ISATIS (Isatis indigotica Fortune) Family: Brassicaceae, formerly Cruciferae A STORY OF VIRUSES by Linda Hall

There is potency in the anti-viral mechanisms found in the herb Isatis indigotica fort, offering us no small amount of reassurance at a time when humans have discovered all over again the terror of a plague. Learning this herb’s usefulness and proper handling, Isatis may help dull somewhat the sharp edge of our fear of viruses, giving us something with healing potential to turn to in times of infection. 
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“It serves little purpose merely to be scared by viruses.  But it serves a good deal of purpose to understand them.”
The subject of viruses may only hold allure for those invested in the study of their origin, evolution, and behavior; for the rest of us, the recent eye-opening, forced intimacy with a viral plague would have us turning a blind eye and a deaf ear to the academics of viruses, even as Covid-19 continues to spin off new spikey versions of itself.  We don’t have to want to be virologists, yet coming to terms with viruses, especially at a time in human history when viral pandemics may begin to occur with frequency, would be not only prudent but empowering, offering an understanding of viral conduct as well as insight into the astonishing role evidenced by some viruses in acts of creation and benefit within the human genome.
Elegantly trim, being not much more than mere pieces of RNA or DNA inside a protein coat that is sometimes enveloped in a lipid membrane, some scientists are certain viruses are not alive.  Lacking the complete set of tools to sustain life, much less reproduce, viruses are obligate parasites.  Their only opportunity to reach into the future is by hitching rides on other living organisms and worming their way inside where they take over their host’s cellular genetic equipment to make copies of themselves.  Although their particularly persuasive infectious power is recognized (viruses have been caricatured as “bad news wrapped in protein”), still some have placed viruses, at best, on the fence between being naught but chemicals on the one side or a fully alive force on the other; yet those of us who’ve ever been knocked flat on our backs by a flu may not be harboring any doubts about on which side of the fence viruses fall. 
However, if we believe life happens when a collection of non-living things finally interacts at a level of critical complexity; if life is a process of emergence, coming into view only when non-living things have self-organized in a fashion that expresses life’s properties, then we may say, viruses as bits of genetic stuff lack the complexity to certify as living things, and further, being the genetic stuff that builds genomes, viruses themselves can’t be alive.  But neither are they inert; they move bearing influence.  Perhaps, then, viruses’ verge on life, helping to shape life’s quality of emergence.
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Regardless, viruses have, over a period of roughly 3.6 billion years, managed to hammer out extremely sophisticated and successful ways of surviving and replicating, yielding them notable access to areas of highly selective inhabitability:  blazing hot deserts, the deepest, darkest sea floors, the earth’s frozen poles.  They are fiercely durable; even when swept sky-high by dust storms, viruses swim in the atmosphere until, raining down by the millions, they return to earth, and not from whence they came.  Viruses are everywhere, some saying there are more of them than stars in the heavens.  
Staggeringly incomprehensible numbers of viruses inhabit our planet.  Viruses for millennia have sought their host organisms, moving in and out of a world of living things, making it quite likely that most of earth’s genetic information dwells within them.  As Stephen Buhner writes in his book Herbal Antivirals:
“Viruses enter cells, snip off sections of DNA or RNA and weave them into their own genetic structure.  They can then weave those sections, as well as sections of their own genome, into other living organisms.  One of their main functions in fact is the genetic intermingling of all life forms on earth.  Our genome, as that of all life on this planet, contains snippets of the genetic codes of multiple other life forms.  It also contains snippets of viral genes.  Our forms, our shape, are an expression of a communication that has been ongoing since life has been.  We are the enemy we have been fighting.”
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Retroviruses are a type of enveloped RNA virus known to only infect vertebrates, those animals having a spine:  a column made of segmented bone (vertebrae) that encircles and protects a spinal cord.  Appearing on the evolutionary scene 460 million to 550 million years ago, it’s likely that retroviruses originated in the earth’s ancient seas alongside the vertebrates. As a result of following their vertebral hosts out of water and onto land, retroviruses today reveal broad representation in all life forms having a backbone, and that includes us.
Thus, half a billion years ago, vertebrates had to begin developing measures to combat retroviruses just as the retroviruses had to undertake the disarming of those measures. Those early interactions appear to correspond with the origin of vertebrate adaptive immunity, speaking to the very real possibility that those long-ago virus-host interchanges assisted in the development of vertebrate anti-viral defense.
