasis added).'”
“Whatever the real motivation behind the Pentagon’s sudden and recent concern about bats being used as a vehicle for bioweapons, the U.S. military has spent millions of dollars over the past several years funding research on bats, the deadly viruses they can harbor — including coronaviruses — and how those viruses are transmitted from bats to humans.”
“For instance, DARPA spent $10 million on one project in 2018 ‘to unravel the complex causes of bat-borne viruses that have recently made the jump to humans, causing concern among global health officials.’ Another research project backed by both DARPA and NIH saw researchers at Colorado State University examine the coronavirus that causes Middle East Respiratory Syndrome (MERS) in bats and camels ‘to understand the role of these hosts in transmitting disease to humans.’ Other U.S. military-funded studies, discussed in detail later in this report, discovered several new strains of novel coronaviruses carried by bats, both within China and in countries bordering China.”
“Many of these recent research projects are related to DARPA’s Preventing Emerging Pathogenic Threats, or PREEMPT program, which was officially announced in April 2018. PREEMPT focuses specifically on animal reservoirs of disease, specifically bats, and DARPA even noted in its press release in the program that it ‘is aware of biosafety and biosecurity sensitivities that could arise’ due to the nature of the research.”
“DARPA’s announcement for PREEMPT came just a few months after the U.S. government decided to controversially end a moratorium on so-called “gain-of-function” studies involving dangerous pathogens. VICE News explained “gain-of-function” studies as follows:”
“In addition, while both DARPA’s PREEMPT program and the Pentagon’s open interest in bats as bioweapons were announced in 2018, the U.S. military — specifically the Department of Defense’s Cooperative Threat Reduction Program — began funding research involving bats and deadly pathogens, including the coronaviruses MERS and SARS, a year prior in 2017. One of those studies focused on “Bat-Borne Zoonotic Disease Emergence in Western Asia” and involved the Lugar Center in Georgia, identified by former Georgian government officials, the Russian government and independent, investigative journalist Dilyana Gaytandzhieva as a covert U.S. bioweapons lab.”
“The decision to shut down USAMRIID garnered surprisingly little media coverage, as did the CDC’s surprising decision to allow the troubled facility to “partially resume” research late last November even though the facility was and is still not at “full operational capability.” The USAMRIID’s problematic record of safety at such facilities is of particular concern in light of the recent coronavirus outbreak in China. As this report will soon reveal, this is because USAMRIID has a decades-old and close partnership with the University of Wuhan’s Institute of Medical Virology, which is located in the epicenter of the current outbreak.”
The Rockfeller Foundation in Publication titled, “Scenarios for the Future of Technology and International Development, published in May of 2010, discusses a scenario of future pandemic in 2012, that precisely matches what is happening right now:
“In 2012, the pandemic that the world had been anticipating for years finally hit. Unlike 2009’s H1N1, this new influenza strain—originating
from wild geese—was extremely virulent and deadly. Even the most pandemic-prepared nations were quickly overwhelmed when the virus streaked around the world, infecting nearly 20 percent of the global population and killing 8 million in just seven months, the majority of them healthy young adults. The pandemic also had a deadly effect on economies: international mobility of both people and goods screeched to a halt, debilitating industries like tourism and breaking global supply chains. Even locally, normally bustling shops and office buildings sat empty for months, devoid of both employees and customers. The pandemic blanketed the planet—though disproportionate numbers died in Africa, Southeast Asia, and Central America, where the virus spread like wildfire in the absence
of official containment protocols. But even in developed countries, containment was a challenge. The United States’s initial policy of
“strongly discouraging” citizens from flying proved deadly in its leniency, accelerating the spread of the virus not just within the U.S. but across borders. However, a few countries did fare better—China in particular. The Chinese government’s quick imposition and enforcement of mandatory quarantine for all citizens, as well as its instant and near-hermetic sealing off of all borders, saved millions of lives, stopping the spread of the virus far earlier than in other countries and enabling a swifter postpandemic recovery.” Please remember these words were written in a Rockefeller publication ten years ago.
The report concludes what it sees are the implications for the various scenarios presented. “First, the link between technology and governance is critical to consider in better understanding how technology could be
developed and deployed. In some futures, the primacy of the nation-state as a unit of analysis in development was questioned as both supra- or sub-national structures proved more salient to the achievement of development goals. In other futures, the nation-state’s power strengthened and it became an even more powerful actor both to the benefit and to the detriment of
the development process, depending on the quality of governance. Technologies will affect governance, and governance in turn will play
a major role in determining what technologies are developed and who those technologies are intended, and able, to benefit.”
“At first, the notion of a more controlled world gained wide acceptance and approval. Citizens willingly gave up some of their sovereignty—and their privacy—to more paternalistic states in exchange for greater safety and stability. Citizens were more tolerant, and even eager, for top-down direction and oversight, and national leaders had more latitude to impose order in the ways they saw fit. In developed countries, this heightened oversight took many forms: biometric IDs for all citizens, for example, and tighter regulation of key industries whose stability was deemed vital to national interests. In many developed countries, enforced cooperation with a suite of new regulations and agreements slowly but steadily restored both order and, importantly,
economic growth.”
It is also important to point out the fact that the U.S. military’s key laboratories involving the study of deadly pathogens, including coronaviruses, Ebola and others, was suddenly shut down last July after the Center for Disease Control and Prevention (CDC) identified major ‘biosafety lapse’ at the facility.'” Again, I urge your to read the whole report by Whitney Webb, with its impeccable research and incredible implications.
Others think the virus emerged from labs in China. “A theory put forward by French professor Luc Montagnier — award-winning co-discoverer of the AIDS virus but also mocked by some colleagues for some outrageous theories — has sparked a scientific firestorm. According to the Nobel Prize winner in medicine, a man used to controversy, the SARS-CoV-2 virus is the result of an attempt to manufacture a vaccine against the AIDS virus, Agence France Presse reported.”
“Montagnier says the presence of elements of HIV in the genome of the new virus and even elements of the “germ of malaria” are highly suspect, the report said. Interviewed on the French CNews channel, he said the characteristics of the new coronavirus could not have arisen naturally. The ‘industrial’ accident was said to have taken place in the Wuhan National Bio-safety Laboratory, he added.”
What if the goals and agenda behind Covid-19-HIV are a multi-fold magnitude worse than the most evil mind could conceive? What if the Covid-19-HIV is only a delivery system, with collateral damage to the elderly and infirm, but whose main goal is infertility, long term health issues and population control in the asymptomatic Covid-19 cohort. What groups or nations are behind its development is a question for another day. Today we need to just understand the goal of this awakening plague on mankind.
