Top left: The nuclei of human cells appear in blue. The green signal indicates the presence of a dengue virus protein.
Top right: The nuclei of human cells appear in teal. The magenta signal indicates the presence of a dengue virus protein.
Bottom left: The nuclei of human cells appear in grey. The red signal indicates the presence of a dengue virus protein.
Bottom right: The nuclei of mosquito cells appear in blue. The red and green signal indicates the presence of two dengue virus proteins.
Today it's the turn of researchers at Oklahoma's Stowers Institute for Medical Research to expose the brilliance of creationism's divine malevolence in the way it's designed the Dengue virus to enable it to spread out of the tropics and infect more people. Currently, according to the World Health Oragnisation, the mosquito-borne virus, infects around 400 million people a year and there is no cure.
The Stowers Institute team led by Predoctoral Researcher Luciana Castellano in the lab of Associate Investigator Ariel Bazzini, Ph.D., has discovered how it, and hundreds of other viruses, replicate in their hosts.
Creationism't intelligent designer, for those who believe in magic, uses it's tried and tested mosquito delivery system, especially the Aedes eagypti mosquito which it used so successfully to spread the Zika virus to cause microcephaly in children.
The sneaky trick it used to get past the immune system it allegedly designed to protect us from things like its viruses, is breathtaking in its simplicity. In order to replicate inside a host cell, the virus needs some specific protein enzymes. It has the RNA code for these enzymes, but the problem is, the host's immune system would recognise those as foreign and launch an attack, so the virus uses the hosts enzymes. Proteins are coded for with a three-nucleotide code, one for each amino acid in the chain. However, the same amino acid can be coded for by several different triplet codes, some of which are more efficient than others. To ensure the cell makes its own enzymes for the virus, the virus uses less efficient codons in its own RNA!
This way, the virus tricks the cell into cooperating in its own destruction.
Neat, eh?
It's a classic example of how an apparently deleterious mutation works in favour of a parasite, and something creationists will find impossible to explain away with the biologically nonsensical 'genetic entropy' causing 'devolution' because the mutation was undoubtedly evolutionary, enabling the dengue virus (DENV) to produce very many more copies of itself than before, and something better can't be less perfect than the original.
Tell me all about Dengue and the virus that causes it, please. Dengue is a mosquito-borne viral infection that has become a major international public health concern in recent decades. The virus responsible for dengue is the dengue virus (DENV), which belongs to the Flavivirus genus within the Flaviviridae family. Here is a comprehensive overview of dengue and the virus that causes it:The Stowers, team's results are published, open access, in the journal Molecular Systems Biology and explained in a Stowers Institute New release:
Dengue Virus (DENV)
Structure and Serotypes
- Structure: Dengue virus is an enveloped virus with a single-stranded RNA genome. It is spherical in shape and about 50 nm in diameter. The RNA genome is approximately 11 kilobases long.
- Serotypes: There are four distinct serotypes of dengue virus, designated as DENV-1, DENV-2, DENV-3, and DENV-4. Each serotype can cause dengue fever, and infection with one serotype provides lifelong immunity to that specific serotype but only short-term immunity to the other three.
Transmission
- Mosquito Vectors: Dengue virus is primarily transmitted to humans through the bites of infected female mosquitoes, mainly of the species Aedes aegypti and, to a lesser extent, Aedes albopictus.
- Cycle: The virus is taken up by the mosquito when it feeds on the blood of an infected person. It then replicates in the mosquito and is transmitted to another person when the mosquito feeds again.
Symptoms and Clinical Presentation
Dengue Fever
- Symptoms: High fever, severe headache, pain behind the eyes, joint and muscle pain, rash, and mild bleeding (such as nose or gum bleed).
- Duration: Symptoms typically last for 2-7 days.
Severe Dengue (Dengue Hemorrhagic Fever/Dengue Shock Syndrome)
- Symptoms: Severe abdominal pain, persistent vomiting, rapid breathing, bleeding gums, fatigue, restlessness, and blood in vomit.
- Risk: This condition can be life-threatening due to plasma leakage, fluid accumulation, respiratory distress, severe bleeding, or organ impairment.