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Once inside its vertebrate host, a retrovirus locates its target cell and integrates (injects) its genes into that cell’s DNA, uniting both genomes. Unique among viruses, it’s the necessary mixing of the two genomes that sets the retrovirus apart, for only through such union can it drive the process of infection and secure its continuing survival.  In Virolution, author Frank Ryan writes about retroviruses:
“Every day, in the vast proliferation of virus-host interactions that are taking place throughout the biological world, wholly disparate genomes are fusing, virus with host.”
Although retroviruses are singularly obligated to unite their genome with their host genome to reproduce, evidence of incidental union of virus/host genomes by diverse other virus types has been found.  Interestingly, controversy swirls around the possibility of Covid-19, another type of enveloped RNA virus, inserting its RNA into human DNA.  Proof of this, however, remains elusive.

  ​Author Frank Ryan continues:
“The normal ecology of a virus is the host genome and its immediate hinterland, the chromosomes, with their component genes, and the translational machinery that enables the genes to code for proteins, and the vast complexity of the bureaucratic apparatus.  We might note in passing that this is a remarkable situation – viruses are the only organisms small enough, and primal enough, to inhabit the genetic landscape.  It is one of the reasons why viruses, despite their miniscule size, are immensely powerful from the evolutionary and infectious point of view.”
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Owing to inefficient transmission from vertebrate to vertebrate in the wild, a retrovirus has had to guarantee its evolution in the earth’s natural settings by establishing within its host a persistent, life-long infection with little, if any, pathogenic effect, thus allowing the host to live long enough to transmit it.  A stable ecosystem where enduring low-grade infection circulates among its members, reflecting deeply rooted compatibility between retrovirus and host, warns, however, of intrusion and cross-species contamination.  Humans, for instance, straying into long-abiding ecosystems with intent to clear land or hunt the meat of wild animals, can contract from circulating infection, what is for them, a novel virus.  Where no compensatory balance exists between the infecting actions of a virus and its host’s immune mechanisms, a virus free to replicate can pose harmful, if not deadly, effects.  An example of this is when the HIV-1 retrovirus crossed species to humans, its emergence among us thought to result from human handling of the meat of primates.  
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In the human body, most of the retrovirus/host genome fusions occur within the soma (parts of the body other than the reproductive cells); fusions occurring at the germ line level (within an egg cell or a sperm cell) result in the virus sacrificing freedom of movement to become a fixed component of our reproductive nuclear machinery.  No longer able to proceed with its original intent to replicate and infect, it has instead secured a survival lasting the length of all our future generations. Inheritable and now nearly immortal, permanently embedded amongst our own genes, it has acquired formidable potential to influence our species’ evolution.  Now, rather than an obligatory parasite, the retrovirus is a symbiont, a participant in a mutualistic interaction whereby virus and host gain benefit from their relationship.

To begin to understand the significance of this, it’s important to note that stretches of retroviral genetic sequences comprising over 500,000 individual elements left over from multiple, highly contagious, pandemic-producing ancient retroviruses that ultimately integrated the germ line of our ancestors, make up 8% to 10% of the human genome.  (Also, important to note is that we modern humans are descended from those who managed to survive such viral onslaught). These genetic sequences, sitting firmly within our genome at the convergence point of foreign genes and the self’s genes, have been conserved over vast passages of time.  Finding accommodation, they’ve trotted right along beside us during our species’ development.  Once thought to be “fossilized” and inert, they bear varying degrees of influence; they’ve been acted upon by natural selection as has our own genetic material. As a result, some of them have eroded over time and may have little, if any, function left; some remain only partly intact; and some are dormant with potential for reactivation.
Still other of these ancient genetic sequences are actively expressed in many different types of human tissue, turning on at many different points in time during our species’ development; and their expression has offered up raw viral genetic material from which our cells have sometimes been able to pick and choose bits and pieces for the shaping of new, highly impactful physiological functions that have further turned us in an improved evolutionary direction.  For example, the ability to securely fuse, undetected by our immune system, with target cells is a viral function that was co-opted millions of years ago and woven into the development of the mammalian placenta, for crucial to the survival of an embryo is a tightly fused placental wall that maintains control over maternal immunosuppression and, ironically, protects against viral infection.  The earliest known ancestor to all placental mammals was a small, chipmunk-like creature that evolved after the mass extinction of the dinosaurs.  It was the germ line invasion of a retrovirus that helped this ancestor give rise to a diverse lineage of placenta-bearing mammals, a lineage that today includes more than 5,000 known species ranging from the tiny bumblebee bat to the huge blue whale. ​

Snuggled into the human genome, retroviral genetic material is softening the boundary between human and virus.  In a very real sense, humans are part of the virus.
