Some disputes on the origins of SARS-CoV-2: coincidences and speculations

The emergence of SARS-CoV-2 in late 2019 and the subsequent COVID-19 pandemic triggered an unprecedented global scientific effort. Understanding the virus, developing drugs and vaccines, and determining its origin became public health imperatives. Although most consolidated scientific evidence points to a zoonotic origin – a spillover event from an animal reservoir, likely bats, possibly via an intermediate host yet to be identified – the possibility of a laboratory leak or an artificial origin has generated considerable controversy. This dispute ignited due to certain genetic "coincidences" that, when taken out of context, fueled widespread speculation and misinformation.

Luc Montagnier and HIV sequences in SARS-CoV-2
One of the most significant of these controversies involved Nobel laureate Luc Montagnier. In the spring of 2020, at 88 years old, Montagnier publicly claimed an artificial origin for the SARS-CoV-2 virus. His primary argument supporting this thesis was the alleged presence of short nucleotide sequences in the SARS-CoV-2 genome with an unusual similarity or "homology" to those found in key HIV-1 proteins (like gp120 and Gag) and other simian immunodeficiency viruses (SIVs). Furthermore, within the context of these presumed "insertions" (from HIV), he also mentioned the Furin Cleavage Site (FCS) in the SARS-CoV-2 Spike protein. We'll delve deeper into the characteristics of this site, which was perceived as unique compared to other known viruses at the time, later in this article.
Luc Montagnier and Jean Claude Perez's first pre-print on the subject, "HIV men-manipulated coronavirus genome evolution trends," published on Zenodo on August 2, 2020 (an article that had not yet been peer-reviewed), was voluntarily withdrawn by the authors from the pre-publication platform due to serious methodological and interpretive flaws, pending a much more in-depth investigation. Subsequently, however, the authors produced other articles asserting the same claims.
Given the stature of the authors, this theory quickly spread, including through media outlets, fueling arguments for an engineered origin of the virus and undermining trust in scientific institutions. However, these claims were widely and rapidly refuted by the global scientific community. The main reason is that the SARS-CoV-2 genome is vast, comprising approximately 30,000 nucleotides (more precisely, estimates vary slightly, but hover around 29,900 nucleotides or 29.9 kilobases, kb). In a genetic code of such magnitude, the appearance of short sequences (like the 8-12 amino acids identified by Montagnier) showing random similarities with other proteins, including those from HIV, is statistically expected and not unusual.
These short sequences are small portions of amino acids that repeat in nature across various unrelated proteins for functional or structural reasons, or simpl by pure chance. They are not indicative of a direct genetic relationship, much less deliberate engineering. In-depth, independent analyses of the SARS-CoV- 2 genome have never found any evidence of HIV-characteristic genes or protein structures, nor any mechanism that could justify their functional integration.

In summary, the "coincidence" of HIV sequences is a classic example of how extrapolating minimal data from a vast genomic context can lead to scientifically unfounded and misleading conclusions, fueling misinformation.
How could a scientist of Luc Montagnier's caliber, a Nobel laureate, make such a glaring error? It must be said that Montagnier, like many other great scientists, always sought to understand previously inexplicable phenomena. This commendable drive to push beyond established scientific guidelines, a characteristic often found in brilliant minds, nevertheless progressively led him away from the traditional scientific path.
His case is an emblematic example of how the scientific mind can slip into irrationality. Montagnier appears to have been influenced by cognitive biases (pre-existing judgments), which led him to interpret evidence selectively. This reinforced personal convictions on concepts like "water memory" (2009) and "DNA teleportation" (2015), theories that, while suggestive, lacked empirical foundation. His obstinacy, in the face of lack of reproducibility and rejection by the scientific community, transformed his innovative research into a veritable fideism, where pure belief replaced proof. Such an almost religious adherence to his own ideas then generated active proselytism, spreading unvalidated theories that fueled skepticism and misinformation, definitively distancing him from the methodological rigor that had characterized his brilliant earlier career.