Diagnosis
- Clinical Diagnosis: Based on symptoms and patient history, especially if the patient has recently been in an area where dengue is endemic.
- Laboratory Tests: Confirmation is typically done through blood tests such as:
- PCR (Polymerase Chain Reaction): Detects viral RNA.
- NS1 Antigen Test: Detects the presence of dengue virus antigen.
- Serology: Detects antibodies against dengue virus (IgM and IgG).
Treatment
- No Specific Antiviral Treatment: There is no specific antiviral treatment for dengue. Management focuses on relieving symptoms.
- Supportive Care: Includes maintaining hydration, pain relief with acetaminophen (not aspirin or NSAIDs due to the risk of bleeding), and monitoring for complications.
- Hospitalization: Severe dengue cases may require hospitalization for fluid replacement and supportive care.
Prevention and Control
Mosquito Control
- Elimination of Breeding Sites: Removing stagnant water where mosquitoes lay eggs.
- Insecticides: Use of insecticides to kill adult mosquitoes.
- Biological Control: Introduction of natural mosquito predators and use of genetically modified mosquitoes.
Personal Protection
- Mosquito Repellents: Using DEET or other effective repellents.
- Protective Clothing: Wearing long-sleeved shirts and long pants.
- Mosquito Nets: Using mosquito nets while sleeping, especially in areas with high mosquito activity.
Vaccination
- Dengvaxia: The first dengue vaccine, developed by Sanofi Pasteur, is available in some countries for individuals aged 9-45 years who have had at least one prior dengue infection. However, it is not recommended for those who have never been infected with dengue due to the risk of severe dengue upon subsequent infection.
Epidemiology
- Global Distribution: Dengue is prevalent in tropical and subtropical regions worldwide, particularly in urban and semi-urban areas.
- Incidence: The incidence of dengue has grown dramatically around the world in recent decades. According to the World Health Organization (WHO), approximately half of the world's population is now at risk.
- Outbreaks: Dengue outbreaks are common in regions such as Southeast Asia, the Western Pacific, the Americas, Africa, and the Eastern Mediterranean.
Challenges and Research
- Vaccine Development: Ongoing research aims to develop more effective and broadly protective vaccines.
- Antiviral Drugs: Efforts are being made to discover and develop antiviral drugs specifically targeting dengue virus.
- Vector Control Innovations: New strategies are being explored, such as Wolbachia-infected mosquitoes which reduce mosquito populations and their ability to transmit dengue.
Conclusion
Dengue is a significant global health issue with a complex interplay of factors influencing its transmission and severity. Effective management and control require a multi-faceted approach involving public health measures, medical treatment, and ongoing research to develop better preventive and therapeutic tools.
Exposing dengue’s invasion strategies
Stowers scientists uncover fundamental rules for how dengue virus infects its mosquito and human hosts, providing hope for identifying therapeutic approaches
Mosquito-borne viral infections once confined to tropical regions are spreading. Dengue virus infects up to 400 million people worldwide each year according to World Health Organization estimates, and no available treatments exist for this disease. Now, research from the Stowers Institute for Medical Research has uncovered surprising strategies for how dengue and hundreds of other viruses replicate in their hosts, with the potential to aid in developing novel antiviral treatments and vaccines.
Led by Stowers Predoctoral Researcher Luciana Castellano in the lab of Associate Investigator Ariel Bazzini, Ph.D., the study, published in Molecular Systems Biology on July 22, 2024, revealed that the dengue virus genome uses less efficient codons, or “vocabulary,” to make its own proteins using the host’s machinery to replicate, and spread. A codon is a sequence of three nucleotides, or “words” in the genetic code that help make proteins. The researchers found that hundreds of other viruses also use “words” in their genetic code that are less efficient in their mosquito and human hosts.
Now that we know what dengue and other viruses use when they infect our cells, we have clues for how we may be able to help prevent these deadly diseases.
Dr. Ariel A Bazzini, lead author
Stowers Institute for Medical Research
Kansas City, MO, USA.