Lest we allow this information to overtake us with a thrill, and gladly widen our hearts to these embedded genetic pieces, we require also knowing that they can play upon us in either one of two ways, wielding the classic double-edged sword:  we can credit them with helping to shape our anti-viral immune defense mechanisms as well as awarding us moments of true evolutionary progress; yet,  roaring back to life should we acquire a virus such as Epstein-Barr, herpes, HIV-1, influenza, or Covid-19, they have the potential to create within us  infectious, autoimmune, neurological, or malignant disease.
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Well beyond the scope of this article is the ever-broadening study of the effects of our retroviral heritage.  Shaped impressively as we are by our ability to balance the gain against the loss provided our species by these embedded genetic pieces, the coupling of retrovirus and human has, in the long run, helped generate change, diversity, and a continuing forward movement within both genomes.  Retroviruses and humans have long been partners in a perpetual dance of co-evolution, and the embrace endures.
The what and how of this is in active pursuit by scientists; the answer to why leads us beyond understanding that interspecies gene flow (reference Buhner’s excerpt above) creates a variety of living forms supportive of life’s overall success on this planet; that all sizes, shapes, and colors of earth’s vertebrates continue to be strung together on one endless genetic strand, fashioned into jewels of diversity by tiny, microscopic hands.  Rather, it leads us onto the terrain where epiphanies grow where the seed of understanding blooms into the highest order of judicious appreciation, without which we, as humans, certainly could not continue to evolve, this fact brought home to us by the 8% to 10% of the human genome belonging to retroviruses.
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As many viruses as there are on our planet, we humans are not falling ill with viral infection at every turn, nor are we dying from any infection we do acquire.  Some of our interactions with viral infections are benign; symptoms are manageable and self-limiting (not in need of treatment).  Some infections are acute, occurring suddenly and resolving either in our recovery or our demise (such as the flu, Covid-19, or rabies).  However, viruses have evolved many strategies by which to chronically persist at the level of the individual, the population, or even the species (for example, living the remainder of life with HIV-1/AIDS).  Further, some viruses persist by remaining dormant within us, snoozing for long periods of time before reactivating (herpes, for example). 
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Mammals, birds, and insects are reservoir hosts of large numbers of diverse viruses that exist and multiply freely within them with little or no pathogenicity.  A forbearance of the one for the other has developed, a pause born of equal parts tension, a co-existence where the host has the immune ability to attack the virus; but the virus owns an array of immune evasion techniques to escape killing.  Carried along in an environment of pressurized equanimity, the virus lives, biding its time, attentive to the possibility of transmission.
Bats host rabies, SARS, and Ebola; aquatic birds host influenza A; mosquitoes are reservoirs of dengue, yellow fever, west Nile, and zika; domestic pigs, wild boars, and chickens host Hepatitis E; and rats and mice carry hantavirus disease.  Such viral reservoirs can become sources of prominent disease outbreak and spread, and critical among them is the bat.  Comprising about 22% of known mammal species (about 50% in tropical ecosystems) and, as a noteworthy aside, host to more than 200 novel coronaviruses, the bat’s ability to fly and develop many large and dense social structures across almost every type of habitat; its means of deftly defying the chronic conditions of aging over its long life; and its exceptional ability to host many viruses without presenting any evidence of disease, attest to how easily bats can intersect with other species and enable the transmission of numerous infections.
The great numbers of bats, and the great numbers of viruses they carry, as well as human mammalian relatedness to bats and our encroaching proximity to their wildlife habitats, allow for two likely pathways to human infection a bat virus may take:  direct bat to human contact or contact through an amplifying (intermediate) host when, for instance, a bat virus passes to us through our livestock or a pet.