Moderna's US9359392B2 patent (2016): a therapeutic context
Subsequently, another controversy arose from the similarity between a 19-nucleotide sequence patented by Moderna and a key region of the SARS-CoV-2 genome.
The patent in question is US9359392B2 (also US9587003B2), filed by Moderna Inc. on February 24, 2016, and granted on May 31, 2016, titled "Modified polynucleotides for the production of human MSH3 protein and uses thereof." It was created by: Paolo Forni, Romain B. M. D. De Beukelaer, Sayumi Asahara, Martin Andrew Stahl, Holly Ann Stefl, and Jeffrey B. Brown. This patent concerns the development of modified and optimized messenger RNA (mRNA) sequences designed to encode the human MSH3 protein, a fundamental component of the DNA mismatch repair (MMR) system (an error in the DNA sequence where two complementary nitrogenous bases do not pair correctly). The objective was therapeutic, particularly for conditions associated with MSH3 gene dysfunctions, such as certain types of cancer. Within this patent, as an example of a "codon-optimized" mRNA sequence – meaning modified to improve the production of a specific protein – there is also the sequence 5'-CTCCTCGGCGGGCACGTAG-3'. The similarity between the sequence 5'-CTCCTCGGCGGGCACGTAG-3' and a portion of the Furin Cleavage Site (FCS) of the SARS-CoV-2 Spike protein (specifically, a 19 nucleotide section that includes the FCS) was noted by Ambati et al. in a study published in 2022 in Frontiers in Virology.
This study highlighted a 100% sequence homology between this portion of the SARS-CoV-2 genome and the reverse complement of a patented sequence related to the human MSH3 gene (MutS Homolog 3), which had been codon-optimized.

What is the Furin Cleavage Site (FCS)?
The Furin Cleavage Site (FCS) is a short amino acid sequence present in the Spike protein of some viruses, including SARS-CoV-2. The Spike protein is fundamental for infecting host cells, as it allows the virus to bind to and enter them.
Furin is an enzyme (a protease) abundantly present in many human cells, including those in the lungs, intestines, and blood vessels. When a virus's Spike protein contains an FCS, furin can "cleave" or "cut" the protein at that specific point. This cleavage is crucial because it activates the Spike protein, making the virus much more efficient at penetrating cells and replicating. In the case of SARS-CoV-2, the presence of this FCS in its Spike protein has been considered one of the key characteristics that make it so transmissible and pathogenic to humans, as it facilitates its ability to infect a wide range of cells and tissues. The discovery of this similarity with a patented sequence raised questions about the origin of the furin cleavage site in SARS-CoV-2, fueling scientific debates and hypotheses about the virus's origin.
In reality, the document describes innovations in the field of modified messenger RNA (mRNA) sequences, designed to optimize the production of the human MSH3 (MutS Homolog 3) protein, a crucial component of the DNA mismatch repair (MMR) system, which plays a fundamental role in maintaining genomic integrity and preventing cancer. The declared objective of the patent was the development of mRNA-based therapies to address medical conditions associated with MSH gene dysfunctions, such as types of cancer where MMR system defects are found, including:

Solid Tumors:
• Colorectal Cancer (CRC): This is the most classically and strongly associated tumor with MMR defects, particularly in Lynch Syndrome (previously
known as HNPCC - hereditary nonpolyposis colorectal cancer), which is caused by germline mutations in MMR genes (MLH1, MSH2, MSH6,
PMS2, and sometimes EPCAM which silences MSH2).
• Endometrial Cancer (Uterus): It's the second most common cancer in Lynch Syndrome and often presents microsatellite instability (MSI).
• Gastric Cancer (Stomach): Especially when associated with Lynch Syndrome, it shows MMR defects.
• Ovarian Cancer: Certain subtypes are associated with MMR deficiency.
• Pancreatic Cancer: Less frequent, but can show MMR defects.
• Prostate Cancer: A subpopulation may present MMR deficiency.
• Hepatobiliary Tract Tumors: Includes liver and bile duct cancers.
• Urinary Tract Tumors: Kidney pelvis, ureter, and bladder cancers.
• Small Intestine Tumors.
• Glioblastoma (a type of brain tumor).
• Some skin cancers: such as sebaceous carcinomas.

