|Posted on October 23, 2021 at 11:35 AM||comments (0)|
Endogenous retroviruses high levels help to understand early mortality in COVID-19 patients
Cristina Azevedo (Fiocruz News Agency)
A study coordinated by the Oswaldo Cruz Foundation (Fiocruz) is helping to understand why some critically ill patients submitted to mechanical ventilation manage to leave the ICU, while others do not survive. The research indicates that the presence of the human endogenous retrovirus K (HERV-K) is associated not only with worsening disease but also with early mortality.
From March to December 2020, the study Human endogenous retrovirus K activation in the lower respiratory tract of severe COVID-19 patients associates with early mortality followed 25 critically ill patients who required mechanical ventilation. With an average age of 57, they were admitted to the D'Or Institute (ID'Or) and the Paulo Niemeyer State Brain Institute (IECPN, acronym in Portuguese).
The progression from mild to severe cases had been associated with hypoxia, uncontrolled inflammation, and coagulopathy. However, the mechanisms involved with mortality in very severe cases are not yet well known. To this end, the study sought to understand the tracheal aspirates virome — that is, the viruses present in the sample — from individuals on mechanical ventilation. The tests showed high levels of HERV-K, compared to the patients with mild cases and of uninfected persons.
"We checked the virome of a population with very high severity, in which the mortality rate reaches 80%, to see if some other virus was coinfecting this patient who is debilitated, immunosuppressed," says study coordinator Thiago Moreno, from the Center for Technological Development in Health (CDTS/Fiocruz). "Our surprise was to find this endogenous retrovirus K high levels. It is the kind of research that starts from a completely unbiased approach. That gives a lot of strength, a lot of credibility to the finding."
HERV-K is an endogenous retrovirus, an ancestral virus that infected the human genome when humans and chimpanzees were decoupling on the evolutionary scale. Some of these genetic elements are present in our chromosomes. Many are silent for most of our lives, but it seems that somehow SARS-CoV-2 has reactivated this ancestral retrovirus. The death rate in severe COVID-19 patients is as high as 50% among those with HERV-K high levels.
The study also established a direct link: by infecting a healthy person's cell with SARS-CoV-2 in the laboratory, there was an increase in HERV-K levels. "We established, in fact, that SARS-CoV-2 is the trigger for the increase in these endogenous retroviruses, to awaken the silent genes," says Thiago Moreno.
Along with HERV-K increased levels in the patients, the researchers noticed that clotting factors were more consumed, more inflammatory processes occurred, and the numbers of factors necessary for the immune system cells survival decreased. As HERV-K levels increased, the activated inflamed monocytes numbers also increased.
"These HERV-K levels correlated with what was called early mortality, such as less than 28 days of hospitalization," Thiago says.
The research is still the first evidence of this retrovirus presence, in the severe COVID-19 patients' respiratory tract and plasma. The HERV-K presence — which also occurs in other diseases, such as cancer and multiple sclerosis — can be used as a biomarker associated with severity in COVID-19 cases. Its early detection could reinforce certain strategies use, such as anticoagulants and anti-inflammatory drugs, comments Thiago Moreno.
But it is still difficult to know why this occurs in some people and not in others. "This silent genes awakening is what can make the difference in evolutions. Perhaps the signal for silencing certain endogenous retroviruses is stronger in some people than in others. The new coronavirus ability to change the host cell epigenetic profile, activating even ancestral viruses, some of which should be dormant in our genome, seems to be associated with gravity", comments the study coordinator.
In addition to Thiago Moreno, Jairo Temerozo (Oswaldo Cruz Institute, IOC/Fiocruz), Natalia Fintelman-Rodrigues, Monique Cristina Santos, Carolina Sacramento, Aline Silva, Samuel Mandacaru, Emilly Caroline Moraes, Monique Trugilho, João Gesto, Marcelo Ferreira, Felipe Betoni, Remy Martins-Gonçalves, Isacláudia Azevedo-Quintanilha, Cassia Righy, Carlos Morel, Dumith Bou-Habib, Fernando Bozza and Patricia Bozza (Fiocruz); Eugênio Hottz (Federal University of Juiz de Fora); Juliana Abrantes (Federal University of Rio de Janeiro); Pedro Kurtz (Paulo Niemeyer State Brain Institute); and Hui Jiang and Hongdong Tan (MGI Tech) took part in the study.