During infection, host cells and viral invaders are at war. Like building weapons, both viruses and cells need to build proteins to fight and defend themselves.
Luciana A Castellano, first author
Stowers Institute for Medical Research
Kansas City, MO, USA.
Dengue virus needs the proteins encoded in its single-stranded RNA genome to propagate, but the virus can’t produce them on its own. The virus must use the host cell’s protein production machinery, so the researchers hypothesized that dengue virus would use codons or “vocabulary” similar to that of mosquitos and humans.
The genetic code is universal for all living organisms and contains 64 codons, the three-nucleotide ‘words’ of RNA, that specify the amino acids that make up proteins.
Dr. Ariel A Bazzini.
The nature of the genetic code allows for more than one codon to specify the same amino acid. Functioning like synonyms in language, codons that specify the same amino acid are called synonymous codons.
But just as each synonym is a distinct word, each synonymous codon has individual properties that can impact a cell’s efficiency for manufacturing proteins as well as the stability of RNA. In addition, a particular synonymous codon can be efficient and optimal in one species but inefficient and nonoptimal in another. This concept is called codon optimality. The Bazzini Lab studies the codon optimality code in humans and other vertebrates, and in this study, the researchers identified for the first time that the mosquito genome also follows its own optimality code.
The researchers found that dengue virus tends to use synonymous codons that are deemed less optimal in their mosquito and human hosts, contrary to their original prediction.
We were surprised to find that dengue virus preferentially uses the host’s less efficient codons, possibly as a strategy to evade an antiviral response by the host.
Luciana A Castellano.
Viruses accumulate mutations during infection of their hosts. We were surprised to find that mutations in the dengue virus genome toward these less efficient codons increased dengue virus fitness in both mosquito and human cells.
Ryan McNamara, co-author
Bioinformatics Analyst in the Bazzini Lab Stowers Institute for Medical Research
Kansas City, MO, USA.
The team analyzed hundreds of other human-infecting viruses and found that many of them, including HIV and SARS-CoV-2, preferentially use less efficient codons relative to humans, suggesting they have evolved an “inefficient” genome as a strategy to use host cell resources in a way that benefits the virus. The conserved preference among viruses has implications to understand not only how viruses evolve but also how the host-pathogen relationship changes over time.
Fundamentally, this work has altered how we think about the relationship between a virus and a host cell.
Dr. Ariel A Bazzini.
In the future, we hope to better understand the mechanism by which viruses are benefitting from using these inefficient codons, and which molecules viruses may be manipulating to gain control.
Luciana A Castellano.
The Centers for Disease Control and Prevention reported that cases of dengue have doubled since just last year in the Americas, and warn of an increased risk of infection in the U.S.
As mosquitos are spreading to broader, more global regions, we need to start thinking very seriously for how to combat dengue and other mosquito-borne viral infections.
Dr. Ariel A Bazzini.
Additional authors include Horacio Pallarés, Ph.D., from the Stowers Institute; Andrea Gamarnik, Ph.D., from Fundación Instituto Leloir-CONICET, Argentina; and Diego Alvarez, Ph.D., from Universidad Nacional de San Martín-CONICET, Argentina.
This work was funded by the National Institute of General Medical Sciences of the National Institutes of Health (NIH) (award: R01GM136849), the NIH Office of the Director (award: R21OD034161), the PEW Innovation Fund award, and institutional support from the Stowers Institute for Medical Research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
AbstractIt really is time creationists stopped trying to blame something else for these nasty little parasites and gave full credit to the brilliant malevolence of their divine pestilential sadist of a god.
Codon optimality refers to the effect that codon composition has on messenger RNA (mRNA) stability and translation level and implies that synonymous codons are not silent from a regulatory point of view. Here, we investigated the adaptation of virus genomes to the host optimality code using mosquito-borne dengue virus (DENV) as a model. We demonstrated that codon optimality exists in mosquito cells and showed that DENV preferentially uses nonoptimal (destabilizing) codons and avoids codons that are defined as optimal (stabilizing) in either human or mosquito cells. Human genes enriched in the codons preferentially and frequently used by DENV are upregulated during infection, and so is the tRNA decoding the nonoptimal and DENV preferentially used codon for arginine. We found that adaptation during single-host passaging in human or mosquito cells results in the selection of synonymous mutations towards DENV’s preferred nonoptimal codons that increase virus fitness. Finally, our analyses revealed that hundreds of viruses preferentially use nonoptimal codons, with those infecting a single host displaying an even stronger bias, suggesting that host–pathogen interaction shapes virus-synonymous codon choice.
