Antibiotics such as Penicillin-streptomycin are commonly used in cell cultures in order to control bacterial contamination. However, it has become increasingly clear that they have various unwanted effects on the cells as well as any results obtained from the cell culture experiments.
From the study “Use antibiotics in cell culture with caution: genome-wide identification of antibiotic-induced changes in gene expression and regulation:”
“Standard cell culture guidelines often use media supplemented with antibiotics to prevent cell contamination. However, RELATIVELY LITTLE IS KNOWN ABOUT THE EFFECT OF ANTIBIOTIC USE IN CELL CULTURE ON GENE EXPRESSION AND THE EXTENT TO WHICH THIS TREATMENT COULD CONFOUND RESULTS.”
“Our results suggest that PenStrep treatment CAN SIGNIFICANTLY ALTER GENE EXPRESSION AND REGULATION in a common liver cell type such as HepG2, advocating that antibiotic treatment SHOULD BE TAKEN INTO ACCOUNT WHEN CARRYING OUT GENETIC, GENOMIC OR OTHER BIOLOGICAL ASSAYS
IN CULTURED CELLS.”
“It is possible that antibiotics such as penicillin-streptomycin and gentamicin also induce a functional state that is significantly different from the basal state of these cell types. FURTHER EVALUATION OF THE BIOLOGICAL IMPACT OF ANTIBIOTIC TREATMENT ACROSS CELL LINES IS HIGHLY WARRANTED. However, we provide some evidence that using antibiotics in cell culture SHOULD BE AVOIDED- especially in studies focused on drug response as well as cell cycle regulation, differentiation, and growth. DATA FROM STUDIES IN WHICH ANTIBIOTICS ARE USED FOR CELL CULTURE SHOULD BE EXAMINED WITH CAUTION.”
The authors state that while little is known about the effects of antibiotics on gene expression, their study showed that significant alterations can occur in the expression and regulation of genes which can alter the results of cell culture and genomic experiments.
This is not the only source claiming such things. From a guide on the use of antibiotics in cell culture:
Antibiotics for DNA, RNA and Protein Modification
“Many antibiotics are effective against bacteria because they modify, interfere with, or inhibit protein synthesis in bacterial cells. Numerous antibiotics can modify bacterial DNA and RNA, inhibit cell wall formation, cause misreading of ribosome codons, and block signal transduction. As a result, antibiotics can be valuable research tools for intentionally modifying nucleic acids, DNA and RNA. Antibiotics predominately interfere and inhibit DNA and RNA synthesis by blocking cellular enzymes like topoisomerase II (DNA gyrase) and RNA polymerase. This interference typically occurs at the 30S or 50S subunits of the 70S bacterial ribosome. Additionally, other antibiotics block peptidoglycan bacterial cell wall formation, cause premature chain termination of proteins, or act as ionophores by disrupting the cellular ionic content and destroying bacteria. Below is a selection of our numerous antibiotics useful for proteomics research due to their modifying actions on nucleic acids, DNA, RNA and protein synthesis.“
So we can add interfering with and inhibiting protein synthesis, modifying DNA/RNA, inhibiting cell wall formation, misreading of ribosome codons, and blocking signal transduction to the list of antibiotics unwanted effects on cell cultures. Some may argue that the article was referring to the effects on bacteria, however other sources show that antibiotics indeed affect not only bacterial DNA/RNA but also human as well:
New insights into how antibiotics damage human cells suggest novel strategies for making long-term antibiotic use safer
“Clinical levels of antibiotics can cause oxidative stress that can lead to damage to DNA, proteins and lipids in human cells“
“Sameer Kalghatgi, Ph.D., a former postdoctoral fellow in Collins’ laboratory who is now Senior Plasma Scientist at EP Technologies in Akron, Ohio, and Catherine S. Spina, a M.D./Ph.D. candidate at Boston University and researcher at the Wyss Institute, first tested whether clinical levels of three antibiotics — ciprofloxacin, ampicillin, kanamycin — each cause oxidative stress in cultured human cells.”
“Kalghatgi and Spina then did a series of biochemical tests, which showed that the same three antibiotics damaged the DNA, proteins and lipids of cultured human cells — exactly what one would expect from oxidative stress.“
Antibiotics-induced oxidative stress
“A large set of ATBs can also damage mammalian tissues and cells; however their modes of action are not as well characterized as in bacteria . Deleterious effects are usually produced by clinically relevant doses of bactericidal ATBs in only few treated patients. Regardless of their molecular targets, the major classes of bactericidal ATBs quinolones, b-lactams, and aminoglycosides can induce mitochondrial dysfunction in various mammalian cell types . Studies in in vitro cell models and in mice have revealed parallel ATB-target interactions in mammalian mitochondria and bacteria [9e11]. Thus, quinolones target bacterial gyrases  and mitochondrial DNA topoisomerase 2 , b-lactams disturb bacterial cell wall functioning  and mitochondrial carnitine/acylcarnitine translocase , and aminoglycosides target both bacterial  and mitochondrial ribosomes . The present review focuses on the induction of oxidative and endoplasmic reticulum (ER) stress by ATBs in mammalian cells, especially hepatocytes, and highlights protective molecular mechanisms involved in response to stress induced by the penicillinase-resistant ATB (PRA) family.”
