*
Pepper Mild Mottle Virus, PMMoV, pictured in Wikipedia
*
Part One: Planting Viruses –From Plants! https://jenniferlake.wordpress.com/2021/01/15/planting-viruses-from-plants/
Part Two: Planting Viruses Two https://jenniferlake.wordpress.com/2021/01/21/planting-viruses-two/
*
*
Self-assembling nano machines are not simply “inspired by biology”. They are biology. Biology is Nanotechnology.
The revelation of the present –and the point of Planting Viruses—is to show how plant viruses, derived from the original ‘filtrate’ methods made of diseased specimens from Tobacco Mosaic Virus (TMV), have evolved into the bio-nano-technology of today. On the way, we’ll see how human viruses took the same path and ask a bigger Question based on evidence: Are modern (20th century) “emerging” virus diseases derived from plant viruses? The expanding scope of the virus industry recognizes more and more pathogens infecting a greater range of hosts, phenomena known as species jumping and host-switching, but read almost any biology research document from a lab of the modern era and you can observe the species-jumping-host-switching activity for yourself by human intervention. Laboratory science in biological ‘evolution’ is not just a practice of learning methods but a goal in itself with a very long technology-dependent history.
The field of virology is looking for “common ancestors” to prove evolutionary lineage but the ancestors I’m postulating are not viruses at all. We know their names, like Wendell Stanley, Hilary Koprowski, Aaron Klug, Craig Venter, etc. etc. Their names include mathematicians and physicists as well as contemporary software designers and gamers. (–the learning game ‘Plague, Inc.’, for example)
Do viruses evolve? –well, that’s a trick question. Viruses and their stuff can disassemble and reassemble, inside or outside of host cell environments. Viruses, like poliovirus, have been made from scratch with laboratory chemicals and formulas but then so has human DNA.
Entire living organisms such as E.coli bacteria have been made from scratch in labs. This puts the trick in evolution. Nature does have some ‘keepers’ among the genetic fragments and “virus-like particles” spread over the earth, and those are called “conserved regions” in protein language. Conserved regions, which are small and dispersed orderly segments of proteins, show up along the replicated strings of genetic material in reproducing entities. They may or may not be evidence of evolution, but for the time being, evidence of identity and ‘targets’ for gene testing. PCR tests, for example, are designed to target and “amplify” conserved regions in genetic specimens. In effect, PCR is a factory for making those certain ‘codes’ of interest and the reason you can stop wondering why a COVID PCR test is not a ‘heath’ test.
*
Covid testing is switching to sewerage anyway –despite the ‘social benefits’ of maintaining individual testing –and we’ll look at the sewerage situation with plant viruses. Vaccines made from fecal matter extracts –as it appears all the older vaccines were—injected plant virus particles directly into the bloodstream. It prompts another set of questions about CoV positive tests: if COVID positivity is the outcome of prior vaccination for polio. They have the same ancestors. Poliovirus likeness to plant virus is demonstrated in Part Two.
*
Part Three is going to focus on plant viruses infecting humans directly, without the need for an intermediate vector, like insects and vertebrates. It will also describe the peculiar differences between “infection” and “infectious” as it’s used in the literature, therefore determining a qualitative interpretation of “safety” as “non-infectious”, and I’ll apply that to TMV-derived nano-products. And, my favorite part –Pictures!—micrographs and progressive comparisons of “real” plant viruses, and some comparisons to “fake virus” images like the “clathrin-coated vesicels” pictured in Part One.
Here’s the Worksheet first (with clips from ‘search)
*
“Humans have antibodies against a plant virus: evidence from tobacco mosaic virus”
https://pubmed.ncbi.nlm.nih.gov/23573274/
*************************************************************************************
Can a plant virus make you sick?
29 April 2010
“Pepper mild mottle virus is present worldwide in field-grown peppers. It is composed of an RNA genome wrapped with many copies of a viral protein that forms a rod-like particle with helical symmetry (pictured)… https://www.virology.ws/2010/04/29/can-a-plant-virus-make-you-sick/
*************************************************************************************
Pepper Mild Mottle Virus, a Plant Virus Associated with Specific Immune Responses, Fever, Abdominal Pains, and Pruritus in Humans
*
Conclusions
Our study identified a local source of PMMoV and linked the presence of PMMoV RNA in stool with a specific immune response and clinical symptoms. Although clinical symptoms may be imputable to another cofactor, including spicy food, our data suggest the possibility of a direct or indirect pathogenic role of plant viruses in humans.
… PMMoV is a non-enveloped, rod-shaped, single-stranded positive sense RNA virus classified in the genus Tobamovirus, which includes viruses extremely resistant to physical and chemical agents [8]–[9]. It is one of the major pathogens of Capsicum spp (chili peppers). Complementary data from Zhang et al.‘s study have shown that PMMoV could be detected in non-diarrheic stool from 12 out of 18 individuals living in San Diego, USA or in Singapore, suggesting it might be geographically widespread, and in 3 out of 22 fresh and processed pepper samples. Moreover, the fecal PMMoV was viable and could infect host plants.