The main goal of Covid-19-HIV as a biological weapon would be to have a devastating initial impact, which would then be followed by a stealth, deadly, infection, through a virus inserted with HIV. This would be magnificently effective. Since initial HIV and flu both present with very similar symptoms, it would be probable that the HIV might be missed by practitioners, where it then could lay in the body to cause long term damage. Even if it was designed as a benign vaccine delivery system it contains the same potential devastating attributes.
Rethinking all of this in the light of recent revelations, what if Covid-19-HIV was developed by very evil people as a delivery system for population control? What if the HIV component has been inserted into the virus to cause mass infertility issues among one nation or the global population? What if the Covid-19-HIV is a fertility inhibitor that would linger in asymptomatic younger population?
All of this became front of mind with recent studies showing that Covid-19-HIV is present in the Ace receptors of the testicles of men. This led me to recent studies in Asia which have shown that Covid-19-HIV is causing fertility problems in infected men.
“This report is from an article from the Thailand Medical News, showing that the Coronavirus rendered certain males infertile, published on February 16, 2020. The latest coronavirus research by medical scientists from Nanjing Medical University and Suzhou Hospital lead by Dr Jianqing Wang, Head of the Department of Urology, at Suzhou Hospital say that certain males affected by the SARS-Cov2 coronavirus which causes the Covid-19 disease might likely become infertile even if they recover from the infection. According to the new researched published in medrxiv, an open source online medical journal, the coronavirus typically attacks the ACE2 (Angiotensin Converting Enzyme 2)) receptors in human tissues.”
“The team of urology researchers that comprised of Dr Jianqing Wang, Dr Caibin Fan, Dr Kai Li, Dr Yanhong Ding and Dr Wei Lu focused primarily on renal and testicular tissues as these were also ‘rich’ with ACE2 receptors especially the renal tubular cells, Leydig cells and cells in seminiferous ducts in the testis.”
“The study results showed that the new coronavirus expressed potent pathogenicity to both renal and testicular tissues with resultant lesions. The damaged testicular tissues could lead to infertility in most of the male patients. The researchers advised that during drug treatments with coronavirus infected patients, clinicians should pay careful attention to renal function evaluation as some of the antivirals which known to exhibit renal toxicity can aggravate the and virus damaged kidneys.”
“The researchers also advised that all clinicians pay attention to the risk of testicular lesions in patients during hospitalization and later clinical follow-ups, especially the assessment and appropriate intervention in male patients’ fertility.”
“The research was based on the data-sets of 146 male patients in three different settings. Thailand Medical News notes that the research has yet to have been peer reviewed. However, the results on this research could have large implications and effect on the thousands of male patients infected with the coronavirus.”
The referenced paper, ACE2 Expression in Kidney and Testis May Cause Kidney and Testis Damage after 2019-nCoV Infection, by Caibin Fan, Et.al is cited below.
“In December 2019 and January 2020, novel coronavirus (2019-nCoV) – infected pneumonia (NCIP) occurred in Wuhan, and has already posed a serious threat to public health. ACE2 (Angiotensin Converting Enzyme 2) has been shown to be one of the major receptors that mediate the entry of 2019-nCoV into human cells, which also happens in severe acute respiratory syndrome coronavirus (SARS). Several researches have indicated that some patients have abnormal renal function or even kidney damage in addition to injury in respiratory system, and the related mechanism is unknown. This arouses our interest in whether coronavirus infection will affect the urinary and male reproductive systems. Here in this study, we used the online datasets to analyze ACE2 expression in different human organs. The results indicate that ACE2 highly expresses in renal tubular cells, Leydig cells and cells in seminiferous ducts in testis. Therefore, virus might directly bind to such ACE2 positive cells and damage the kidney and testicular tissue of patients. Our results indicate that renal function evaluation and special care should be performed in 2019-nCoV patients during clinical work, because of the kidney damage caused by virus and antiviral drugs with certain renal toxicity. In addition, due to the potential pathogenicity of the virus to testicular tissues, clinicians should pay attention to the risk of testicular lesions in patients during hospitalization and later clinical follow-up, especially the assessment and appropriate intervention in young patients’ fertility.”
“Angiotensin converting enzyme 2 (ACE2) belongs to the angiotensin-converting enzyme family of dipeptidyl carboxydipeptidases, which is homologous to human angiotensin 1 converting enzyme. The expression distribution of ACE2 suggests that it might play critical roles in the regulation of cardiovascular and renal function, as well as fertility…Here in this study, we analyzed the online datasets to uncover the expression pattern of ACE2 in urinary and male reproductive systems, which is the potential mechanism of abnormal renal function or even kidney damage in patients infected with 2019-nCoV. Moreover, we emphasized high ACE2 expression level in testis because of the potential pathogenicity of the virus to testicular tissues, especially the potential risks affecting fertility.”
“Another major point in this study is the high expression level of ACE2 in testicular cells. It is well known that viruses such as HIV, HBV and mumps could enter the testicular cells and cause viral orchitis. Besides, in some cases, virus-induced testicular tissue damage might result in male infertility and testicular tumor [19]. SARS-CoV is just like the ‘cousin’ of 2019-nCoV and shares the receptor ACE2 with 2019-nCoV. Previous research has also investigated the possible damage of the testis in SARS patients and the effects of SARS on spermatogenesis. Their findings suggested that orchitis is a complication of SARS and that spermatogenesis could be affected after infection [20]. Current clinical data show that a large proportion of the novel coronavirus (2019-nCoV) – infected pneumonia patients are young adults and even children, so the potential testicular damage caused by the virus may exist as a late complication. However, limited information is available regarding the involvement of reproductive organs in patients infected with 2019-nCoV. Therefore, our findings suggest that clinicians should take care of the possible occurrence of orchitis. Following-up and evaluation of the reproductive functions should be done in recovered male SARS patients, especially the young male patients.”