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|Posted on October 23, 2021 at 11:00 AM||comments (0)|
Exogenous Coronavirus Interacts With Endogenous Retrotransposon in Human Cells
Ying Yin1,2,3,4, Xiao-zhao Liu1,3,4, Ximiao He1,3,4* and Li-quan Zhou2*
1Department of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
2Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
3Center for Genomics and Proteomics Research, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
4Hubei Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation, Huazhong University of Science and Technology, Wuhan, China
There is an increased global outbreak of diseases caused by coronaviruses affecting respiratory tracts of birds and mammals. Recent dangerous coronaviruses are MERS-CoV, SARS-CoV, and SARS-CoV-2, causing respiratory illness and even failure of several organs. However, profound impact of coronavirus on host cells remains elusive. In this study, we analyzed transcriptome of MERS-CoV, SARS-CoV, and SARS-CoV-2 infected human lung-derived cells, and observed that infection of these coronaviruses all induced increase of retrotransposon expression with upregulation of TET genes. Upregulation of retrotransposon was also observed in SARS-CoV-2 infected human intestinal organoids. Retrotransposon upregulation may lead to increased genome instability and enhanced expression of genes with readthrough from retrotransposons. Therefore, people with higher basal level of retrotransposon such as cancer patients and aged people may have increased risk of symptomatic infection. Additionally, we show evidence supporting long-term epigenetic inheritance of retrotransposon upregulation. We also observed chimeric transcripts of retrotransposon and SARS-CoV-2 RNA for potential human genome invasion of viral fragments, with the front and the rear part of SARS-CoV-2 genome being easier to form chimeric RNA. Thus, we suggest that primers and probes for nucleic acid detection should be designed in the middle of virus genome to identify live virus with higher probability. In summary, we propose our hypothesis that coronavirus invades human cells and interacts with retrotransposon, eliciting more severe symptoms in patients with underlying diseases. In the treatment of patients with coronavirus infection, it may be necessary to pay more attention to the potential harm contributed by retrotransposon dysregulation......
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|Posted on October 23, 2021 at 9:30 AM||comments (0)|
Novel coronavirus (COVID-19) is causing global mortality and lockdown burdens. A compromised immune system is a known risk factor for all viral influenza infections. Functional foods optimize the immune system capacity to prevent and control pathogenic viral infections, while physical activity augments such protective benefits. Exercise enhances innate and adaptive immune systems through acute, transient, and long-term adaptations to physical activity in a dose-response relationship.
Functional foods prevention of non-communicable disease can be translated into protecting against respiratory viral infections and COVID-19. Functional foods and nutraceuticals within popular diets contain immune-boosting nutraceuticals, polyphenols, terpenoids, flavonoids, alkaloids, sterols, pigments, unsaturated fatty-acids, micronutrient vitamins and minerals, including vitamin A, B6, B12, C, D, E, and folate, and trace elements, including zinc, iron, selenium, magnesium, and copper.
Foods with antiviral properties include fruits, vegetables, fermented foods and probiotics, olive oil, fish, nuts and seeds, herbs, roots, fungi, amino acids, peptides, and cyclotides.
Regular moderate exercise may contribute to reduce viral risk and enhance sleep quality during quarantine, in combination with appropriate dietary habits and functional foods. Lifestyle and appropriate nutrition with functional compounds may offer further antiviral approaches for public health.
Keywords: COVID-19; exercise; functional food; immune system; lifestyle prevention; viral infection
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|Posted on October 23, 2021 at 9:25 AM||comments (0)|
|Posted on October 23, 2021 at 7:15 AM||comments (0)|
|Posted on October 23, 2021 at 7:10 AM||comments (0)|
Stealth adaptation is a generic immune evasion mechanism, which can potentially
occur with all viruses [1-4]. It involves the deletion or mutation of the genes coding for the
relatively few virus components typically targeted by the cellular immune system. A further
characteristic of certain stealth adapted viruses is the incorporation of additional genetic
sequences of cellular and bacterial origins [5-8]. These “renegade” genetic sequences can
be subsequently transmitted between humans as components of infectious stealth adapted
viruses. The best characterized stealth adapted virus, referred to in GenBank as stealth virus
1, is a derivative of an African green monkey simian cytomegalovirus (SCMV) [2,4,9]. It was
repeatedly cultured from a patient with the chronic fatigue syndrome (CFS) . A similar
virus (stealth virus-2) was isolated from the cerebrospinal fluid of a comatose patient with
a 4-year history of a bipolar psychosis . Stealth virus-1 was cloned and the complete or
partial DNA sequences of 248 clones were submitted to GenBank. Of these clones, 200 of the
sequences correspond to regions of the SCMV genome. The sequences are unevenly distributed
over the genome of the originating SCMV, with clear evidence of major deletions and genetic
instability. Fourteen clones contained genetic sequences that were derived from non-coding
regions of the human genome. These incorporated cellular sequences have also undergone
genetic changes indicative of the genetically unstable stealth adapted virus genome .
