Despite what you have been led to believe, antibiotics DO have anti-viral effects!
By: James Paul Roguski September 26, 2020 310-619-3055
Do a "google" search for "antibiotics not effective against viruses" and you will receive a nearly endless list of results claiming that antibiotics do NOT work against viruses. Those articles are in error. Those articles are "fake news."
The propaganda machines have been working overtime to hide the truth from both doctors and the general public. The reason is simple: "incurable" diseases caused by viruses are big business.
The industry that is designed to create "vaccines" for these "incurable" diseases will CRUMBLE once the vast majority of Americans learn this truth: There are many safe, affordable, medications that are effective against a wide variety of viruses.
This information is being hidden due to the fact that it is NOT profitable for pharmaceutical companies to study or produce these medications because their patents expired long ago.
If you want to see the plain and simple truth, then use your favorite internet search engine to search for "the antiviral effects of doxycycline" or "azithromycin" or "ivermectin" (or the name of just about any other antibiotic or antiparasitic drug).
You will immediately be able to see for yourself just how much evidence there is in support of the fact that the propaganda machine continues to hide the fact that many existing drugs have anti-viral effects that can be helpful to people who are suffering from a wide variety of ailments, including COVID-19.
Below is an excerpt from an article written by Dr. Lee D. Merritt, M.D. in the fall 2020 issue of the Journal of American Physicians and Surgeons (download PDF in the ARTICLES section below).
Prior to reading this article, you may forgive yourself for being unaware of the studies that provide ample evidence that antibiotics and anti-parasitic drugs DO inhibit viruses.
YOU are NOT supposed to be aware of this information.
This information can be good for YOUR health, but it is very, very bad for those who stand to profit from your ongoing dis-ease.
There is NO moral, ethical or legal justification to mandate vaccines of any type on a healthy human being when effective treatments exist.
It is okay if the importance of this information escapes you.
However, if you "get it," then please feel free to contact me directly at 310-619-3055.
*NOTE:
We are NOT claiming that ivermectin nor doxycycline are zinc ionophores.
We are NOT claiming that ivermectin nor doxycycline are zinc ionophores.
The excerpts from the article below explains just some of the reasons why Doxycycline is included in many doctors' protocols to treat their patients with COVID-19.
Doxycycline as a potential partner of COVID-19 therapies
https://www.sciencedirect.com/science/article/pii/S2214250920301724
https://www.sciencedirect.com/science/article/pii/S2214250920301724
Antiviral effects of doxycycline
The mechanism of the antiviral effects of tetracycline derivatives may be secondary to transcriptional upregulation of intracellular zinc finger antiviral protein (ZAP), an encoding gene in host cells [11,12].
ZAP can also bind to specific target viral mRNAs and represses the RNA's translation [13,14].
Experimental studies have used tetracycline to induce the overexpression of host ZAP in HEK293, rats and monkeys cell lines (Vero cells), which contributed to inhibition of RNA viruses such as the Dengue, Ebola, Human Immunodeficiency Virus, Zika, and Influenza A viruses [11,12,[15], [16], [17], [18]].
Also, in vitro studies have showed that doxycycline can repress Dengue virus infection in Vero cells through the inhibition of dengue serine protease enzymes and of viral entry [17,19].
Doxycycline showed the capacity to inhibit dengue virus replication in Vero cells culture and likely it interacts with the dengue virus E protein that is required for virus entry [19].
Similarly, doxycycline controls Chikungunya virus (CHIKV) infection through the inhibition of CHIKV cysteine protease of Vero cells and showed significant reduction of CHIKV blood titer of mice [20].
In addition, tetracycline derivatives such as doxycycline are highly lipophilic antimicrobials that chelate zinc compounds on matrix metalloproteinases (MMPs) of mammalian cells [21],
and an in vitro study showed that murine coronaviruses rely on MMPs for cell fusion and viral replication [22].
Other mechanisms of viral fusion and replication by coronaviruses utilize host proteases [22], could be a possible target to doxycycline.
Anti-inflammatory effects of doxycycline
Doxycycline and other tetracycline derivatives such as minocycline exhibit anti-inflammatory effects along with in vitro antiviral activity against several RNA viruses. Use of these agents have been associated with clinical improvement, even reversal of cytokine storm in some infections caused by RNA viruses, such as dengue fever [10].
In COVID-19, elevated levels of blood interleukin (IL)-6 have been more commonly observed in severe COVID-19 illness and among non-survivors, suggesting that mortality might be due to virally-driven hyperinflammation and to cytokine storm [23].
Intense proinflammatory state has a central role in the pathogenesis of dengue and hemorrhagic fever, leading to cytokine storm [24].
Importantly, doxycycline reduced pro-inflammatory cytokines, including IL-6 and tumor necrosis factor (TNF)-α, in patients with dengue hemorrhagic fever, and the mortality rate was 46 % lower in the doxycycline-treated group (11.2 %) than in the untreated group (20.9 %) [24].
Moreover, doxycycline was more effective than tetracycline in the reduction of these pro-inflammatory cytokines [25].
Similarly, an in vitro study suggested that treatment with minocycline had dual anti-inflammatory effects and viral replication in cells infected with Enterovirus 71 infection, as minocycline reduced the viral cytopathic effect, viral protein expression, viral titers, levels of IL-6 and IL-8, and relative mRNA expression of TNF-α. Also, in a murine model, minocycline inhibited IL-6 and granulocyte colony-stimulating factor in plasma and TNF-α in the cerebellum [26].