“In another study cited below which was funded by the National Institute of Health and published on February 21, 2020 by Zhengpin Wang and Xiaojiang Xu. A series of studies have provided the bioinformatics evidence of potential routes of SARS-CoV-2 infection in respiratory, cardiovascular, digestive and urinary systems. SARS-infected male patients show wide-spread germ cell destruction, few or no spermatozoon in the seminiferous tubules, and a thickened basement membrane in the testes. However, whether the reproductive system is susceptible to SARS-CoV-2 infection has not yet been determined. In this study, we investigate the RNA expression profiles of ACE2 in adult human testes at single-cell resolution. Our study documents that ACE2 is predominantly enriched in spermatogonia and Leydig and Sertoli cells. ACE2-positive cells possess higher abundance of transcripts associated with viral reproduction and transmission, and lower abundance of transcripts related to male gametogenesis. Thus, the reported ACE2 expression in human testes suggests that SARS-CoV-2 could infect the male gonad and risk male reproductive dysfunction.”
“…In summary, our study provides bioinformatics evidence that the testis may be potentially vulnerable to SARS-CoV-2 infection. These investigations suggest that the reproductive functions should be followed and evaluated in recovered COVID-2019 male patients. Our findings may also have translational implications for the treatment of reproductive defects caused by SARS-CoV-2 infection.”
In another study cited below, ACE2 angiotensin I converting enzyme 2 [ Homo sapiens (human) ] Gene ID: 59272, updated on 5-Apr-2020, the summary states: The protein encoded by this gene belongs to the angiotensin-converting enzyme family of dipeptidyl carboxydipeptidases and has considerable homology to human angiotensin 1 converting enzyme. This secreted protein catalyzes the cleavage of angiotensin I into angiotensin 1-9, and angiotensin II into the vasodilator angiotensin 1-7. The organ- and cell-specific expression of this gene suggests that it may play a role in the regulation of cardiovascular and renal function, as well as fertility.
Should the fact that these last two studies were funded by the National Institute of Health in Bethesda Maryland be troubling? Does the federal government know more about Covid-19-HIV than they have told the public? Do they understand the reproductive risk of infection with Covid-19-HIV?
General studies regarding fertility and HIV have also noted a link between the disease and a reduction in fertility. Shari Margoles in the Body Pro states that, “Biological mechanisms also influence fertility rates in HIV-positive women and men. Research has shown that women with HIV may find it more difficult to conceive than their HIV-negative counterparts. HIV infected women experience reduced pregnancy rates and higher rates of both planned abortion and miscarriage. HIV/AIDS may induce sterility, increase fetal mortality, decrease production of spermatozoa, and sometimes decrease frequency of sexual intercourse, all contributing to declining fertility.”
“Amanda Ross of the Swiss Tropical Institute in Basel and colleagues studied a cohort of 191 women (92 HIV positive and 99 HIV negative at enrollment), aged 15-49, in southwest Uganda between 1990 and 2001 to better understand the association between HIV disease progression and the incidence of pregnancy. Among the women with HIV, sexual intercourse became less frequent as HIV disease progressed. In their analysis, Ross’ team found that “fertility is reduced from the earliest asymptomatic stage of HIV infection resulting from both a reduced incidence of recognized pregnancy and increased fetal loss. The greatest reduction in fertility was observed following progression to AIDS when there was a very low incidence of recognized pregnancies.” (A recognized pregnancy refers to the implantation and survival of an embryo in the lining of the uterus.) These data were published in the March 26, 2004 issue of AIDS.”
“An earlier study of 412 HIV-positive women in Paris and southeastern France from 1988 to 1993 by Isabelle De Vincenzi of Saint-Maurice National Hospital and colleagues found that the incidence of pregnancy decreased by more than half, from 20.4 per 100 person-years before HIV diagnosis to 7.9 per 100 person-years after HIV diagnosis. (A person-year is a shorthand term used by epidemiologists to make comparisons.) The study also showed that the proportion of pregnancies voluntarily interrupted more than doubled from 29% to 63% after HIV diagnosis. The percentage of miscarriages and ectopic (outside the womb) pregnancies increased significantly from 8.3% to 25.4% of those conceived before and after HIV diagnosis, respectively. Also, the proportion of women who were sexually inactive rose four-fold, from 5% before to 20% after HIV diagnosis. These data were published in the March 11, 1997 issue of AIDS.”
“…D’Ubaldo’s team offered possible explanations for increased spontaneous abortion (miscarriage) in HIV-positive women. They suggested that HIV affects the placenta by interfering with the transfer of important nutrients to the fetus, or that the virus causes abnormal development of the embryo. Other theories include a direct relationship between HIV and the fetal thymus gland, as well as an increased risk of infection due to the weakened immune system of the mother. HIV may also directly influence the ability of HIV-positive men to produce healthy sperm.”
In the article, HIV/AIDS and Infertility: Emerging Problems in the Era of Highly Active Antiretrovirals, authored by Vitaly A. Kushnir, M.D. and William Lewis, M.D. there are detailed descriptions of how HIV affects male fertility. “Male infertility also can impact reproductive efficacy in HIV/AIDS. Sperm parameters that reflect fertility are significantly impaired in HIV-1 infected men. Measurements including semen volume, sperm motility, concentration and morphology are adversely affected. Semen parameters correlate positively with CD4 counts, which suggests that patients with full blown AIDS are less fertile than healthier HIV-1 infected males. HIV-1 infected men are more likely to have orchitis, hypogonadism, and leukospermia which could account for oligospermia and teratozoospermia. Barboza et al employed atomic force microscopy to examine sperm morphological and topographical changes in HIV/AIDS patients receiving HAART and revealed that damage to the spermatozoa was due to HAART rather than the HIV-1 virus. These ultrastructural findings contrast earlier ones where no adverse effect on sperm resulted from AZT treatment. Recent data indicate that HAART significantly decreased total sperm count, progressive motility, and post-preparation count while it significantly increases the proportion of abnormal sperm forms…Orhchitis and acute epididymitis in HIV positive men has been reported involving opportunistic infections including CMV, salmonella, toxoplasmosis, Ureaplasma, Urealyticum, Corynebacterium and Mima Polymorphia, fungi and mycobacteria. Kaposi’s sarcoma and lymphoma involving the testes have also been described”
“Hypogonadism, diminished libido and impotence are major issues in HIV infected men. Erectile and ejaculatory dysfunction is estimated to affect 60% of men with advanced disease. Caution should be used when treating erectile dysfunction with inhibitors of PDE5 in patients who are also taking protease inhibitors as both families of drugs are metabolized by cytochrome P450 3A4 95–97. In general, the lowest dose of PDE5 inhibitor should be started to avoid risk of adverse events including priapism.”