Hematological Tumors (Blood and Lymphatic System):
• MMR defects are considered rarer in hematological tumors compared to solid ones, but can still be present, especially in certain circumstances:
• Acute Myeloid Leukemia (AML): Especially in those arising after chemotherapy or radiotherapy for a primary cancer.
• Myelodysplastic Syndrome (MDS): Especially those with therapy-related forms.
• Other hematological disorders.
It is important to emphasize that the detection of an MMR defect or MSI in a tumor has become a crucial biomarker, as these tumors tend to respond particularly well to immunotherapy with immune checkpoint inhibitors, thanks to their high genomic instability leading to the production of numerous neoantigens.
Thus, the MMR system is an essential cellular mechanism that acts as a "proofreader" for our DNA. Its main function is to recognize and correct errors that occur during DNA replication or as a result of certain types of DNA damage. It also plays a role in suppressing the integration of foreign or retroviral DNA into the host genome. Cells with MMR defects have shown a reduced ability to detect and correct errors in DNA replication, leading to an accumulation of mutations and genomic instability, a key factor in the development of various types of cancer, as well as a greater tendency to integrate linear or retroviral DNA into chromosomes. This implies that a functional MMR system helps prevent the undesirable integration of viral elements, including potentially active Human Endogenous Retroviruses (HERVs) or other retroelements. Therefore, the goal to be achieved is to restore the function of the deficient gene or produce a functional protein that the body cannot synthesize correctly due to the genetic anomaly. mRNA-based therapies address these dysfunctions primarily through two strategies: protein/gene replacement therapy (producing the missing/defective MSH protein) and mRNA cancer vaccines (immunotherapy).

The correspondence with the SARS-CoV-2 genome: an apparent homology
Within the patent claims and descriptions, a series of exemplary nucleotide sequences are presented, including a specific 19-nucleotide sequence: 5'- CTCCTCGGCGGGCACGTAG-3'. This sequence was included as an example of a "codon-optimized" mRNA sequence to improve the efficiency of human MSH3 protein translation, and the patent specified that it represented a portion of human mRNA or its reverse complement. It is crucial to understand that the patent fits into a broad line of research aimed at developing mRNA therapies, a rapidly expanding field long before the pandemic.
The controversy erupted when, in the context of investigations into the origin of SARS-CoV-2, it was highlighted that the patented 19-nucleotide sequence showed a near-perfect homology (or reverse complementarity) with a specific portion of the SARS-CoV-2 genome. Specifically, it was noted that the patented sequence is the reverse complement (or, in some cases, a direct match with a few mismatches) of a 19-nucleotide sequence within the region encoding the Furin Cleavage Site (FCS) of the SARS-CoV-2 Spike (S) protein.
The furin cleavage site (with the characteristic amino acid sequence PRRAR or similar variations, encoded by nucleotide sequences like CCTCGGCGGGCACGTAG) is a distinguishing feature of SARS-CoV-2 that significantly differentiates it from closely related coronaviruses found in nature, such as the bat RaTG13 or pangolin coronaviruses, which either lack a functional FCS or possess it in a less efficient form. The FCS is believed to play a crucial role in the virus's pathogenicity and transmissibility, as it facilitates the cleavage of the Spike protein by furin, making the virus more efficient in cellular entry and replication. The presence of a functional FCS has been a key point in the debate about the virus's origin, with some theories suggesting it might have been artificially inserted. The discovery of a similar sequence patented by Moderna inevitably fueled and reinvigorated these speculations, amplified by social media and non-scientific sources.

The contestations and conspiracy theories: misinformation based on misinterpretation
The news of the coincidence, often presented without the necessary scientific context, quickly found fertile ground in conspiracy theories and narratives supporting an artificial or manipulated origin of SARS-CoV-2. The main contestations and erroneous conclusions can be summarized as follows:
• "Proof of manipulation": The presence of a patented sequence in a crucial region of the virus was interpreted as direct evidence of genetic engineering and manipulation of SARS-CoV-2 by third parties, including Moderna or related entities.
• "Premeditation or pre-existing knowledge": It was suggested that Moderna somehow had pre-existing knowledge of the virus or was working on sequences related to SARS-CoV-2 years before the pandemic, which would imply involvement in its "creation" or "leak."
• "Lab leak": The coincidence was used to reinforce the lab leak argument, hypothesizing that the sequence might have been part of experiments conducted in the laboratory to induce the acquisition of a new function or the enhancement of a pre-existing "Gain-of-Function" (GoF) aimed at making the virus more aggressive.
It is fundamental to reiterate that these contestations are based on a misinterpretation of scientific data, a poor understanding of the principles of molecular genetics and bioinformatics, and often a lack of context.