SynopsisIntroduction
Analyses of viral genome adaptation to the host optimality code, reveal that hundreds of human-infecting viruses preferentially use non-optimal codons and suggest that host-pathogen interactions can shape virus synonymous codon choice.
- Dengue virus (DENV) preferentially uses non-optimal codons and avoids codons that are defined as optimal in either human or mosquito cells.
- Codon optimality mechanism exists in mosquito cells.
- Human genes enriched in the codons preferentially and frequently used by DENV are up-regulated during DENV infection, as well as tRNAs decoding the non-optimal codon that DENV preferentially uses.
- Hundreds of human-infecting viruses preferentially use non-optimal codons suggesting that host-pathogen interaction shapes virus synonymous codon choice.
Dengue is the most prevalent mosquito-borne viral disease in the world, causing an estimated 390 million infections each year (Bhatt et al, 2013). This disease is caused by four (DENV1-4) distinct but genetically related serotypes. DENV is a single-stranded positive-sense RNA virus that is transmitted to humans by infected Aedes species (Ae. Aegypti or Ae. Albopictus) mosquitoes (Henchal and Putnak, 1990). Besides the strict dependence on the host translation machinery to synthesize their protein components, RNA viruses display compact genomes with a limited coding capacity and have evolved to adapt the host cell translation resources (Ahlquist, 2006). Beyond the amino acid composition of viral coding sequences, selective pressures acting on virus genomes determine their particular nucleotide composition (Fros et al, 2021; Kustin and Stern, 2021.1; Sexton and Ebel, 2019). On the one hand, the presence of cis-acting regulatory sequence and structural motifs often pose a constraint to mutation as changes in these elements can be detrimental or even deleterious (Fros et al, 2021; Gumpper et al, 2019.1; Sexton and Ebel, 2019). On the other hand, as the redundancy of the genetic code allows most amino acids to be specified by more than one synonymous codon, selection leads to various forms of compositional bias in viral genomes, including nucleotide bias (Balzarini et al, 2001; Berkhout et al, 2002; Jenkins et al, 2001.1; Kapoor et al, 2010; Lobo et al, 2009; Muller and Bonhoeffer, 2005; Shackelton et al, 2006.1; van der Kuyl and Berkhout, 2012; van Hemert and Berkhout, 2016; van Hemert et al, 2007), codon bias (Adams and Antoniw, 2004; Bahir et al, 2009.1; Belalov and Lukashev, 2013.1; Berkhout et al, 2002; Bouquet et al, 2012.1; Butt et al, 2014; Cai et al, 2009.2; Chen, 2013.2; Fu, 2010.1; He et al, 2017; Jenkins and Holmes, 2003; Jenkins et al, 2001.1; Kumar et al, 2016.1; Li et al, 2012.2; Liu et al, 2010.2; Nougairede et al, 2013.3; Plotkin and Dushoff, 2003.1; Tao et al, 2009.3; van Hemert et al, 2007; Wong et al, 2010.3; Zhao et al, 2003.2; Zhong et al, 2007.1), dinucleotide bias (Antzin-Anduetza et al, 2017.1; Atkinson et al, 2014.1; Di Giallonardo et al, 2017.2; Gaunt et al, 2016.2; Kunec and Osterrieder, 2016.3; Shackelton et al, 2006.1; Simmonds et al, 2015; Tao et al, 2009.3; Tulloch et al, 2014.2; Upadhyay et al, 2014.3; Washenberger et al, 2007.2; Witteveldt et al, 2016.4) and codon pair bias (Coleman et al, 2008; Gao et al, 2015.1; Le Nouen et al, 2014.4; Leifer et al, 2011; Li et al, 2018; Martrus et al, 2013.4; Mueller et al, 2010.4; Ni et al, 2014.5; Wang et al, 2015.2; Yang et al, 2013.5) that are often related to host tropism. For example, CpG dinucleotides were shown to be underrepresented in vertebrate viruses, while invertebrate viruses lack this CpG suppression (Gaunt and Digard, 2022; Simmonds et al, 2015; Simmonds et al, 2013.6). While many studies have proposed the idea that codon bias in viral genomes may be selected as a strategy for regulating the translation