“Men tend to have normal testosterone levels early in the course of HIV disease. As the disease progresses to AIDS, testosterone levels decline. Androgen deficiency is particularly common in AIDS wasting syndrome. The progressive decline in testosterone has been attributed to both gonadal and extragonadal causes. Secondary hypogonadism is more commonly seen than primary hypogonadism due to testicular atrophy.”
Part II: The Virus
Recent testing in Boston has shown that a large number of residents in Pine Street Inn, a homeless facility have asymptomatic Covid-19-HIV. Are these people without symptoms because many are intravenous drug users who already infected HIV? Further study will be done to uncover the link to lack of symptoms among the people with HIV with heretofore undiscovered health issues which might impact Covid-19-HIV.
The first clue of the quest began with all of the odd attributes of this supposed coronavirus. These attributes really didn’t fit the profile of a virus. These questions were raised and well-articulated by Dr. Cameron Kyle-Siddell and other doctors in Italy. Why was this virus acting so strangely?
Of course, the place the medical community has refused to go to is to the unthinkable. This virus is lab generated.
A recent article from the Global Times which quote doctors in China says that Covid-19 is “like a combination of SARS and AIDS.” “Autopsies show severe damage to COVID-19 patients’ lungs and immune system, according to a doctor in Wuhan reached by the Global Times, who called for measures to prevent fibrosis of the lungs at an early stage of the disease. ‘The influence of COVID-19 on the human body is like a combination of SARS and AIDS as it damages both the lungs and immune systems,’ Peng Zhiyong, director of the intensive care unit of the Zhongnan Hospital of Wuhan University in Wuhan, told the Global Times on Friday.”
Peng said he had just talked to Liu Liang, a forensic specialist from the Tongji Medical College at Huazhong University of Science and Technology. Liu’s team has reportedly conducted nine autopsies on deceased COVID-19 patients as of February 24. The autopsy results Liu shared inspired me a lot. Based on the results, I think the most important thing now is to take measures at an early stage of the disease to protect patients’ lungs from irreversible fibrosis,’ Peng noted.”
A recent Thailand Medical News Report states, “To add to many studies already showing that the deadly and potent ways the SARS-Cov-2 has of attacking various human host cells and also critical proteins and cellular pathways in the human cells, a new collaborative study by researchers from the United States and China now shows that the SARS-CoV-2 coronavirus also attacks the T Lymphocytes similarly to the way that HIV viruses act. The human immune system has many components that work together in protecting the body from foreign invaders. One of the most important types of immune cells is T lymphocytes or T cells, a type of white blood cell that acts as the core of adaptive immunity, the system that modifies the immune response to specific pathogens.”
“Researchers from the New York Blood Centre and also from Fudan University in Shanghai have discovered that the SARS-CoV-2 coronavirus which causes the COVID-19 disease that often results severe acute respiratory syndrome also attacks the immune system’s T lymphocytes. The worrying findings highlight the destructive power of the novel coronavirus, which can destroy the immune system, leaving the patient vulnerable and unable to fight off the infection. The researchers’ surprise discovery has shed light on the potency of the novel coronavirus is killing powerful immune cells, which are supposed to kill the virus instead.”
“Already Thailand Medical News had warned about a mutated gene that the SARS-CoV-2 coronavirus had that was similar to HIV virus and also a discovered manner it had in attacking human host cells using the furin cleavage that was also similar in the HIV virus in February 2020 but few researchers paid any attention to it. The researchers had studied the virus’s action on T-lymphocyte cell lines. T lymphocytes or T cells work by identifying and eliminating foreign invaders in the body. However, surprisingly, the researchers found that when the SARS-Cov-2 coronavirus and the T cell came into contact with each other, the T cell became prey to the coronavirus, wherein a structure in the spike of the coronavirus triggered the attachment of a viral envelope to the cell membrane of the T cells. After, the genes of the virus entered the T cell and overwhelmed it and took it hostage, the SARS-Cov-2 coronavirus deactivated its ability to protect the human host body.”
The researchers also experimented with the SARS virus, and another coronavirus, but these pathogens were not able to infect T cells. The researchers suspect that the SARS virus, which caused an outbreak in 2002 to 2003, lacks a membrane fusion or binding function capability. The virus can only infect cells that have a particular receptor protein called the angiotensin-converting enzyme 2 (ACE2). T cells contain only a few ACE2 receptor proteins.”
“The research is a major breakthrough as knowing the effect of the SARS-CoV-2 on T cells may show why the disease is spreading so quickly, and infecting so many across the world. It also explains why certain vulnerable populations are at a high risk of dying from the infection, including those who are more than 65, those who are immunocompromised, and those with underlying medical conditions like lung disease, heart disease, diabetes, and hypertension.”
“Additional research also showed that patients who died from COVID-19 had damage to their bodies similar to both SARS and HIV. Also, the team found that unlike HIV that replicates faulty T cells, the coronavirus does not replicate, showing that the T cells and the virus may end up dying together. The new study has also a lot of implications on recovered patients and also asymptomatic patients and their future health conditions as long as there are residual amounts of the coronavirus in their bodies. One virologists who wanted to remain anonymous commented, “These findings show that we have a super potent virus that is evolving and behaving like an airborne HIV ‘cousin’!”
An article from February 27, 2020 in the Inkstone News states, “The new coronavirus has an HIV-like mutation that means its ability to bind with human cells could be up to 1,000 times as strong as the Sars virus, according to new research by scientists in China and Europe. The discovery could help to explain not only how the infection has spread but also where it came from and how best to fight it. Scientists showed that the virus that causes Sars (severe acute respiratory syndrome) entered the human body by binding with a receptor protein called ACE2 on a cell membrane.”
“Some early studies suggested that the new coronavirus, which shares about 80% of the genetic structure of Sars, might follow a similar path. But the ACE2 protein does not exist in large quantities in healthy people, and this partly helped limit the scale of the Sars outbreak of 2002-03, which infected about 8,000 people around the world. Other highly contagious viruses, including HIV and Ebola, target an enzyme called furin, which works as a protein activator in the human body.When looking at the genome sequence of the new coronavirus, also known as 2019-nCoV, Professor Ruan Jishou and his team at Nankai University in Tianjin found a section of mutated genes that did not exist in Sars, but were similar to those found in HIV and Ebola. “This finding suggests that 2019-nCoV may be significantly different from the Sars coronavirus in the infection pathway,” the scientists said in a paper published this month on Chinaxiv.org, a platform used by the Chinese Academy of Sciences to release scientific research papers before they have been peer-reviewed. This virus may use the packing mechanisms of other viruses such as HIV.”