Critical analysis
Hypothesis of the insertion of the 19 nucleotides from Moderna, or other fragments, into the genome of an already existing coronavirus in nature, with the intent of making it more aggressive for humans.
If a sequence is inserted into a genome, especially at a point that confers a new advantage (such as a furin cleavage site that makes the virus more infectious to human cells), scientists look for signs of this insertion. Such signs include: Unusual junction sequences: Genetic engineering techniques tend to leave molecular "scars" at junction points. These scars are small DNA sequences not commonly found in nature or that indicate the use of specific laboratory tools. In the case of SARS-CoV-2, extremely detailed analyses of the genome have not revealed such signatures around the furin cleavage site or in other potentially "inserted" regions. The furin cleavage site sequence in SARS-CoV-2, while unique among closely related sarbecoviruses, integrates seamlessly into the genome in a manner consistent with naturally occurring insertion/deletion events and point mutations. Furthermore, if a sequence had been artificially inserted, one would expect an evolutionary "discontinuity." In the case of SARS-CoV-2, phylogenetic analysis shows evolutionary continuity with other bat coronaviruses, suggesting gradual evolution.

Probability of genomic coincidences
To rigorously evaluate the significance of the coincidence between Moderna's patented sequence and the SARS-CoV-2 genome, it's essential to consider several scientific and statistical factors: Molecular context of Moderna's 2016 patent: a clarifying analysis Moderna's 2016 patent, which we've already discussed, focused specifically on optimizing mRNA sequences for the production of human MSH3 protein.
This is the core of the entire document, not research on viruses. The sequence in question was designed to significantly increase the efficiency of protein synthesis by cells, ensuring optimal production of the MSH3 protein. This result was achieved by modifying specific groups of three nucleotides in the mRNA, a process called 'codon optimization.' The sequence in question was generated using two main components: a "human transcript," which is simply a piece of RNA derived directly from our body's DNA, and a "reverse complement" (i.e., a kind of "mirror image" or complementary sequence read backward) of a specific portion of human mRNA. It is crucial to understand that the inclusion of this sequence in the patent had a single, well-defined purpose: it was purely functional for the production of the MSH3 protein. There was no relationship, implicit or explicit, with coronaviruses or any other type of virological research. The patent was not about viruses at all. Consequently, arguing that there is a correlation between this patent and the origin of a virus means extrapolating the sequence from its original scientific context, attributing a meaning to it that is completely extraneous to the purpose for which it was conceived and patented.

The concept of “random homology” and statistical probabilities
The debate surrounding the 19-nucleotide sequence patented by Moderna has generated much confusion, but a scientific analysis clarifies its limited significance. The crucial point is the extreme brevity of this sequence compared to the entire SARS-CoV-2 genome, which is approximately 30,000 nucleotides long.
Imagine you have a book with 30,000 letters. Finding a specific sequence of 19 letters, even if it's identical to one found in another book, is not nearly as surprising as it might intuitively seem. Here's the detail of why this "coincidence" is scientifically explainable: The theoretical probability of a 19-nucleotide sequence: the Moderna patent case In the context of discussions related to specific biotechnology patents, such as Moderna's (US Patent US9359392B2), a 19-nucleotide sequence has sometimes been referenced. Let's analyze the theoretical probability that a sequence of such length could appear by pure chance, an exercise that highlights its extreme improbability without targeted intervention. DNA (and RNA, as in the case of mRNA technologies) is made up of four fundamental "letters," the nucleotide bases: Adenine (A), Thymine (T) – or Uracil (U) in RNA – Cytosine (C), and Guanine (G). For this simplified calculation, we adopt two assumptions:
• Equal probability for each base: Let's assume that each of the four bases has the same probability of appearing in each single position of the sequence. Thus, the probability (P) for a specific base is 1/4, or 0.25. P(single base)=1/4=0.25
• Random and independent sequence: We assume that the choice of a base in one position does not influence the choice of bases in subsequent positions in any way. The events are, therefore, statistically independent. Calculation of probability for Moderna's 19 nucleotides: To determine the probability P that a specific sequence of N nucleotides forms by pure chance, we multiply the probability of each single position. For a sequence 19 nucleotides long (so N=19), the calculation becomes: P=(0.25)19 Solving the power: (0.25)19=(1/4)19=1/419 Calculating 419: 419=274,877,906,944 Therefore, the probability is: P=1/274,877,906,944 Expressed in scientific notation, this value is approximately: P≈1.45×10−12

Interpretation of Results: The Probability of Genetic Coincidences and the Moderna Patent
The probability calculation we examined, 1.45×10−12, highlights an incredibly small number. This means that the probability of a specific 19-nucleotide sequence generating spontaneously and randomly, respecting our simplified assumptions (equally probable bases, independent events), is almost zero. Such a result suggests that a purely random event of this nature is almost impossible. However, it is crucial to clarify that this calculation is misleading if interpreted without adequate context, as it ignores several crucial factors that drastically increase the probability of a coincidence in the real world of biology and genomics.