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Viruses are said to spill over from one species to another when a reservoir host with a high pathogenic load meets with a receptive target.  Such an event, albeit infectious, doesn’t necessarily send the virus careening through the target species, possibly due to the viral source being a species distantly related to the target, where the virus doesn’t bring with it a pre-evolved command of the target’s immune defenses.  Bird flu H5N1 (a type of influenza A) easily transmits between wild and domesticated birds, and those of us in close contact with either may contract it, just as may the caretakers of those fallen ill; otherwise, there seems to be no concrete evidence that this virus can spread unchecked and with little provocation among us.
On the other hand, a virus that makes a species jump has undergone the type of genetic change that makes it not only able to easily infect but also spread well, where the virus is coming from a species biologically like its target. Able to take effortless command of the host immune mechanisms rising against it, the virus moves with swift ease through the target species.
In the case of Covid-19, we met with a novel coronavirus making a species jump; a virus pre-evolved, ready, and able to overtake the human immune system and spread through our species. Although the origin of Covid-19 has yet to be definitively known, bats, as large capacity reservoir hosts of coronaviruses, are high on the list for consideration:  
Bats and humans (both mammals) share a common ancestor, thus biological similarity.
A wet market localizes a large and diverse range of animal species in an environment strange and stressful.  Kept from their normal food sources, retained in cages that ultimately fill and overflow with urine and excrement, and fearful of their captors’ intent, the animals suffer lowered immunity, leaving them wide open to various unfamiliar and unsolicited pathogens circulating in their crowded conditions.  Possibly hosts already to numerous viruses, in wet market animal pathogenic loads elevate and to one degree or another tip the scales in favor of species jumps.  The animal waste and bloody butchering increase the risk already attendant upon human handling.  Inherent in the construct of a wet market, it would seem, is an inhumanity shaped by negligence, profiteering, and possibly an abject unwillingness to look directly in the eye of the beast of a pandemic that waits behind the capture, forced unsanitary imprisonment, and slaughter of these hapless animals.
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Investigative research has documented “47,381 individuals from 38 species, including 31 protected species, sold between May 2017 and November 2019 in China’s Wuhan markets.”  The absence of bats in the survey data points to the fact that bats are not usually eaten in Central China, but trading of animals susceptible to bat coronaviruses is a possible disease link worthy of investigation.
Is it conceivable, then, that Covid-19 jumped species from a bat in China (as reservoir host), to an amplifying host (an animal ultimately captured for sale in a Wuhan wet market), to humans . . . and with wings, took off from there?
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Unfortunately, humans strengthen viral disease outbreak and transmission through a great number of deeply ingrained ways:  population growth, migration from rural land to dense city centers, worldwide travel, expansion of global trade, destructive manipulation of well-established ecosystems, wet markets, crowded domestic animal operations, war, neglect of the impoverished, and through encouragement of climate change, which alters habitats and spreads disease into new geographic areas.
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Albeit uniquely structurally simple, without any of the characteristics we humans deem the necessary descriptors of life, it's a virus’ ability to accurately interpret its surroundings external and internal to its host; its awareness and proper analysis of the host immune weaponry, and its skill at altering itself or that weaponry to dodge host attempts at defense, that seem indications of viral reasoning.  Other indications might include the various means viruses employ for entry into and travel through the host, their pinpointing of the host target cell, and the ways in which that cell is made to submit to viral control.  What underlies all these highly successful maneuvers is keen perception, accurate assessment, agile genetic juggling, and a billion-year-old steady and resolute will to survive.
We may wonder, again, if a virus is truly alive.
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Granted only a few hours or a few days in the outer world, a virus, in a seed-like waiting state on a tabletop or in the soil, on food, or in water or air, actively receives and analyzes information about its external environment.  Should we appear on the scene as an accommodating host, the virus infiltrates us.  Scoping out the design of our immune system, it engages strategies to hide from it.  Succeeding, it searches, under the radar, for the right cell to infect.  Finding its target cell, it engages strategies to deceive the cell’s receptors into allowing its attachment.  Succeeding, docking snugly on the surface of the cell, the virus plants its flag on the moon - espionage, shapeshifting, and trickery having greased the wheels all the way.   
We have yet to feel the virus’ presence.  
Entering the cell either through fusion with the cell membrane (enveloped viruses) or penetration directly into the cell (non-enveloped viruses), the virus topples the established working order, claiming the cell’s ability to replicate for its own purpose.  The coup accomplished, the virus prepares to infect us with its own will to survive and replicate.
