July 24, 2020 | David F. Coppedge

Plagues Can Arise Quickly Without Evolution

Smallpox and mosquitoes illustrate how diseases can arise quickly and spread through human populations.

This year, or late in 2019, a virus jumped from an animal host (probably a bat) to humans, and within months, the world is suffering the consequences of SARS-CoV-2. Is this an example of “evolution”? We can see from two other plagues reported in science news this week that pathogenicity can arise quickly by gene inactivation or opportunism – not evolution.


Anopheles mosquito gorged with human blood. (PD)

How mosquitoes got their taste for human blood and what it means for the future (Science Daily). Mosquitos are such iconic pests, it may be hard to believe that of the more than 3,000 species known, very few have acquired a taste for human blood. Malaria is spread by a species of Anopheles mosquito. Some other human-biters around the world, while not deadly to humans and mammals, cause itchy rashes. Most species ignore us. A new study reported in Current Biology cannot say for sure when the vector species Aedes aegypti started biting humans:

People tend to think of all mosquitoes as major pests to people. But, in fact, the researchers explain, mosquitoes are quite diverse. Some of them won’t bite humans at all. Only a few species specialize in biting people. In the new study, the researchers focused their attention on Aedes aegypti, the primary spreader of dengue, Zika, yellow fever, and Chikungunya virus.

Researchers Carolyn McBride and Noah Rose from Princeton University gathered Aedes aegypti mosquito eggs from 27 sites around sub-Saharan Africa and tested to see which ones were attracted to human odor. The results were not straightforward; the best theory they came up with is that the taste for human blood arose in this species in urban areas or places with long dry seasons; otherwise, they would have used available water for rearing their young. That pattern does not match Anopheles, however. New Scientist implies that the taste was acquired just thousands of years ago, not millions.

A long dry season is a problem for A. aegypti, says Rose, because these mosquitoes depend on standing water to rear their young. But humans often create sources of standing water, whether by storing rainwater in barrels or by irrigating crop fields. Mosquitoes that lived thousands of years ago may have been drawn to these places and thus evolved to bite humans.

The story may well be different for Anopheles mosquitoes, which spread malaria, says Rose. These mosquitoes are only distantly related to A. aegypti and have a different life cycle. “The adults can go into a state called aestivation, where they dry out through the dry season,” says Rose.

The Princeton team is also unsure which genes changed to “evolve” a taste for human blood; Science Daily concludes its coverage with unfinished business: “They’d also like to understand why mosquitoes specialize on certain hosts to begin with and which specific genes and genetic changes are most important.” It seems possible that mosquitoes’ biting equipment served other purposes—perhaps sawing into plants and sucking out the juice—but worked just as well on human or animal skin. If that took less energy, it would make sense that genes might be down-regulated in the process. Existing sensory organs intended to detect plant hosts could be switched to follow carbon dioxide from mammal breath instead of volatile compounds from plants.

A summary of the research in Nature says, “Their genetic analysis suggests that the taste for humans evolved just once.” This should strike evolutionists as surprising, since they assume flying insects evolved hundreds of millions of years before mammals and birds arrived on the scene. How did they get by without blood before blood evolved? Another unanswered question is how the mosquito is unharmed by viruses and bacteria in its body that cause disease in mammals.

The point is that the jump to human blood could have been recent and involved horizontal changes to existing equipment in the mosquito – not the evolution of some innovative apparatus and genetic information.


One of the deadliest plagues in history has been smallpox. The last two remaining samples of smallpox virus are kept in secure facilities for research before they are scheduled to be destroyed. If they got out, the world could quickly suffer a devastating pandemic before vaccination could catch up. In a Perspective piece in Science Magazine today (July 23), Antonio Alcami tells what is known about the origin of this deadly pathogen.

Was smallpox a widespread mild disease? (Science Magazine). Surprisingly, smallpox might have started as a rather mild virus not that long ago.

Smallpox—caused by variola virus (VARV), a poxvirus—was one of the most virulent diseases known to humans, killing up to 30% of infected individuals and 300 million to 500 million people in the 20th century. The year 2020 commemorates the 40th anniversary of smallpox eradication, the first human disease eradicated after a global vaccination campaign led by the World Health Organization (WHO). The last samples of VARV are kept in two high-security laboratories pending destruction, and fears about reemergence or deliberate release of VARV have not subsided. Smallpox eradication is one of the most successful stories of public health, but the origin of the deadly virus remains an enigma. On page 391 of this issue, Mühlemann et al. (2) report the identification of VARV in archaeological remains from the Viking Age (600 to 1050 CE) that reveals new information about the origin of VARV and its evolution in human populations.