Factors that drastically increase the probability of a coincidence
When we talk about genetic sequences, it's easy to think that every match is an extraordinary event. But in reality, in the vast and complex world of DNA and RNA, finding short identical or very similar fragments can be much more probable than one might believe, even without a direct or intentional link. This is especially true for functional biological sequences: they aren't random, but have been shaped by evolution or created for a purpose. The point is that, even if created for a purpose, short segments can reappear randomly elsewhere.
Let's see why it's so easy to encounter these "coincidences":
1. The genome is a huge target: Imagine searching for a specific word in a book. If you only search on one specific page, the chances are low. But if you can search for it in every single line of every single page of the entire book, the possibilities increase dramatically. Similarly, we aren't looking for a 19-nucleotide sequence (the "building blocks" of DNA/RNA) at a fixed point in SARS-CoV-2. This virus's genome is about 30,000 nucleotides long, and the sequence we're looking for could start at any of the approximately 30,000 possible starting positions. This enormously multiplies the opportunities to find a purely random match.
2. No perfect match needed: Often, perfect identity isn't necessary. If we accept that the "matching" sequence can have one or two different nucleotides (so-called "mismatches") compared to the original, the probabilities of finding a match increase exponentially. In the case of the Moderna sequence and SARS-CoV-2, some early analyses showed a very high similarity, but not always 100% identical, which makes the coincidence even more probable.
3. "Mirror image" also counts: When searching for genetic similarities, we consider not only the sequence in one direction on a DNA or RNA strand, but also its "reverse complementarity." This means searching for the sequence that would bind to it on the other strand, or the sequence read backward. Think of it like having two sides of a coin: instead of just looking for "heads," you also look for "tails." This, in effect, doubles the chances of finding a random match.
4. The enormous amount of available data: The comparison isn't just between Moderna's patent and a single viral genome. The search is conducted in immense public genomic databases, like GenBank, which contain trillions of nucleotide sequences from thousands of different organisms: bacteria, viruses, plants, animals, humans. In such a vast universe of sequences, finding short identical or highly similar fragments is a statistically predictable and common event. It's somewhat like the "birthday paradox": in a relatively small group of people, the probability that two share the same birthday is much higher than one might think. Similarly, in an immense sea of genetic sequences, short similar segments will simply reappear by chance. In conclusion, while a single, long, and specific identical sequence in two unrelated contexts would be extremely improbable, the search for short fragments with some tolerances, within vast genomes and databases, makes the discovery of these "coincidences" a perfectly normal and statistically explainable event.

Mechanisms of viral evolution and the origin of the Furin Cleavage Site (FCS)
RNA viruses like SARS-CoV-2 evolve extremely rapidly through natural mechanisms such as random mutations, recombination, and natural selection. The acquisition of a Furin Cleavage Site (FCS) has been observed in various coronaviruses independently (for example, in some lines of avian infectious bronchitis virus, IBV, or in other coronaviruses infecting mammals).
The emergence of a functional FCS in SARS-CoV-2 is believed to be the result of:
• Gradual mutations and positive selection in a host viral population, which confer an evolutionary advantage.
• Natural recombination events with other animal coronaviruses. Coronaviruses are known for their high capacity for recombination. This means they can exchange portions of their genetic material when two different viruses infect the same cell. It is a primary source of genetic variability and can lead to the acquisition of new characteristics, such as a furin cleavage site. It is not necessary to invoke an artificial origin or deliberate intervention to explain the presence of an FCS. Robust phylogenetic analyses have traced the evolution of SARS-CoV-2, suggesting a divergence from a common ancestor with other betacoronaviruses that supports the zoonotic origin.

Bat CoV CD35: a crucial proof
Recent discoveries have further strengthened the natural hypothesis. In 2023, Wu and colleagues identified a new bat betacoronavirus, Bat CoV CD35, which possesses a polybasic furin cleavage site identical to that found in SARS-CoV-2. Its Spike protein contains the amino acid sequence PRRAR, encoded by the nucleotide sequence 5'-CCU CGG CGG GCA-3' (referring to the key insert), identical to that of SARS-CoV-2. This discovery is of fundamental importance because it provides direct proof that a furin cleavage site sequence identical to that of SARS-CoV-2 can exist naturally in a bat coronavirus. This refutes the argument that such a sequence is an intrinsic "signature" of laboratory manipulation and lays the groundwork for possible natural recombination with other animal coronaviruses.