“According to the study, the mutation can generate a structure known as a cleavage site in the new coronavirus’ spike protein.The virus uses the outreaching spike protein to hook on to the host cell, but normally this protein is inactive. The cleavage site structure’s job is to trick the human furin protein, so it will cut and activate the spike protein. The activation causes a “direct fusion” of the viral and cellular membranes. Compared to the Sars virus’s way of entry, this binding method is “100 to 1,000 times” as efficient, according to the study. In a follow-up study, a research team led by Professor Li Hua from Huazhong University of Science and Technology in Wuhan, Hubei province, confirmed Ruan’s findings.”
One of the interesting attributes of this particular virus is that it causes rashes similar to those found in HIV in patients. The report that Covid-19 patients had rashes on their bodies was a clue to the underlying possibility that HIV may have been inserted into the virus. A Cleveland Clinic article by Sarah Young MD states that skin rashes are and important manifestation of Covid-19. “An early report from dermatologists working with COVID-19 patients in Italy found that, in a group of 88 confirmed positive patients, 20% developed skin symptoms, with a little under half developing a rash at the onset of disease, and a little more than half developing it after hospitalization. Of the affected patients, the most common manifestation was erythematous rash, or a patchy red rash. A few developed urticaria, or hives, and one developed chickenpox-like blisters. The trunk was the most commonly involved site.” So then the question becomes, if the rash is caused by the HIV insertion, not the virus, than maybe some of the other symptoms also be generated by HIV rather than influenza. When the body’s immune system is weakened by HIV, it can lead to skin conditions that cause rashes, sores, and lesions. Skin conditions can be among the earliest signs of HIV and can be present during its primary stage. They may also indicate disease progression, as cancers and infections take advantage of immune dysfunction in later stages of the disease. About 90 percent of people with HIV will develop a skin condition during the course of their disease. These skin conditions usually fall into one of three categories: inflammatory dermatitis, or skin rashes infections and infestations, including bacterial, fungal, viral, and parasitic ones skin cancers. As a general rule, skin conditions caused by HIV are improved with antiretroviral therapy.” So then the question becomes, if the rash is caused by the HIV insertion, not the virus, than maybe some of the other symptoms also be generated by HIV rather than influenza.
One of the interesting aspects of Covid-19 is the raging pneumonia that plagues the lungs and affects their ability to deliver oxygen to the blood. A Scientific American article, COVID-19 Patients Need to be Tested for Bacteria and Fungi, Not Just the Coronaviru, which was just published, April 16, 2020, helps to highlight the significant correlation between Covid-19 pneumonia and Pneumocystis carinii pneumonia for the HIV impaired.
“Many studies have already found that a significant number of hospitalized COVID-19 patients have and are continuing to develop dangerous secondary bacterial co-infections such as bacterial pneumonia and sepsis. Rapid diagnostic tests that identify the presence of bacterial or fungal infections and drug-resistant pathogens can and will play a critical role in the ongoing public health response to COVID-19.” This article posits that patients are developing bacterial coinfections because of hospitalizations. What it the fungal and bacterial infections are the result of the virus itself, with it HIV insertion?
A recent article in Science states, “If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.”
“Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration. Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.”
“But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computerized tomography scans, their lungs are riddled with white opacities where black space—air—should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells (see graphic).”
There are also reports out of Africa that Hypoxia is one of the early symptoms of HIV AIDS. “Chronic lung diseases are increasingly recognized complications of vertically-acquired HIV among adolescents in sub-Saharan Africa and may manifest with hypoxia or tachypnea. We sought to determine the prevalence of and risk factors for hypoxia and tachypnea among adolescents with vertically-acquired HIV in Nairobi, Kenya.
“Overall, 11% of adolescents had hypoxia and 55% had tachypnea. Advanced HIV (adjusted OR [aOR] 2.41) and low CD4 (aOR 1.74)
“Hypoxia and tachypnea are common among adolescents with vertically-acquired HIV. There was a suggestion that advanced HIV and low CD4 were associated with greater hypoxia risk. Low CD4, lack of ART use and stunted growth are risk factors for tachypnea. Our findings highlight the chronic lung disease burden in this population and may inform diagnostic algorithms.”
“Some clinicians suspect the driving force in many gravely ill patients’ downhill trajectories is a disastrous overreaction of the immune system known as a “cytokine storm,” which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what’s needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.”
“Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.”
“Pneumocystis carinii pneumonia (PCP) is a life-threatening lung infection that can affect people with weakened immune systems, such as those infected with HIV, the virus that causes AIDS. More than three-quarters of all people with HIV disease will develop PCP if they do not receive treatment to prevent it.”
“PCP is caused by a tiny parasite. In addition to the lungs, the parasite can infect the eyes, ears, skin, liver and other organs. The organism probably infects most people during childhood, but it usually does not cause illness in healthy people. Because the parasite remains in the body for life, it can cause disease at any time if the immune system becomes severely damaged, as in HIV infection, or is suppressed by drugs. People with HIV infection are particularly prone to PCP when their CD4+ T-cell levels fall below 200. CD4+ T cells (also called T4 cells or T helper cells) are important immune system cells targeted by HIV.”
“The respiratory symptoms of PCP include a dry cough, chest tightness and chest tightness and difficulty breathing. People with this infection can experience fever, fatigue and weight loss for weeks or even months before having any respiratory symptoms. If a person with PCP is not treated, the infection can seriously impair the lungs’ ability to transport oxygen from inhaled air into the blood, which can lead to death. People with respiratory symptoms usually undergo a chest x-ray to determine if signs of pneumonia are present. Doctors diagnose PCP itself by detecting the organism in sputum or in fluid removed from the lung by bronchoscopy, a procedure in which a tiny tube is threaded through the patient’s airways. Rarely, doctors may have to surgically remove a sample of lung tissue for examination.”
“The standard treatment for people with PCP is either a combination of trimethoprim and sulfamethoxazole (TMP/SMX, also called Bactrim or Septra), or pentamidine. Both treatments are highly effective and their widespread use for both the treatment and prevention of PCP has made the likelihood of dying from a PCP infection less than ten percent.”
“Patients take TMP/SMX orally or through a vein for at least three weeks. More than half of the patients who receive the combination drug experience such side effects as skin rashes, a decrease in the number of red or white blood cells, nausea, vomiting or kidney impairment. Some of these side effects may be severe enough to discontinue treatment.”