Scientists are not agreed on where smallpox came from. “The current hypothesis,” Alcami continues, “is that thousands of years ago, a variola-like virus ancestor from Africa was transmitted from rodents, which are common reservoirs of poxviruses, to humans, in which it evolved to become VARV.” But again, the “evolution” may not have been from acquisition of some new innovative genetic information, but from downregulation of existing genes.

A notable feature of all modern VARV genomes is the inactivation (deletion, truncation, or mutation) of 29 genes involved in host immune evasion and in infection of a wider host range. Deletion of all these genes in VARV major and minor strains suggests that they were not required for human infection.

Alcami notes that the ancestor of the current smallpox virus could have been better equipped genetically:

Virulent poxviruses are believed to have evolved from a common ancestor encoding the full collection of about 200 genes, likely similar to cowpox virus, which causes limited pathology and infects a broad range of species. The concept that the loss of immune evasion genes may increase virulence is counterintuitive, but it illustrates that much of the damage caused by viruses is due to excessive host immune responses. For example, poxvirus-encoded cytokine decoy receptors may dampen the cytokine storm that would otherwise cause pathology.

This implies that smallpox is actually less evolved – i.e., devolved – from the common ancestor. Even as recently as the Viking era in medieval Europe, it had not yet reached the deadly form.

Once VARV was established in humans, the findings of Mühlemann et al. suggest that the inactivation of genes occurred gradually over the centuries, leading to the generation of a highly virulent, human-specific modern VARV that caused smallpox. Notably, different virus clades (subtypes) coexisted, and the ancient VARV sequenced from Viking corpses corresponds to an extinct clade of VARV.

It would not make sense for a virus to drive itself extinct by killing all its hosts. Consequently, a virus may lose virulence as it adjusts to co-exist with its host, and the host immune system becomes aware of it, as may be happening with the current SARS-CoV-2 virus.

Poxviruses do not establish persistent infections and individuals recovered from infection develop lifelong protective immunity, so poxviruses are forced to constantly infect naïve individuals. The observed pattern of gene inactivation may have conferred to VARV a more efficient transmission and replication capacity, but perhaps the virus became extremely virulent. Maybe this drove the evolution of the modern VARV clade that caused the devastating smallpox epidemics, whereas less aggressive and less transmissible, low-pathogenic ancient VARV clades became extinct.

Viruses, as Bergman reported in CEH earlier (2 April 2020), serve many beneficial functions. There is a complex interplay between a virus and the immune system of its host. When some existing genes get down-regulated, such that the virus has free rein in the host for awhile, rampant disease can occur.

The origin of natural evil is certainly a difficult question, but it is even more difficult for the evolutionist. Natural evil, in their thinking, is not evil at all; it is survival of the fittest, and the germ must be the fittest if it kills the human patient. And as this article points out, evolutionists have serious questions of their own: How did germs exist before their hosts evolved? If modern humans existed up to 3 million years ago, and their hominid ancestors even before that, why are we still vulnerable to viruses now in 2020?

The Biblical story tells of a perfect creation and a balanced ecology. When sin entered the world (just thousands of years ago, not millions), creation was cursed with pain, sweat and death. The curses could have involved not so much the creation of evil things, but the relaxing of controls on perfect things such that errors and modifications wreaked havoc on the original perfect order. In a sense, God took his “hands off” the creation to some degree and let bad things happen, rather than causing bad things to happen. Genes, instead of being repaired perfectly each time, could be subject to mutations that caused aging and health issues, which accumulated over thousands of years. Opportunism would result, as each member of an ecosystem is left to downgrade to new relationships with its neighbors in order to survive. Thorns, as modified leaves, might prevent opportunistic predators from eating everything.

Sanford’s book examines the impact of mutations that are invisible to selection.

John Sanford’s book Genetic Entropy shows why the human genome could not be millions of years old, due to the growing mutational load (about 100 new mutations each generation). These are only partially offset by modern medicine. While natural evil is a difficult problem in philosophy and theology, what we observe fits with a recent creation that started perfect and has degraded over time. We’re seeing it now with a zoonotic virus that quickly became a global problem not millions of years ago, but within months; a new equilibrium would probably render it harmless in short order once “herd immunity” is reached by the immune systems of the population. Since that would take a higher death toll, human intelligence is applying its cumulative knowledge of genetics and microbiology to beat it sooner with vaccines that can share that immunity instantly, as well as alleviate suffering with well-designed therapeutics.


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