Thirty-four sequences from stealth virus-1 correspond to modified bacterial protein-
coding sequences. These sequences may have arisen from coinfection of cells with both
stealth adapted viruses and intracellular bacteria, with the bacteria-derived sequences
providing specific metabolic functions and/or substituting for some of the ordinary virus
capsids proteins. The overall genome of stealth virus-1 is genetically fragmented leading to
the likelihood of the cellular and bacteria-derived sequences becoming incorporated into the
virus genome by the cross-linking of fragments from the originating SCMV. Cellular sequences
incorporated into the stealth adapted viruses isolated from certain other CFS patients
(designated in Gen Bank as stealth virus numbers 3,4,5) include sequences from the rhesus
monkey genome [13-16]. There are also human-derived cellular sequences in stealth virus-5
The presence of these human-derived sequences is consistent with homologous
recombination, which would allow for the replacement of some of the original rhesus-derived
sequences in stealth virus-5 with human cellular sequences. A similar explanation can
apply to the finding of human cellular sequences instead of African green monkey cellular
sequences in stealth virus-1 [7-8]. The incomplete inclusion and genetic instability of the
originating virus sequences, along with further replacements of virus sequences with cellular
and bacteria-derived sequences have impeded efforts by many virologists to detect these
viruses in patients. The existence of stealth adapted viruses has
unfortunately been disregarded by public health authorities despite
the unequivocal DNA sequence data. The biased, not-wanting-to-
know ignorance of the public health system led to the declaration
in 2002 that the clinical culturing of stealth adapted viruses had
put the Nation’s health into Immediate Jeopardy. All clinical testing
had to cease under threat of criminal charges and financial penalty.
The purpose of this article is to raise the possibility of stealth
adapted viruses capturing the Covid-19 S-protein mRNA sequence
used in the Pfizer and Moderna vaccines [15,16]. This could lead
to the overproduction of the S-protein and to a major disruption
in the functioning of the angiotension-converting enzyme-2
(ACE2) receptor [17-19]. Arguably, there could be either excessive
activation or inhibition of the functions of the ACE2 receptor. In
either event, the biological effects would be potentially profound.
Additionally, there could be continuing formation of antigen-
antibody complexes as well as enhanced tissue-destructive cellular
immunity directed to the Covid-19 S protein. Because stealth
adapted viruses are infectious, the potential deleterious effects
of a Covid-19 S protein coding stealth adapted virus could spread
throughout the human and animal world. A reasonable request to
those responsible for approving Covid-19 vaccines is to seriously
consider the potential worldwide risks caused by the foreseeable
interactions of the vaccines with stealth adapted viruses.
At a minimum, the FDA should be formally required to scientifically
respond to the concepts embodied in this article. Stealth virus-1
is available from the American Type Culture Collection (VR-2343,
deposited September 17, 1991). Candidate mRNA vaccines could be
added to stealth virus-1 cultures to determine the ease with which
the Covid-19 S protein coding mRNA can become included into a
replicating stealth adapted virus. Additional considerations should
also be given to other possible interactions between the Covid-19
vaccine and its included adjuvants and stealth adapted viruses.
Vaccine science has previously failed the world, including the likely
inadvertent development of HIV. It is still reluctant to address
vaccine-derived stealth adapted viruses as an explanation for the
rising incidence of brain damaging illnesses, including autism and
CFS. Although typically non-immunogenic, residual components
on stealth adapted viruses can become antigenic targets if the
immune system is sufficiently stimulated with adjuvants. This can
explain the instances of vaccine induced neurological illnesses. It
would indeed be tragic if the future of mankind were to be further
imperiled by a continuing FDA disregard of the existence of stealth
1. Martin WJ (1994) Stealth viruses as neuropathogens. CAP Today 8(10):
2. Martin WJ (1999) Stealth adaptation of an African green monkey simian
cytomegalovirus. Exp Mol Pathol 66(1): 3-7
3. Martin WJ (2014) Stealth adaptation of viruses: Review and updated
molecular analysis on a stealth adapted African green monkey simian
cytomegalovirus (SCMV). Journal of Human Virology & Retrovirology 1:
4. Martin WJ (1998) Cellular sequences in stealth viruses. Pathobiology
5. Martin WJ (1999) Bacteria related sequences in a simian cytomegalovirus-
derived stealth virus culture. Exp Mol Pathol 66(1): 8-14.