“Pneumocystis jirovecii has a predilection to infect the lung in at-risk individuals. Microscopic examination reveals that Pneumocystis attaches to Type I alveolar epithelium, which allows the fungus to transition from its small trophic form to the larger cystic form. Adherence of Pneumocystis to alveoli is not the singular cause of diffuse alveolar damage, but rather it is the host’s own inflammatory response that causes significant lung injury and impaired gas exchange, leading to hypoxia and possibly respiratory failure. Pneumocystis is primarily an alveolar pathogen, but in the setting of severely immunocompromised individuals, the rare disseminated form may be seen. Examples of extra-pulmonary manifestations may be seen in those patients who are undergoing non-systemic or second-line prophylaxis and include hepatosplenomegaly and thyroid, ocular, ear, or skin lesions.”
“A chest radiograph will typically reveal diffuse bilateral peri-hilar interstitial infiltrates. These changes become increasingly homogenous as the disease course progresses. Other radiographic findings seen may include solitary or multiple nodules which may progress to become cavitary lesions, lobar infiltrates such as upper lobe lesions in patients receiving certain antimicrobial medications and pneumothorax in some cases. If there is a clinical concern for infection with Pneumocystis and negative chest radiograph, CT of the chest should be performed and may show ground glass attenuation or cystic lesions with high sensitivity.”
“Pneumocystis pneumonia (PCP) is a serious infection caused by the fungus Pneumocystis jirovecii neumocystis Carinii Pneumonia (PCP), now referred to as Pneumocystis Jirovecii Pneumonia is a fungal infection that most commonly affects the immunocompromised and, in some cases, can be severely life-threatening. Typically, patients at risk are those with any underlying disease states that alter host immunity such as those with cancer, the HIV, transplant recipients, or those taking immunosuppressive therapies and medications. Patients presenting with PCP may show signs of fever, cough, dyspnea, and, in severe cases, respiratory failure. Pneumocystis is thought to be transmitted from person to person through an airborne route. Asymptomatic lung colonization can occur in people with normal immune systems, and they may unknowingly become reservoirs (asymptomatic carriers) for the spread of Pneumocystis to immunocompromised individuals.”
“Most people who get PCP have a medical condition that weakens their immune system, like HIV/AIDS, or take medicines that lower the body’s ability to fight germs and sickness. In the United States, people with HIV/AIDS are less likely to get PCP today than before the availability of antiretroviral therapy (ART). However, PCP is still a substantial public health problem.1-3 Much of the information we have about PCP and its treatment comes from caring for patients with HIV/AIDS.”
The symptoms of PCP include1,6
Fever
Cough
Difficulty breathing
Chest pain
Chills
Fatigue (tiredness)
“In people with HIV/AIDS, PCP symptoms usually develop over several weeks and include a mild fever. In people who have weakened immune systems for reasons other than HIV/AIDS, PCP symptoms usually develop over a few days, often with a high fever.6,7”
“PCP is diagnosed using a sample from a patient’s lungs. The sample is usually mucus that is either coughed up by the patient (called sputum) or collected by a procedure called bronchoalveolar lavage. Sometimes, a small sample of lung tissue (a biopsy) is used to diagnose PCP. The patient’s sample is sent to a laboratory, usually to be examined under a microscope.” “Polymerase chain reaction (PCR) can also be used to detect Pneumocystis DNA in different types of samples. A blood test to detect β-D-glucan (a part of the cell wall of many different types of fungi) can also help diagnose PCP.19”
“Before the beginning of the HIV/AIDS epidemic in the 1980s, PCP was uncommon. In fact, clusters of PCP were one of the first signs that the HIV/AIDS epidemic was beginning in the United States.20 PCP soon became one of the main AIDS-defining illnesses in the United States. In the late 1980s, an estimated 75% of people living with AIDS developed PCP.21 Since then, PCP in people living with HIV/AIDS has decreased substantially due to antiretroviral therapy (ART) and preventive treatment with TMP/SMX.2,22,23 However, PCP is still a serious health concern for people living with HIV/AIDS or other conditions that weaken the immune system. It is an opportunistic infection, which means an infection that occurs more frequently and is more severe in people with weakened immune systems.” (Section needs citation)
So is there a correlation between blood clotting in Covid-19 and in HIV?
“Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.”
“The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.
D-Dimer in HIV-AIDS is discussed in Inflammatory and Coagulation Biomarkers and Mortality in Patients with HIV Infection: “Increases in hsCRP, IL-6, and D-dimer from study entry to the visit preceding the death were associated with an increased risk of death. Whether the activation of tissue factors secondary to inflammation is the key event is likely but unproven in this study. Several alternative hypotheses are possible. One study showed that tissue factor, an initiator of coagulation, is generated by HIV-related proteins and could have pathologic effects [35]. Another study found that HIV-infected leukocytes transmigrate across the endothelium [36], and this dissemination of virus could result in damage to multiple organs. Alternatively, circulating lipopolysaccharide, which has been shown to be higher in HIV-infected compared to uninfected individuals [37], induces tissue factor transcription, which in turn decreases F1.2 and soluble fibrin, resulting in fibrin split products such as D-dimer [38]. Lipopolysaccharide also activates monocytes to produce inflammatory cytokines, including IL-6 [39]. It is also possible that elevations of inflammatory markers, such as hsCRP and IL-6, and of D-dimer are independent events. In analyses that considered the joint influence of IL-6 and D-dimer, each remained strongly associated with all-cause mortality. Specific therapies that reduce the inflammatory response to HIV and decrease hsCRP, IL-6, and D-dimer levels may warrant investigation as an approach for reducing risk of death among HIV-infected individuals [40–42]”
“‘The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19,” Bikdeli says. Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes—a reduction in blood flow that can lead to swollen, painful digits and tissue death. In the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It’s possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. “One theory is that the virus affects the vascular biology and that’s why we see these really low oxygen levels,’ Levitt says.”
“If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease—but nearly as many had diabetes, and fully half had pre-existing high blood pressure.”
“Mangalmurti says she has been ‘shocked by the fact that we don’t have a huge number of asthmatics” or patients with other respiratory diseases in HUP’s ICU. ‘It’s very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension.’”
“Scientists are struggling to understand exactly what causes the cardiovascular damage. The virus may directly attack the lining of the heart and blood vessels, which, like the nose and alveoli, are rich in ACE2 receptors. Or perhaps lack of oxygen, due to the chaos in the lungs, damages blood vessels. Or a cytokine storm could ravage the heart as it does other organs.”