“ATBs with different chemical structures can cause adverse side effects in various human tissues and cells, especially the liver. ATBs frequently cause cholestasis which is often associated with hepatocellular injury typified by mitochondrial dysfunction and over-expression of ROS, leading to oxidative stress and cell death.“
Effects of antibiotics on mitochondria in mammalian cells
“Bactericidal and bacteriostatic antibiotics have been shown to target mitochondrial components. In mammalian cells, the mitochondrial ETC is a major source of ROS during normal metabolism because of leakage of electrons. According to the endosymbiotic theory, mitochondria originated from free-living, aerobic bacteria (Lesnefsky et al., 2001). It is likely then that antibiotics target mitochondria and mitochondrial components, similar to their action in bacteria. Indeed, previous studies in mammalian systems have revealed parallel antibiotic-target interactions in mitochondria. It has been shown, for instance,that aminoglycosides target both bacterial and mitochondrial ribosomes, quinolones target bacterial gyrases and mtDNA topoisomerases, and β-lactams inhibit bacterial cell wall synthesis and mitochondrial carnitine/acylcarnitine transporters (Hobbie et al., 2008; Lowes et al., 2009; McKee et al., 2006;
Pochini et al., 2008).”
“Using live cell imaging of primary human mammary epithelial cells, the morphological changes in mitochondria was measured and found short, swollen,
fragmented mitochondria (smaller aspect ratio) with highly reduced branching (smaller form factor) in bactericidal antibiotic–treated cells compared to long, tubular (larger aspect ratio), and extensively branched (larger form factor) mitochondria in untreated cells. These results suggest that bactericidal antibiotics shift the balance toward a profission state. A profission state can lead
to a loss of membrane potential, loss of metabolic activity, and an overall increase in oxidative stress (Seo et al., 2010).”
“The constant exposure of mitochondrial DNA to the oxidative environment in the cells has made it more prone to mutations. These mitochondrial mutations and genetic variability may have implications in influencing antibiotic selectivity and sensitivity to the host cell (Singh et al., 2014).”
Beyond Bacteria: How Antibiotics Impact Mitochondria
“Mitochondria are organelles that live within the cell to produce the energy source known as adenosine triphosphate (ATP). They play a role in many cellular activities spanning from energy homeostasis and detoxification to cell death. These organelles have evolved from endosymbiotic alpha-proteobacteria, making them similar to bacteria in many ways. For instance, they maintain a distinct circular genome separate from the nuclear genome and have genes that are homologous to bacterial genes. They also have independent DNA replication and division, and that makes them vulnerable to the effects of antibiotics. Most antibiotics target the growth processes or function of the bacteria—some target the cell wall or cell membrane, some interfere with essential enzymes, and others target protein synthesis. These effects translate to the infectious bacteria, the microbiome, and the bacteria-like organelles known as mitochondria.
We can no longer subscribe to the idea of antibiotics killing bacteria and causing no harm to our cells. According to a study published in 2013 titled, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells,” bactericidal antibiotics induced intracellular ROS in various human cell lines, and this increase in ROS led to damage in DNA, proteins and lipids. It was shown that the bactericidal antibiotics caused this damage by disrupting the mitochondrial electron transport chain, which led to a buildup of free radicals. These antibiotics impaired mitochondrial function after just four days, which is a shorter duration than typical antibiotic protocols.”
As can be seen from these sources, antibiotics can target the same pathways in Mitochondria as they do in bacteria. This leads to oxidative stress which damages DNA, lipids, and proteins in human cells. This can lead to cell death which is exactly what Virologists see when they claim “viruses” as the cause of the cytopathic effects they observe in their cell culture experiments.
However, beyond the cytopathogenic effect antibiotics have on the cell culture experiments, their use also influences genomic studies when they damage Mitochondria as they are essential to genomic stability. This is highlighted in three sources:
Mitochondria damage checkpoint in apoptosis and genome stability
“Studies described in this paper suggest a role for mitochondria in maintaining genomic stability. Genomic stability appears to be dependent on mitochondrial functions involved in maintenance of proper intracellular redox status, ATP-dependent transcription, DNA replication, DNA repair and DNA recombination.”
Mitochondrial dysfunction leads to nuclear genome instability: A link through iron-sulfur clusters
“Here we report that in Saccharomyces cerevisiae, loss of mtDNA leads to nuclear genome instability, through a process of cell cycle arrest and selection we define as a cellular crisis.”
“These results suggest mitochondrial dysfunction stimulates nuclear genome instability by inhibiting the production of ISC-containing protein(s), which are required for maintenance of nuclear genome integrity.“
“Normal mitochondrial function appears to be important for nuclear genome integrity.”