of viral proteins (Bahir et al, 2009.1; Belalov and Lukashev, 2013.1; Berkhout et al, 2002; Chen, 2013.2; Cristina et al, 2015.3; Jenkins and Holmes, 2003; Jenkins et al, 2001.1; Li et al, 2012.2; Moratorio et al, 2013.8; Tao et al, 2009.3; van Hemert and Berkhout, 2016; van Weringh et al, 2011.1; Wong et al, 2010.3), it has also been proposed that viral codon bias is dictated primarily by the nucleotide composition of the viral RNA genome (Atkinson et al, 2014.1; Burns et al, 2009.4; Kunec and Osterrieder, 2016.3; Moura et al, 2007.3; Tulloch et al, 2014.2; van Hemert et al, 2016.5). Untangling these conflicting drivers of evolution has remained challenging (Gaunt and Digard, 2022; Gumpper et al, 2019.1). For instance, the DENV genome has been subjected to various evolutionary constraints and selective pressures, as shown by the presence of evolutionary conserved cis-acting regulatory motifs and adaptation to the divergent dinucleotide and codon frequencies, along with codon pair preferences exhibited by genes encoding proteins in humans and mosquitoes (Chin et al, 2023; de Borba et al, 2015.4). Synonymous variations were shown to critically influence the viral life cycle (Chin et al, 2023; Martinez et al, 2016.6). In this sense, vaccines were generated by viral attenuation due to synonymous mutations, illustrating that synonymous mutation are not silent from the regulatory point of view (Broadbent et al, 2016.7; Coleman et al, 2008; Fan et al, 2015.5; Goncalves-Carneiro and Bieniasz, 2021.2; Le Nouen et al, 2014.4; Mueller et al, 2010.4; Nogales et al, 2014.6; Shen et al, 2015.6; Wang et al, 2015.2; Yang et al, 2013.5).
Synonymous codon can also influence protein abundance across species by a post-transcriptional mechanism known as codon optimality (Bazzini et al, 2016.8; Boel et al, 2016; Burow et al, 2018.1; Forrest et al, 2020; Medina-Munoz et al, 2021.3; Mishima and Tomari, 2016.9; Narula et al, 2019.2; Presnyak et al, 2015.7; Richter and Coller, 2015.8; Wu and Bazzini, 2018.2; Wu and Bazzini, 2023; Wu et al, 2019.3). “Codon optimality” is the mechanism by which mRNA translation affects mRNA stability and translation efficiency in codon-dependent manner (Bazzini et al, 2016.8; Presnyak et al, 2015.7; Wu et al, 2019.3). Codons that enhance mRNA stability are defined as “optimal codons”, while “nonoptimal” codons have the opposite effect (Wu et al, 2019.3) (Fig. EV1A). Thus, mRNAs enriched in optimal codons tend to be more stable and more efficiently translated than mRNAs enriched in nonoptimal codons (Bazzini et al, 2016.8; Presnyak et al, 2015.7; Wu et al, 2019.3). While the molecular mechanisms involved in codon optimality remain poorly characterized, optimal codons are associated with higher levels of tRNA and higher charged to uncharged tRNA ratios (Bazzini et al, 2016.8; Despic and Neugebauer, 2018.3; Frumkin et al, 2018.4; Presnyak et al, 2015.7; Rak et al, 2018.5; Richter and Coller, 2015.8; Wu et al, 2019.3). Unlike codon usage, which refers to the frequency of each codon in a given transcriptome, “codon optimality” refers to the effects that specific codons have on mRNA stability and translation efficiency (Hanson and Coller, 2018.6). Frequently, these two terms are employed interchangeably, however codon usage and optimality do not exhibit a strong correlation in vertebrates (Bazzini et al, 2016.8; Wu et al, 2019.3). For example, the codon GAA is one of the most frequently used codons in human cells but it is nonoptimal (Wu et al, 2019.3). While it has been previously shown that vertebrate viruses exhibit codon bias that does not mimic their hosts usage (Castells et al, 2017.3; Chen et al, 2020.1; Cristina et al, 2015.3; Moratorio et al, 2013.8; Simon et al, 2021.4), the relationship between viral codon preference and host codon optimality remains unexplored.