One sign of Covid-19 is the loss of tastes and smell in patients. Loss of taste and smell is associated with worsing conditions of HIV-AIDS patients. “Overall the results suggest abnormalities in the peripheral and central nervous systems, and subjective distortion of taste and smell. A significant correlation was not established between CDC classification of HIV infection and taste and smell function, although trends were observed suggesting worsening function with progression of HIV disease. These results document significant taste and smell losses in HIV infected subjects which may be of clinical significance in the development or progression of HIV associated wasting.”
“Chemosensory losses in HIV infected individuals may result from a variety of pathophysiologic processes which affect taste and smell receptors or the peripheral and central nervous systems. These processes may include oral pathology, opportunistic infections, neoplasms, HIV associated neurological disease, and medications. Infections of the mouth are common in HIV infection, and oropharyngeal candidiasis has been cited as a cause of
loss of taste in these patients (25). Other opportunistic infections and neoplasms, by virtue of their location, might affect taste and smell perception. An HIV encephalopathy has been described which preferentially affects the amygdala, hippocampus, and frontal and temporal cortex, regions important for smell and taste perception (6). In addition, cranial and peripheral neuropathies have been described due to HIV itself and due to secondary infections such as cytomegalovirus. A number of drugs have been shown to affect taste and smell, some of which are prescribed for HIV infected individuals. Antimicrobial drugs, including amphotericin B, ampicillin, metronidazole, and tetracyclines can cause a loss or distortion of taste. Nebulized pentamidine, which is commonly used as prophylaxis against Pneumocystis carinii pneumonia, can cause a metallic taste… This study demonstrates both taste and smell deficits occurring in HIV infected patients when compared with control subjects matched for age, race, gender, number of years of education, and smoking behavior. The losses occur in both peripheral (documented by significantly higher taste and smell detection thresholds) and central (documented by significantly impaired taste identification tasks) taste and smell pathways. The etiology of these deficits cannot be determined from this study and is probably the result of multiple processes including HIV associated
neurological disease, complicating opportunistic infections and neoplasms, and medications.”
On the open ended questionnaire,
Neurological issues have also been widely reported with Covid-19. Neurological issues can are also found in the beginning stages of HIV-AIDS. “HIV invades the CNS early, during the first days-weeks of primary infection. Approximately 24% of patients with primary HIV infection will have symptoms of an aseptic meningitis. HIV infection can result in progressive cognitive, motor, and behavioral abnormalities, particularly in persons who receive no ART, begin ART late in their disease, or receive inadequate ART that does not fully suppress HIV.”
“HIV-associated neurocognitive disorder” or “HAND” (previously known as “HIV encephalopathy”, “HIV–associated dementia”, or “AIDS dementia complex”) (2, 3) is the most common CNS disorder caused by HIV infection. It is characterized by the subacute onset of cognitive deficits, central motor abnormalities, and behavioral changes. Although cognitive decline is the defining feature in HAND, many patients have mild deficits that are detectable only by neuropsychological testing, and do not reach the functional criteria required to diagnose a dementia (e.g., inability to perform activities of daily living).”
“In an article in the journal Nature from 2003 highlights the similarities between HIV and SARS-CoV. “So far two types of coronavirus surface receptor have been identified5. The group II coronavirus mouse hepatitis virus (MHV) uses murine carcinoembryonic antigen-related cell adhesion molecules (CEACAMs), members of the immunoglobulin superfamily of receptors6. A number of group I coronaviruses, for example human coronavirus 229E, transmissible gastroenteritis virus and feline infectious peritonitis virus, require the zinc metalloprotease aminopeptidase N (APN, CD13) for entry into their target cells7,8,9. Recently, a distinct coronavirus has been identified as the aetiological agent of SARS, an acute pulmonary syndrome characterized by an atypical pneumonia that results in progressive respiratory failure and death in close to 10% of cases10,11,12,13. Analysis of the SARS-CoV genome suggests that this virus does not belong to any of the three defined coronavirus groups, and that the SARS-CoV S protein is similarly distinct14,15. Similar to the analogous human immunodeficiency virus (HIV) and influenza proteins, the S proteins of some coronaviruses—including MHV and the group III coronavirus infectious bronchitis virus—are cleaved into two subunits (S1 and S2) by a cellular protease in virus-producing cells16,17. The S proteins of other coronaviruses, including those of group I and probably SARS-CoV, are not cleaved in virus-producing cells14,15,18. Nonetheless, S1 and S2 domains of these latter S proteins can be identified through their homology with the S1 and S2 subunits of cleaved coronavirus S proteins. The S1 domains of all characterized coronaviruses mediate an initial high-affinity association with their respective receptors19,20,21.”
“Perhaps the most urgent question is whether soluble ACE2 (sACE2), and various fusion constructs or fragments, can serve as potent inhibitors of the virus infection in vivo. The analogy to HIV could help to avoid costly clinical trials and save time. After the failure of recombinant soluble CD4 (sCD4) to affect HIV replication in humans, it took more than a decade to develop a potent multivalent CD4-IgG fusion protein, which is now showing promising results in recent clinical trials. Like sCD4, sACE2 is likely to have a short half-life in vivo, and may not be a very potent inhibitor in a monovalent form.”
“‘We’re still at the beginning,” Krumholz says. “We really don’t understand who is vulnerable, why some people are affected so severely, why it comes on so rapidly … and why it is so hard [for some] to recover.’”
Simon Wain-Hobson PhD has said in a paper, warning about the dangers of GOF and virus research conducted in labs around the world, and cited below that, “By resorting to semantics, or hiding behind the cloak of freedom to investigate, or whipping up fears about increased regulation, yet continuing GOF work, these researchers are showing themselves to be remarkably cavalier, disdainful of public opinion, and totally averse to discussion, which is a contradiction in terms for scientists. Their imperviousness will ultimately boomerang on the flu community that has shown an esprit de corps typical of a medieval guild. Ultimately, society will have the last word. My fear is that before the issue is settled there will be an accident or an incident resulting in a terrible backlash on biomedicine. Thereafter, the new dynamics will harsher. I do not even want to contemplate the nightmare of a man-made pandemic.” Simon Wain-Hobson 2014
“So What is the similarity between the SARS-CoV-2 spike protein and the HIV ‘exoprotein’? Researchers have used public-domain genetic sequence of the SARS-CoV-2 virus. It was first published by Chinese researchers from the Shanghai lab on January 11. That lab, was shut down on January 12, 2020.The same genetic sequence, however, was used by researchers in different countries to develop a test kit to identify the virus using a highly-reliable reverse transcription PCR (polymerase chain reaction).”