6. Martin WJ (2019) Renegade cellular and/or bacterial genetic sequences
in stealth adapted viruses. Journal of Human Virology & Retrovirology
7. Martin WJ (2020) Cellular and bacterial genetic sequences in monkey-
derived stealth adapted viruses. Cohesive Journal of Microbiology and
Infectious Diseases 3(4).
8. Martin WJ, Ahmed KN, Zeng LC, Olsen JC, Seward JG, et al. (1995) African
green monkey origin of the atypical cytopathic ‘stealth virus’ isolated
from a patient with chronic fatigue syndrome. Clin Diagn Virol 4(1): 93-
9. Martin WJ, Zeng LC, Ahmed K, Roy M (1994) Cytomegalovirus-related
sequences in an atypical cytopathic virus repeatedly isolated from a
patient with the chronic fatigue syndrome. Am J Pathol 145(2): 441-452.
10. Martin WJ (1996) Simian cytomegalovirusrelated stealth virus isolated
from the cerebrospinal fluid of a patient with bipolar psychosis and
acute encephalopathy. Pathobiology 64(2): 6466.
11. Martin WJ (1996) Genetic instability and fragmentation of a stealth viral
genome. Pathobiology 64(1): 917.
12. Martin WJ (2020) Virus transmission to humans of genetically unstable
rhesus monkey cellular sequences: A possible forerunner of complex
human illnesses. Journal of Human Virology & Retrovirology 8(3): 74-
13. Martin WJ (2020) Stealth adapted viruses with genetically unstable
rhesus monkey cellular sequences A possible forerunner of complex
human illnesses. Cohesive Journal of Microbiology and Infectious
14. Martin WJ (2020) Infectious rhesus monkey-derived cellular DNA
sequences in certain stealth adapted viruses. The FASEB Journal 34(1):
15. Martin WJ (2020) Viruses disguised as self and/or as bacteria.
Microbiology and Infectious Diseases 4(1): 1-5.
16. Samavati L, Uhal BD (2020) ACE2
, much more than just a receptor for
SARS-COV-2 Front. Cell Infect Microbiol.
17. Imai Y, Kuba K, Nakanishi TO, Penninger JM (2010) Angiotensin-
converting enzyme 2 (ACE2
) in disease pathogenesis. Circ J 74(3): 405-
18. Hamming I, Cooper ME, Haagmans BL, Hooper NM, Korstanje R, et al.
(2007) The emerging role of ACE2
in physiology and disease. Journal
Pathology 212(1): 1-11.
19. Martin WJ (2015) Chimpanzees inoculated with cytome ACE galovirus
contaminated polio vaccines may explain origin of HIV-1. Journal of
Human Virology & Retrovirology 2(2): 00035.
Martin*. A Cautionary Tale: What if
Stealth Adapted Viruses Incorporate the
Covid-19 Spike Protein Coding mRNA
into Their Genome?. Cohesive J Microbiol
Infect Dis. 4(4). CJMI. 000593. 2020.
Copyright@ W John Martin. This article is
distributed under the terms of the Creative
Commons Attribution 4.0 International
License, which permits unrestricted use
and redistribution provided that the
original author and source are credited.
|Posted on October 23, 2021 at 6:55 AM||comments (0)|
The continuing emergence of variant forms of the SARS-CoV-2 virus is the probable consequence of using the current Covid-19 vaccines. These vaccines do not induce the same immunity as do naturally occurring infections. First, the vaccines are given by intramuscular injections. This is far less effective than natural infection in stimulating the development of virus specific immunoglobulin A (IgA) producing cells and cytotoxic T cells (CTL) within the respiratory mucosa. Virus exposure in a previously vaccinated individual with limited mucosal immunity increases the risk of a persistent, subclinical infection, which will initially be restricted to the superficial mucosa. NIH and CDC officials have alluded to this possibility in advising those who have been vaccinated to continue wearing masks lest they may infect others.