Mitochondria-nucleus network for genome stability
“The proper functioning of the cell depends on preserving the cellular genome. In yeast cells, a limited number of genes are located on mitochondrial DNA. Although the mechanisms underlying nuclear genome maintenance are well understood, much less is known about the mechanisms that ensure mitochondrial genome stability. Mitochondria influence the stability of the nuclear genome and vice versa. Little is known about the two-way communication and mutual influence of the nuclear and mitochondrial genomes. Although the mitochondrial genome replicates independent of the nuclear genome and is organized by a distinct set of mitochondrial nucleoid proteins, nearly all genome stability mechanisms responsible for maintaining the nuclear genome, such as mismatch repair, base excision repair, and double-strand break repair via homologous recombination or the nonhomologous end-joining pathway, also act to protect mitochondrial DNA. In addition to mitochondria-specific DNA polymerase γ, the polymerases α, η, ζ, and Rev1 have been found in this organelle. A nuclear genome instability phenotype results from a failure of various mitochondrial functions, such as an electron transport chain activity breakdown leading to a decrease in ATP production, a reduction in the mitochondrial membrane potential (ΔΨ), and a block in nucleotide and amino acid biosynthesis. The loss of ΔΨ inhibits the production of iron-sulfur prosthetic groups, which impairs the assembly of Fe-S proteins, including those that mediate DNA transactions; disturbs iron homeostasis; leads to oxidative stress; and perturbs wobble tRNA modification and ribosome assembly, thereby affecting translation and leading to proteotoxic stress. In this review, we present the current knowledge of the mechanisms that govern mitochondrial genome maintenance and demonstrate ways in which the impairment of mitochondrial function can affect nuclear genome stability.”
In other words, antibiotics damage the mitochondria which disrupts genomic stability. Why is this important?
From “The detection and implication of genome instability in cancer:”
“Genomic instability refers to a variety of DNA alterations, encompassing single nucleotide to whole chromosome changes, and is typically subdivided into three categories based on the level of genetic disruption. Nucleotide instability (NIN) is characterized by an increased frequency of base substitutions, deletions, and insertions of one or a few nucleotides; microsatellite instability (MIN or MSI) is the result of defects in mismatch repair genes which leads to the expansion and contraction of short nucleotide repeats called microsatellites; chromosomal instability (CIN) is the most prevalent form of genomic instability and leads to changes in both chromosome number and structure .”
Genomic instability stemming from mitochondrial damage from antibiotics results in alterations to a genome. With the various ways in which antibiotics affect cells and damage DNA/RNA, is it any wonder why, as of this writing, we have over 3 million different “variants” of the same “virus?”
It has been clear that antibiotics should not be used in cell cultures as they are highly toxic and can and will change the cells used with them. Various guidelines recommend against the use of antibiotics but alas, they continue to insist on using them.
So knowing the damage that antibiotics have on cell culture and genomic experiments, let’s look at two of the most cited papers for the evidence of “SARS-COV-2” and see if they used antibiotics:
From “A Novel Coronavirus from Patients with Pneumonia in China, 2019:”
“The viral transport medium was composed of Hank’s balanced salt solution (pH 7.4) containing BSA (1%), AMPHOTERICIN (15 μg ml−1), PENICILLIN G (100 units ml−1) and STREPTOMYCIN (50 μg ml−1).”
“PENICILLIN (100 units ml−1) AND STREPTOMYCIN (15 μg ml−1) WERE INCLUDED IN ALL TISSUE CULTURE MEDIA.”
From “Identification of Coronavirus Isolated from a Patient in Korea with COVID-19:”
“Oropharyngeal samples were diluted with viral transfer medium containing nasopharyngeal swabs and ANTIBIOTICS (NYSTADIN, PENICILLIN-STREPTOMYCIN 1:1 dilution) at 1:4 ratio and incubated for 1 hour at 4°C, before being inoculated onto Vero cells. Inoculated Vero cells were cultured at 37°C, 5% CO2 in 1× Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 2% fetal bovine serum AND PENICILLIN-STREPTOMYCIN.”
Both “SARS-COV-2” papers used antibiotics when culturing their “viruses” which in turn would effect the end results of the cell culture process as well as any genomic data gained from it.
Remember: “Data from studies in which antibiotics are used for cell culture should be examined with caution.”
I want to also point out that the Zhu paper admitted to not fulfilling Koch’s Postulates in order to prove pathogenicity and authors from both papers admitted to not purifying “virus” particles. The “evidence” within them is already faulty even if we were to disregard the overuse of the Cell/DNA damaging antibiotics.
This is the “evidence” used to “confirm” to the world that “SARS-COV-2” exists and was used for the justification of lockdowns, quarantines, social distancing, masks, and vaccines.
It’s time to wake up to the lies and the fraudulent methods used to justify them.