We have yet to feel the virus’ presence.
In, established, and rolling out multitudinous copies of itself, populating ever greater numbers of its target cell type, with infection well under way, our immune system is in full metal battle.  Its actions against the virus begin to rise up in the form of uncomfortable symptoms.
Only now do we feel the presence of the virus.
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Prowess forged over literal eons of time, viruses, those bits, and pieces of microscopic genetic stuff, were already on the planet when we arrived, their magician-like master mindedness in full swing.  Today, we see our position in relation to what we know of viruses and our ability to survive them becoming more precarious in the light of their growing pandemic strength, as they relentlessly emerge and re-emerge into our modern times with the ever-increasing sharpness of a brilliant blade of steel, dividing, one from another of us, those who can withstand the pain and those who cannot.

This brings us back to the herb Isatis indigotica Fortune, known also as Isatis Woad.  Its leaf (Da-qing-ye) and its root (Ban-lan-gen) are both used medicinally.
This species of Isatis is indigenous to southeastern Russia and China, and because the herb grows well, re-seeds easily, and has a pronounced desire for conquest, it transplants quite comfortably; and with a will to penetrate far-reaching territories, it easily becomes invasive.  It can grow in your garden, but if not contained, its impetus to exceed its borders will take over.  Just one plant can put out approximately 500 seeds, and every one of them, if freed from its seed pod, will germinate.
This herb’s formidable will to survive speaks to its ableness as a virucidal agent.  Its considerable strength encompasses a wide array of viral diseases. 
ACTIONS:
Directly virucidal:  inhibits viral attachment to and entry into cells; inhibits viral replication.
Promotes effectiveness of the immune system inhibits virus-induced inflammation; decreases production of inflammatory mediators.
Enhances the effectiveness of viral vaccines.
ACTIVE AGAINST:
SARS and all strains of influenza.
Viral pneumonia, respiratory syncytial virus.
Laryngitis, sore throat, tonsillitis.
Rubella, measles, mumps, chicken pox, herpes simplex virus 1, shingles, Epstein-Barr (especially with acute sore throat at onset), hepatitis B, cytomegalovirus.
Encephalitis.
 
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  ​Even though both plant parts can be used medicinally, please note Isatis leaf is the most anti-viral part of the plant.  Isatis Root is also capable of anti-viral action, yet it appears better at modulating the immune system.  By normalizing, calming, immune function, the root sharpens the immune system’s ability to effectively fight inflammation and infection. 
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Dosing Suggestions:
Combine the leaf and the root in one remedy – preferably a cup of tea as most of the plant’s medicine is water soluble.  Adding Ginger Root or Licorice Root and/or honey to the tea improves the taste of Isatis.  (Reminder, this plant is in the Brassicaceae family – home to the cruciferous vegetables).
A potent decoction of the herb is made by boiling one third – one ounce of root for 30 minutes and adding one third - one half ounce of leaf for the last ten minutes of the boil.  Heated in water and drunk as a decoction is the most effective way to utilize Isatis as an anti-viral.  Better used with active infection as opposed to prophylactically, drink one cup of decoction three times a day for no longer than three weeks.  This length of time should be sufficient to bring about recovery, especially if you’ve added other anti-viral herbs to the decoction.
Let yourself be encouraged to combine Isatis with other anti-viral herbs, which will only increase the power within each herb to move you through infection to the safety of recovery.  Consider Chinese Skullcap Root, Elderberry, Ginger Root, and Licorice Root to enhance anti-viral performance and the taste of the decoction.
Safety Considerations:
Avoid using the herb as a single remedy if you present with a feeling of cold and lack a fever.  
Overuse (longer than three weeks) may cause a deep chill.
Overuse (longer than three weeks) can lead to weakness, dizziness, and an odd sensation in the bones.
High doses of the herb, or long-term use of it, may negatively impact kidney function.  Do not use Isatis if you are in renal failure, on dialysis, or suffer any kidney impairment.
The use of Isatis may interfere with tests that measure bilirubin.
Appropriately, if under medical supervision and using any prescription medicine, please discuss the possibility of the use of Isatis, as well as any other herbs you wish to use in tandem with it, with your physician(s).
Sources available upon request.