The second major distinction between the Covid-19 vaccines and natural infection is the FDA allowance of using only one component as the antigen, namely the spike protein. Deletion or other modifications of a single targeted component can occur more readily as an immune evasion mechanism than concurrent genetic modifications of multiple antigenic components. Covid-19 vaccine evoked immunity will, therefore, exert a strong immunoselective pressure for major modifications or deletion of the spike protein. With successive additional changes in the few remaining viral components that are normally targeted by cellular immunity, as well as the incorporation of sufficient genetic sequences from cells and other microbes; non-immunogenic, pathogenic viruses will then emerge. These viruses will no longer be immunologically restricted to the respiratory mucosa and will become more widespread within the body. The immune evasion/escape mechanism utilized in this manner is termed stealth adaptation. It was initially identified in the cytomegaloviruses of monkeys used to produce polio vaccines. Not only were these viruses probably involved in causing AIDS, but they can account for the rise in many chronic illnesses, such as autism and the chronic fatigue syndrome (CFS). Until proven otherwise, the neuropsychiatric symptoms of the Long Covid syndrome in previously healthy individuals, are consistent with brain infection with stealth adapted coronaviruses. This illness is, therefore, likely to be infectious, including the possibility of transplacental transmission.
Testing for stealth adapted viruses in these patients is best performed using virus cultures followed by genetic sequencing. Even though cellular immunity fails to effectively suppress stealth adapted viruses, these viruses as well as the conventional viruses from which they are derived, are still susceptible to a non-immunological anti-virus defense mechanism mediated by the alternative cellular energy (ACE) pathway. This pathway is reflected in an added kinetic activity of the body's fluids. The environmental life-force energy for the ACE pathway is called KELEA (Kinetic Energy Limiting Electrostatic Attraction). Water with high levels of KELEA is available for clinical studies. Enhancing the ACE pathway in those who are susceptible to severe Covid-19 illness and in Long Covid syndrome patients is arguably preferable to risking the development of new forms of stealth adapted viruses by using the current Covid-19 vaccines.
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|Posted on October 14, 2021 at 5:30 AM||comments (0)|
Purpose of review: The pandemic COVID-19 has affected more than seventy million people globally. The whole world is eagerly waiting for an effective antiviral therapy to combat COVID-19, but it is yet to get. The emergence of COVID-19 makes imperative the need for safe and potent antiviral drugs. Many metal nanoparticles exhibit significant antiviral potential against many viral diseases. The Ayurvedic system of medicine is the treasure of many metal nanoparticulate drugs termed as Bhasma.
Recent findings: Gold, silver, copper, zinc and iron oxide nanoparticles are effective against coronavirus. A possible mechanism of action of the metal nanoparticles against coronavirus is a disruption of outer layers of coronavirus. Swarna Bhasma, Rajata Bhasma, Tamra Bhasma and Yashada Bhasma are recommended for COVID-19 treatment due to the ability to reduce the plasma interleukins, interferons and TNFα levels.
Summary: The Ayurvedic Bhasma preparations are unique metal nanoparticles. These metal nanoparticles are safe, stable in solid state and are having excellent biological activities. Ayurvedic metal nanoparticles, Swarna Bhasma, Rajata Bhasma, Tamra Bhasma and Yashada Bhasma could be proved as novel antiviral agents against SARS-CoV-2 for their anti-inflammatory, immunomodulatory, antiviral and adjuvant activities.
Keywords: Ayurveda; Bhasma; COVID-19; Metal; Nanoparticles; SARS-CoV-2.
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|Posted on October 13, 2021 at 8:40 AM||comments (0)|
European Journal of Epidemiology
Vaccines currently are the primary mitigation strategy to combat COVID-19 around the world. For instance, the narrative related to the ongoing surge of new cases in the United States (US) is argued to be driven by areas with low vaccination rates . A similar narrative also has been observed in countries, such as Germany and the United Kingdom . At the same time, Israel that was hailed for its swift and high rates of vaccination has also seen a substantial resurgence in COVID-19 cases . We investigate the relationship between the percentage of population fully vaccinated and new COVID-19 cases across 68 countries and across 2947 counties in the US.
We used COVID-19 data provided by the Our World in Data for cross-country analysis, available as of September 3, 2021 (Supplementary Table 1) . We included 68 countries that met the following criteria: had second dose vaccine data available; had COVID-19 case data available; had population data available; and the last update of data was within 3 days prior to or on September 3, 2021. For the 7 days preceding September 3, 2021 we computed the COVID-19 cases per 1 million people for each country as well as the percentage of population that is fully vaccinated.