Conclusion: the need for scientific rigor against misinformation
The coincidence between a 19-nucleotide sequence patented by Moderna and a portion of the SARS-CoV-2 furin cleavage site is an interesting scientific fact, but it has been widely misrepresented and distorted in public debate, fueling misinformation and mistrust.
A rigorous and evidence-based scientific analysis leads to the following unequivocal conclusions:
• Contextual functionality of the patented sequence: The patented sequence was functional within its original context; it was part of a Moderna patent focused on optimizing the expression of the human MSH3 protein for therapeutic purposes, with no correlation whatsoever to coronaviruses.
• Statistically explainable coincidence: Given the size of the viral genome, the enormous quantity of sequences present in biological databases and in nature, and the tolerance for "mismatches," the probability of finding short homologies or inverse complementarities by pure chance is not at all negligible. The brevity of the sequence (19 nucleotides) is insufficient to indicate deliberate manipulation or a significant causal relationship.

• No evidence of direct manipulation: Despite speculations, this coincidence provides no scientific evidence that SARS-CoV-2 was artificially created or that Moderna played a role in its origin. Solid scientific evidence on the origin of SARS-CoV-2 refutes the argument that the furin cleavage site sequence is an intrinsic "signature" of laboratory manipulation and demonstrates how a sequence identical to that of SARS-CoV-2 can exist naturally in a bat coronavirus and could have been naturally recombined into SARS-CoV-2.

Conclusion: the need for scientific rigor against misinformation
The coincidence between a 19-nucleotide sequence patented by Moderna and a portion of the SARS-CoV-2 furin cleavage site is an interesting scientific fact, but it has been widely misrepresented and distorted in public debate, fueling misinformation and mistrust.
A rigorous and evidence-based scientific analysis leads to the following unequivocal conclusions:
• Contextual functionality of the patented sequence: The patented sequence was functional within its original context; it was part of a Moderna patent focused on optimizing the expression of the human MSH3 protein for therapeutic purposes, with no correlation whatsoever to coronaviruses.
• Statistically explainable coincidence: Given the size of the viral genome, the enormous quantity of sequences present in biological databases and in nature, and the tolerance for "mismatches," the probability of finding short homologies or inverse complementarities by pure chance is not at all negligible. The brevity of the sequence (19 nucleotides) is insufficient to indicate deliberate manipulation or a significant causal relationship.
• No evidence of direct manipulation: Despite speculations, this coincidence provides no scientific evidence that SARS-CoV-2 was artificially created or that Moderna played a role in its origin. Solid scientific evidence on the origin of SARS-CoV-2 refutes the argument that the furin cleavage site sequence is an intrinsic "signature" of laboratory manipulation and demonstrates how a sequence identical to that of SARS-CoV-2 can exist naturally in a bat coronavirus and could have been naturally recombined into SARS-CoV-2. In an era of rapid information dissemination, it is crucial for the scientific community to continue providing clarity, context, and rigorous analysis of facts to counter unfounded narratives. The history of Moderna's 19-nucleotide sequence serves as an eloquent warning about how scientific data can be decontextualized, misinterpreted, and distorted to support theories not backed by evidence. Scientific rigor and transparency are the only tools to address complex challenges, such as pandemics, relying on knowledge and not speculation.

The economic roots of misinformation
It is crucial to recognize that the proliferation of misinformation, including that related to virus origins and manipulation theories, is not always random or driven solely by misunderstanding. Often, it has significant economic roots. Misinformation can be a profitable business. Online platforms and individuals can generate advertising revenue or increase their visibility and influence by spreading sensational, controversial, or emotionally charged content, regardless of its veracity. Fear, anger, and distrust are powerful emotions that attract much more user attention and engagement than positive, non-sensational information. This directly translates into clicks, shares, and ultimately, profits. Furthermore, misinformation can be used to damage the reputation of companies or sectors (like the pharmaceutical industry), alter public perception of products or policies, or even influence financial markets. This creates an incentive for some actors to invest in the creation and dissemination of misleading narratives, exploiting cognitive vulnerabilities and the complexity of scientific information for profit or strategic advantage. Understanding these economic dynamics is essential to effectively recognize and combat misinformation.

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