“Indian researchers have compared the S (spike) Protein sequence between SARS-CoV-2 (or 2019-nCoV, or Wuhan coronavirus), and SARS. What they found is startling: An uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag. Gag, or group specific antigen, is the major structural protein (of HIV-1 and all other retroviruses) and comprises about 50 per cent of the mass of a viral particle.”
“The Indians discovered the 2019-nCoV (SARS-CoV-2) had 2 new sequences inserted — all of which can be found in HIV genetic sequences.” Of course this Indian research had disappeared and been discredited by other researchers.
“This similarity was found through a simple search in GenBank (a genetic sequence database run by the US National Institutes of Health, NIH). The GenBank sequence database is an open-access, annotated collection of all publicly- available nucleotide sequences and their protein translations. It is produced and maintained by the US National Center for Biotechnology Information as part of the International Nucleotide Sequence Database Collaboration.)”
The supposed HIV genetic insertions on SARS-CoV-2 gene are:
Insert 1: TNGTKR
Insert 2: HKNNKS
Insert 3: RYSL—TPGDSSG
Insert 4: QTNSPRRA
“Chinese virology expert Dr. Shi Zhengli (one of the authors of lab-grown chimera virus mentioned above, published in Nature) reportedly discredited those observations. However, she did not deny the existence of the four inserted sequences. Scientists who mined GenBank database found only three viruses containing all four inserted sequences.”
Then there is the curious case of Dr. Charles Leiber a Harvard University professor and the question of how he fits into all of this Frankensteinish manipulation and research. The timing of his arrest raises many questions. Profession Leiber was being paid by the Chinese government for research which he conducted in Wuhan, China. The following is from a New York Times article. “In 2017 he was named a University Professor, Harvard’s highest faculty rank, one of only 26 professors to hold that status. The same year, he earned the National Institutes of Health Director’s Pioneer Award for inventing syringe-injectable mesh electronics that can integrate with the brain.”
“Harvard’s president at the time, Drew G. Faust, called him ‘an extraordinary scientist whose work has transformed nanoscience and nanotechnology and has led to a remarkable range of valuable applications that improve the quality of people’s lives.’”
“Dr. Lieber has made no secret of his work with Chinese partners, joining five senior Chinese officials and scientists in 2013 to found the WUT-Harvard Joint Nano Key Laboratory at the Wuhan Institute of Technology.” Who knows how or whether he fits into all of this but he is certainly a Dr. Strangelove in all of this.
“Ten years later, Leiber created a transistor so small it can be used to penetrate cell membranes and probe their interiors, without affecting the intercellular functions. The bio-compatible transistor – the size of a virus – can not only measure activities inside a neuron but also heart cells and muscle fibers.” “In 2017, Leiber and his team successfully created flexible 3D nanowires mesh that can inject into the brain or retina of an animal, attach itself to the neurons and monitor electrical signals between the cells.”
And then there are recent reports from Reuters that HIV drugs are being used to treat Covid-19 in China and Russia. “MOSCOW- A black market has developed in Russia for an antiviral HIV drug explored as a possible treatment for COVID-19, the respiratory disease caused by the new coronavirus, according to sellers, HIV activists and the head of the drug’s main Russian producer.More than 20 trials around the world are testing Kaletra as a COVID-19 treatment or post-exposure prophylaxis.”
“…A leading Russian microbiologist has claimed the coronavirus is the result of Wuhan scientists doing ‘absolutely crazy things’ in their laboratory.”
“World renowned expert Professor Petr Chumakov claimed their aim was to study the pathogenicity of the virus and not ‘with malicious intent’ to deliberately create a manmade killer. Professor Chumakov, chief researcher at the Engelhardt Institute of Molecular Biology in Moscow, said: ‘In China, scientists at the Wuhan Laboratory have been actively involved in the development of various coronavirus variants for over ten years. ‘Moreover, they did this, supposedly not with the aim of creating pathogenic variants, but to study their pathogenicity. ‘They did absolutely crazy things, in my opinion. For example, inserts in the genome, which gave the virus the ability to infect human cells. Now all this has been analyzed. The picture of the possible creation of the current coronavirus is slowly emerging.’ He told Moskovsky Komsomolets newspaper: ‘There are several inserts, that is, substitutions of the natural sequence of the genome, which gave it special properties. It is interesting that the Chinese and Americans who worked with them published all their works in the open (scientific) press.
“Russia’s Health Ministry recommended it as a possible treatment for COVID-19 at the end of January after reports from China that it was beneficial, but later added that its efficacy was uncertain. ‘I even wonder why this background comes to people very slowly. ‘I think that an investigation will nevertheless be initiated, as a result of which new rules will be developed that regulate the work with the genomes of such dangerous viruses. ‘It’s too early to blame anyone.’ ‘He said the Chinese scientists created ‘variants of the virus … without malicious intent’ possibly aiming for an HIV vaccine.’”
And then there are recent reports from Reuters that HIV drugs are being used to treat Covid-19 in China and Russia. “MOSCOW- A black market has developed in Russia for an antiviral HIV drug explored as a possible treatment for COVID-19, the respiratory disease caused by the new coronavirus, according to sellers, HIV activists and the head of the drug’s main Russian producer.More than 20 trials around the world are testing Kaletra as a COVID-19 treatment or post-exposure prophylaxis.”
“Russia’s Health Ministry recommended it as a possible treatment for COVID-19 at the end of January after reports from China that it was beneficial, but later added that its efficacy was uncertain.”
So what is to be made of all this information and where exactly does it lead us? It leads us to a lot more questions than answers. Could a virus have been developed either by global organizations or governments that would negatively affect reproductive health in order to bring down populations in an enemy or world-wide? Was a biologic weapon developed using a combination of coronavirus and HIV? I don’t yet have the answer to those questions, but I can tell you my hands are shaking, from the potential of what is lurking behind the Covid-19, Covid-19-HIV pandemic now decimating the world. The unanswered question haunting me, is this; Will the asymptomatic sufferers of Covid-19-HIV eventual develop reproductive or other devastating health issues that will affect national and worldwide population?
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