For the county-level analysis in the US, we utilized the White House COVID-19 Team data , available as of September 2, 2021 (Supplementary Table 2). We excluded counties that did not report fully vaccinated population percentage data yielding 2947 counties for the analysis. We computed the number and percentages of counties that experienced an increase in COVID-19 cases by levels of the percentage of people fully vaccinated in each county. The percentage increase in COVID-19 cases was calculated based on the difference in cases from the last 7 days and the 7 days preceding them. For example, Los Angeles county in California had 18,171 cases in the last 7 days (August 26 to September 1) and 31,616 cases in the previous 7 days (August 19–25), so this county did not experience an increase of cases in our dataset. We provide a dashboard of the metrics used in this analysis that is updated automatically as new data is made available by the White House COVID-19 Team (https://tiny.cc/USDashboard).
At the country-level, there appears to be no discernable relationship between percentage of population fully vaccinated and new COVID-19 cases in the last 7 days (Fig. 1). In fact, the trend line suggests a marginally positive association such that countries with higher percentage of population fully vaccinated have higher COVID-19 cases per 1 million people. Notably, Israel with over 60% of their population fully vaccinated had the highest COVID-19 cases per 1 million people in the last 7 days. The lack of a meaningful association between percentage population fully vaccinated and new COVID-19 cases is further exemplified, for instance, by comparison of Iceland and Portugal. Both countries have over 75% of their population fully vaccinated and have more COVID-19 cases per 1 million people than countries such as Vietnam and South Africa that have around 10% of their population fully vaccinated........
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|Posted on October 3, 2021 at 8:10 AM||comments (0)|
|Posted on October 3, 2021 at 5:35 AM||comments (0)|
A 1999 autopsy study of young adults in the US between the ages of 17 and 34 years of who died from accidents, suicides, and homicides confirmed that coronary artery disease (CAD) is ubiquitous in this age group. The disease process at this stage is too early to cause coronary events but heralds their onset in the decades to follow. These data are similar to those reported in an earlier postmortem analysis of US combat casualties during the Korean conflict, which found early CAD in nearly 80% of soldiers at an average age of 20 years. From these reports, which are 17 and 63 years old, respectively, it is clear that the foundation of CAD is established by the end of high school. Yet, medicine and public health leaders have not taken any steps to forestall or eliminate the early onset of this epidemic. Smoking cessation, a diet with lean meat and low-fat dairy, and exercise are generally advised, but cardiovascular disease (CVD) remains the number one killer of women and men in the US. The question is, why?
Unfortunately, such dietary gestures do not treat the primary cause of CVD. The same can be said of commonly prescribed cardiovascular medications such as beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, anticoagulants, aspirin, and cholesterol lowering drugs and medical interventions such as bare metal stents, drug-eluting stents, and coronary artery bypass surgery.
It is increasingly a shameful national embarrassment for the United States to have constructed a billion-dollar cardiac healthcare industry surrounding an illness that does not even exist in more than half of the planet. If you, as a cardiologist or a cardiac surgeon, decided to hang your shingle in Okinawa, the Papua Highlands of New Guinea, rural China, Central Africa, or with the Tarahumara Indians of Northern Mexico, you better plan on a different profession because these countries do not have cardiovascular disease. The common thread is that they all thrive on whole food, plant-based nutrition (WFPBN) with minimal intake of animal products.
By way of contrast, in the United States, we ignore CVD inception initiated by progressive endothelial injury, inflammatory oxidative stress, decreased nitric oxide production, foam cell formation, diminished endothelial progenitor cell production and development of plaque that may rupture and cause myocardial infarction or stroke. This series of events is primarily set in motion, and worsened, by the Western diet, which consists of added oils, dairy, meat, fish, fowl, and sugary foods and drinks—all of which injure endothelial function after ingestion, making food a major, if not the major cause of CAD.
In overlooking disease causation, we implement therapies that have high morbidity and mortality. The side effects of a plethora of cardiovascular drugs include the risk of diabetes, neuromuscular pain, brain fog, liver injury, chronic cough, fatigue, hemorrhage, and erectile dysfunction. Surgical interventions are fatal for tens of thousands of patients annually. Each year approximately 1.2 million stents are placed with a 1% mortality rate, causing 12,000 deaths, and 500,000 bypass surgeries are performed with a 3% mortality rate, resulting in another 15,000 deaths. In total, 27,000 patients die annually from these two procedures. It is as though in ignoring this dairy, oil, and animal-based illness, we are wedded to providing futile attempts at temporary symptomatic relief with drugs and interventional therapy, which employs an unsuccessful mechanical approach to a biological illness with no hope for cure. Patients continue to consume the very foods that are destroying them. This disastrous illness and ineffective treatments need never happen if we follow the lessons of plant-based cultures where CVD is virtually nonexistent........