In addition, severe acute respiratory syndrome–related coronavirus (SARS-CoV) encompasses a papain-like protease that significantly triggers an early growth response protein 1 (Egr-1)–dependent activation of transforming growth factor beta 1 (TGF-β1), resulting in upregulation of pro-fibrotic responses in vitro and in vivo in the lungs [27,28].
Recent computational methods study identified doxycycline among the drugs that could potentially be used to inhibit SARS-CoV-2 papain-like protease [29].
Severe COVID-19, ARDS, and pathophysiologic and therapeutic considerations
Respiratory failure from ARDS is the leading cause of mortality in COVID-19 patients [30].
Various pro-inflammatory cytokines and chemokines, including IL-6, TNF-α, and profibrotic factors (TGFB1, CCN2, and PDGFA), are also implicated in tissue damage and vascular leakage and can stimulate pulmonary fibrosis in SARS-CoV infection [31].
The pathologic features of COVID-19 closely resemble those of SARS-CoV infection, which causes massive lung tissue remodeling through the urokinase, coagulation, and wound-healing pathways and through extracellular matrix proteins, including MMPs [31].
MMPs are involved in lung remodeling and destruction of the extracellular matrix, leading to damage of the endothelial basal lamina and increased vascular permeability [32,33].
Importantly, mechanical ventilation, which has a primary role in ARDS management, is associated with further lung injury through activation of MMPs, leading to ventilation-induced lung injury [34].
As mentioned earlier, doxycycline is a strong and broad-spectrum inhibitor of MMPs (a family of more than 24 zinc-dependent proteases). Furthermore, experimental studies have showed that treatment with doxycycline conferred a protective role in lung injury [35,36].
A prophylactic use of doxycycline in mice infected with virulent influenza H3N2 virus attenuates the occurrence of acute lung injury [37].
The tetracycline class of antimicrobials overall has proven a clinically useful tool in MMP inhibition through their ability to chelate the catalytic Zn2+ ion, which is essential for MMP activity, independently of their antimicrobial properties [34].
Among the tetracycline derivatives, doxycycline is the most potent MMP inhibitor, even at a subantimicrobial dose (25 mg) [34].
As lung immune injury/ARDS is prominent in patients with severe COVID-19, inhibiting MMPs may help repair the damaged lung tissue and enhance recovery [38].
Doxycycline treatment of high-risk COVID-19-positive patients with comorbid pulmonary disease
https://journals.sagepub.com/doi/full/10.1177/1753466620951053
https://journals.sagepub.com/doi/pdf/10.1177/1753466620951053
https://journals.sagepub.com/doi/full/10.1177/1753466620951053
https://journals.sagepub.com/doi/pdf/10.1177/1753466620951053
| doxycycline_treatment_of_high-risk_covid-19-positive_patients_with_comorbid_pulmonary_disease.pdf |
There are thousands of articles and research papers available to provide evidence in support of the obvious fact that yes, antibiotics and antiparasitic drugs DO have antiviral effects.
Why is this information being suppressed?
A very small sampling of such articles are listed below.
Why is this information being suppressed?
A very small sampling of such articles are listed below.
The Treatment of Viral Diseases: Has the Truth Been Suppressed for Decades?
https://jpands.org/vol25no3/merritt.pdf
https://jpands.org/vol25no3/merritt.pdf
| the_treatment_of_viral_diseases-_has_the_truth_been_suppressed_for_decades.pdf |
ARTICLES:
Doxycycline - Rationale For Use In COVID-19
https://medicaldialogues.in/pulmonology/news/doxycycline-rationale-for-use-in-covid-19-68527
Coronavirus Treatment Could Lie in Existing Drugs
https://www.genengnews.com/news/coronavirus-treatment-could-lie-in-existing-drugs/
Rapid Response:Doxycycline for COVID-19 Prophylaxis in NHS Frontline Workers
https://www.bmj.com/content/368/bmj.m1252/rr-20
PUBLISHED STUDIES:
Antiviral activity of doxycycline against vesicular stomatitis virus in vitro
https://pubmed.ncbi.nlm.nih.gov/26459887/
https://www.researchgate.net/publication/282875000_Antiviral_activity_of_doxycycline_against_vesicular_stomatitis_virus_in_vitro
Inhibitory effect of doxycycline against dengue virus replication in vitro
https://pubmed.ncbi.nlm.nih.gov/24142271/
https://www.researchgate.net/publication/258061560_Inhibitory_effect_of_doxycycline_against_dengue_virus_replication_in_vitro
Tetracyclines: a pleitropic family of compounds with promising therapeutic properties. Review of the literature
https://journals.physiology.org/doi/full/10.1152/ajpcell.00047.2010
Clinical pharmacology perspectives on the antiviral activity of azithromycin and use in COVID-19.
https://pubmed.ncbi.nlm.nih.gov/32302411/
Azithromycin induces anti-viral effects in cultured bronchial epithelial cells from COPD patients
https://pubmed.ncbi.nlm.nih.gov/27350308/
Prophylaxis with tetracyclines in ARDS: Potential therapy for COVID-19-induced ARDS?
https://www.medrxiv.org/content/10.1101/2020.07.22.20154542v1
Topical application of aminoglycoside antibiotics enhances host resistance to viral infections in a microbiota-independent manner
https://www.nature.com/articles/s41564-018-0138-2
Antiviral Effects of Aphidicolin, a New Antibiotic Produced by Cephalosporium aphidicola
https://aac.asm.org/content/4/3/294.short