Here, we demonstrated that codon optimality exists in mosquito cells and defined its codon optimality code to address DENV codon preference relative to both human and mosquito host codon optimality codes. We also investigated whether host gene expression, including tRNA abundance, changes in a codon-dependent manner upon DENV infection and whether selective pressures act on virus-synonymous codon choice. This work revealed that DENV and many other viruses preferentially use nonoptimal codons compared to their host which has important implications for understanding host–pathogen interactions.
Figure EV1. Dengue virus serotypes preferentially use nonoptimal codons relative to human.
(A) Heatmap showing human CSC. Optimal codons highlighted in red, nonoptimal codons highlighted in blue. Scale bar indicated. (B) Scatterplot showing the RSCU fold change (relative to human) for DENV1, DENV3 and DENV4 and human codon stability coefficient (CSC). R = −0.31, P = 0.016 for DENV1, R = −0.28, P = 0.034 for DENV3, R = −0.26, P = 0.047 for DENV4. Spearman rank correlation. (C) Scatterplot showing the RSCU fold change (relative to human) for DENV2 3’UTR in the three frames and human codon stability coefficient (CSC). Spearman correlation coefficients and p values indicated, Spearman rank correlation. (D) Matrix showing the four DENV serotypes’ (DENV1–4) similarity. Lower triangle indicates amino acid similarity, upper triangle indicates nucleotide similarity.
Castellano, Luciana A; McNamara, Ryan J; Pallarés, Horacio M; Gamarnik, Andrea V; Alvarez, Diego E; Bazzini, Ariel A
Dengue virus preferentially uses human and mosquito non-optimal codons Molecular Systems Biology (2024) 1-24; DOI: 10.1038/s44320-024-00052-7
Copyright: © 2024 The authors.
Published by EMBO Press. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Of course, they could really absolve it of any blame in a much more rational way, by accepting that these things are the result of a natural, mindless evolutionary process with no gods involved, but for some reason they can't do that without the risk of being ostracized and vilified by other creationists.
The Unintelligent Designer: Refuting The Intelligent Design Hoax
ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.
Available in Hardcover, Paperback or ebook for Kindle
The Malevolent Designer: Why Nature's God is Not Good
This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.
Illustrated by Catherine Webber-Hounslow.
Available in Hardcover, Paperback or ebook for Kindle
Illustrated by Catherine Webber-Hounslow.
Dengue fever by mosquitoes is one of the more horrific diseases in the world. It takes an evil genius or a Devilish mind to create such a cruel disease. This is a prime example out of countless examples within Nature that illustrates there cannot be an omnibenevolent, omniscient, omnipotent, loving, merciful creator God.
ReplyDeleteMy poor father suffered an episode of Dengue fever a long time ago when he was young. He later on suffered from other serious health issues. Creationists invoke the usual execuse of The Fall or Original Sin of Adam and Eve. They just blame everything on Adam and Eve, which is unrealistic, unscientific, unhistorical, unfair, unjust, unkind, unreasoning, unforgiving. It's fake science, fake history, fake reality which is preached by Kent Hovind and Ken Ham and its believed by ignorant people who don't know any better. Or the blame for Natural evil is thrown on Satan and demons which is the view of Gregory Boyd. But where is the evidence for this?
I often write as anonymous and also as Moral Man. Thank you for reading. Keep up the good work.