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|Posted on September 30, 2021 at 7:05 AM||comments (0)|
Introduction: The COVID-19 caused by a new type of coronavirus has emerged from China and led to thousands of deaths globally. Despite many groups engaged in studying the newly emerged virus and searching for the treatment, the understanding of the SARS-CoV2 target ligand interactions represents a key challenge. Several studies are being conducted to identify potential treatment. Alternatively, the results of numerous studies have shown that protease inhibitors can be a genuine leader in research. The antiviral activity and beneficial effect against respiratory disorders of thymoquinone have been largely demonstrated.
Aim: The aim of this study is to evaluate in silico the inhibition of the replication of SARS CoV2 by thymoquinone.
Methods: This is a molecular simulation study using SARS CoV2 protease and thymoquinone structures provided by Protein Data Bank.
Results: The preliminary results have shown that thymoquinone may have inhibitory activities against SARS CoV2 protease.
Conclusion: Furthermore, given the demonstrated results of thymoquinone, we can conclude that it may be considered as an effective or adjuvant treatment for SARS CoV2 infection.
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Youness Kadil*, Mohammed Mouhcine and Houda Filali, “In Silico Investigation of the SARS CoV2 Protease with Thymoquinone, the Major Constituent of Nigella Sativa”, Current Drug Discovery Technologies 2021; 18(4) . https://doi.org/10.2174/1570163817666200712164406
|Posted on September 10, 2021 at 9:15 AM||comments (0)|
Migraine as an inflammatory disorder
Christian Waeber, Michael A. Moskowitz
First published May 23, 2005, DOI: https://doi.org/10.1212/WNL.64.10_suppl_2.S9
Inflammation is a localized response designed to protect tissues against infection, injury, or disease. The inflammatory response acts to destroy, dilute, or wall off (sequester) both the injurious agent and the injured area. The production and release of chemical agents by cells in the affected tissue result in the four well-known signs of Celsus: pain (dolor), heat (calor), redness (rubor), and swelling (tumor), to which Galen later added loss of function (functio laesa). Histologically, inflammation is characterized by a complex series of events. These include the following: dilatation of arterioles, capillaries, and venules, with increased permeability and blood flow; exudation of fluids, including plasma proteins; and leukocyte migration into the inflammatory focus.
Although pain and inflammation usually go hand in hand, migraine has not classically been considered an inflammatory disease, possibly because it is not obviously associated with heat, redness, and swelling. Instead, a vascular etiology was proposed on the basis of a report that ergotamine tartrate alleviates pain and reduces the amplitude of temporal artery pulsation in migraineurs,1 a small but significantly increased risk for strokes,2 association with vascular malformations,3 and genetic disorders such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).4 For most of the twentieth century, the prevailing theory of migraine held that pain results from an abnormal dilatation of intracranial blood vessels, leading to mechanical excitation of sensory fibers that innervate these vessels. This “vascular” theory, however, has never been validated. No differences in blood flow velocity exist in vertebral and middle cerebral arteries during and outside migraine attacks,5 and a consistent relationship between vessel caliber, cerebral blood flow, and headache has not been established.6
In recent years, accumulating evidence has shifted the emphasis away from vascular smooth muscle and toward mechanisms related to inflammation within cephalic.......
|Posted on September 10, 2021 at 8:45 AM||comments (0)|
Severe COVID-19 arises from the convergence of inadequate pre-existing immunity and a host response that damages, rather than repairs, tissues. We outline clinical presentations of COVID-19 that are likely driven by dysregulated host immunity, discuss potential mechanisms underlying pathological responses, and highlight important areas for basic research on this topic.
The substantial mortality in coronavirus disease 2019 (COVID-19) has been driven largely by an absence of pre-existing immunity that could have provided some protection in vulnerable populations against severe and fatal outcomes. As population immunity increases in some regions, severe COVID-19 has become much less frequent; yet communities lacking protection continue to be ravaged by this disease. In addition to vaccines, having medications that prevent the acute respiratory distress syndrome (ARDS) that is often central in fatal COVID-19 could dramatically reduce the threat of SARS-CoV-2 as a human pathogen. For this reason, understanding mechanisms involved in the pathogenesis of severe COVID-19 is imperative.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections result in a vast spectrum of clinical outcomes, yet most infections are subclinical or mild, even in the absence of pre-existing immunity. The drivers of severe COVID-19 are not entirely clear, but excessive inflammation is nearly always associated with worsening clinical status in this disease. Interestingly, minimal virus is detected in most organs obtained from autopsies of COVID-19 patients, which may suggest that while the virus triggers an initial disease, it is not the ultimate cause of organ failure. Tissue damage often appears driven by excessive accumulation and activation of effector immune cells. Together, the evidence supports a model in which severe and fatal COVID-19 are driven by an aberrant immune response to the infection that causes pathology rather than restoring health. We propose that this aberrant response is the driver of susceptibility to severe COVID-19 in vulnerable populations.
In addition to severe disease, SARS-CoV-2 infections can result in long-term symptoms (here called “long COVID syndromes”) in a large proportion of cases, regardless of severity of the acute infection. Many of the long-term sequelae are likely to be driven by inflammatory pathways. In this article, we outline clinical presentations of COVID-19 that are likely driven by dysregulated host immune responses and discuss potential mechanisms of disease as well as outstanding clinical and research questions on this important topic.
COVID-19 clinical presentations and syndromes related to inflammation
Severe acute COVID-19 Those who develop severe COVID-19 usually worsen after 7 days of mild-to-moderate symptoms. Many of the sequalae in severe cases, such as ARDS, thromboembolism, arrhythmias, and renal failure, are mediated by inflammation and are central in the mortality associated with COVID-19. Some effective treatments have immunomodulatory or immunosuppressive effects. These include compounds with data showing clinical benefit such as corticosteroids, tocilizumab that inhibits the proinflammatory cytokine interleukin-6 (IL-6), the JAK inhibitor baricitinib, and SARS-CoV-2 monoclonal antibodies (mAbs). While we know that severe COVID-19 is associated with an elevation in routine inflammatory markers and an absence of early neutralizing antibodies, we currently lack adequate tools to identify cases that would benefit from early therapeutic interventions. Further, methods are not yet established for guiding treatments based on monitoring of inflammation within affected organs, short of invasive biopsies. As an example, the assessment of lung bronchoscopy fluid for cellular and soluble factors could be very helpful for therapeutic monitoring and potentially for guiding treatment, yet practical methods for dynamic sampling of this fluid and studies correlating results with clinical outcomes are not available. Such methods could also improve our understanding of the mechanisms resulting in long-term sequelae of severe COVID-19.
Multisystem inflammatory syndrome in children/adolescence.......
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Background: Obesity and chronic pain are prevalent concerns. Pain is frequently experienced in weight-bearing joints, but is common in other areas of the body as well, suggesting other factors. Poor diet often contributes to obesity and can directly influence the immune system. We have shown that poor diet prolongs recovery from inflammatory injury. Therefore, our goal was to determine whether poor-quality diet-induced consequences could be prevented or reversed by an anti-inflammatory diet (AID).
Methods: A Standard American Diet (SAD) was developed to investigate the effects of poor diet on pain. The SAD includes amounts of refined sugar, carbohydrates and fats that better model the typical American diet, as compared to high-fat diets. We developed an AID to explore whether the effects of the SAD could reverse or whether the AID would enhance recovery prophylactically. The AID was developed using ingredients (epigallocatechin gallate, sulforaphane, resveratrol, curcumin and ginseng) with known anti-inflammatory properties. Following 15 weeks of diet [SAD, AID or regular (REG)] exposure, male and female mice underwent inflammatory injury, at which point some animals had their diets switched for the remainder of the study.
Results: Animals who consumed the SAD showed longer recovery compared to the AID- and REG-fed animals. Animals switched off the SAD had faster recovery times, with AID-fed animals recovering as fast as REG-fed animals.
Conclusions: Poor diet prolonged recovery from inflammatory injury. Substitution of SAD with AID or REG promoted faster recovery. These findings suggest diet can be used as a non-pharmacological intervention following injury.
Significance: Obesity may increase susceptibility to chronic pain often due to poor diet. Diet has potential to be used as treatment for pain. This study investigates the use of a novel translatable diet to act as a preventative (i.e. prior to surgery) or an intervention (i.e. following an injury).
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