…All N. tabacum cultivar Xanthi NN plants inoculated with each of the three PMMoV RNA-positive food products developed local lesions typical of PMMoV infection within 5–7 days post-inoculation (Figures 2a–h)…
…We also identified statistically significant differences in the occurrence of fever, abdominal pains, and pruritus and the detection of specific immune responses to PMMoV in the case-control study. We, therefore, believe that we provide the first evidence that plant viruses may cause disease in humans…
************************************************************************************
*“Pepper mild mottle virus (PMMoV) is a plant pathogenic virus that occurs worldwide on species of field grown bell, hot and ornamental pepper species. It is caused by members of the plant virus genus Tobamovirus- otherwise known as the tobacco mosaic virus family…
The origin of PMMoV has been linked to Tomato mosaic virus, as they both reside in the Tobacco mosaic virus family. The Tunisian Journal of Plant Protection brought about the link between PMMoV to ToMV from a French study dating back to 1964. ToMV affects a wide range of Solanaceous crops and a strain of this virus likely mutated into PMMoV.[3]”
https://m.blog.naver.com/ehongsik60/221532987034
*************************************************************************************
Tobamoviruses can be frequently present in the oropharynx and gut of infants during their first year of life
…”Plant viruses have been reported to be common in the gut of human adults, presumably as result of food ingestion. In this work, we report that plant viruses can also be found frequently in the gut and oropharynx of children during their first year of life, even when they are exclusively breast-fed. Fecal and oropharynx samples were collected monthly, from birth to 1 year of age, from three apparently healthy children in a semi-rural community and analyzed by next generation sequencing. In 100% of the fecal samples and 65% of the oropharynx samples at least one plant virus was identified. Tobamoviruses in the Virgaviridae family were by far the most frequently detected, with tropical soda apple mosaic virus, pepper mild mottle virus, and opuntia tobamovirus 2 being the most common species. Seventeen complete virus genomes could be assembled, and phylogenetic analyses showed a large diversity of virus strains circulating in the population. These results suggest that children are continuously exposed to an extensive and highly diverse collection of tobamoviruses. Whether the common presence of plant viruses at an early age influences the infant’s immune system, either directly or through interaction with other members of the microbiota, remains to be investigated…
… surprisingly, [plant viruses] were found as early as 2-weeks after birth in exclusively breast-fed infants. Tobamoviruses, in the Virgaviridae family, were the most abundant, and were present in most of the samples analyzed. Of interest, antibodies to plant viruses have been found in animals, including humans3, and it has also been shown that cowpea mosaic virus can disseminate systemically when orally administered to mice12. Whether the common presence of these viruses at an early age has an effect in the infant’s immune system and maturation of the gut remains to be investigated…
https://www.nature.com/articles/s41598-020-70684-w
*************************************************************************************
*
Antibodies in the bloodstream are taken as an unequivocal sign of infection by public health authorities. Livestock farmers have, many times over, had their antibody-positive (seropositive) animal herds seized and destroyed as a heavily enforced cautionary measure against the “presence of disease” even when no other signs of disease were manifest. In the animal world, this kind of “herd immunity” can get you killed. Despite our understanding of antibodies as proof of immunity against disease, this seemingly paradoxical situation is used to define “infection” with pathogenic entities. A pathogen (as I was taught in nursing school) is a microbe outside of its natural place. We recognize pathogens only in their ability to induce changes, but in the dynamic biosphere of our planet which is continuously building-up, breaking-down and on the move, pathogens are everywhere. Pathogens, in fact, are the “cause” of evolution if we stick to my foundation principle of out-of-place microbes.
Antibodies problems: http://theothersideofvaccines.com/2018/12/7-reasons-why-antibodies-cant-possibly-provide-immunity/
So, where are the “natural places” of some of these pathogens making us sick? Many of them, of the least in size, belong on a long string of RNA and DNA. The evolution of microscopic technology itself took decades of unrelenting improvement and investigation into the tiniest classes of genetic fragments (made of nucleic acids) that amounted to something “microbe-like”. A new class of ‘subunit’ entities discovered by science learning methods is called “subviral agents” and has emerged to categorize these genetic fragments. In plants these ultra-small pathogens are called “viroids”.
*
“Viroids are small (about 300 nucleotides), single-stranded, circular, non-encapsidated pathogenic RNA molecules. They do not code for proteins and thus depend on plant host enzymes for their replication and other functions. They induce plant diseases by direct interaction with host factors but the mechanism of pathogenicity is still unknown [in 2004]. They can alter the expression of selected plant genes important for growth and development…” https://pubmed.ncbi.nlm.nih.gov/15448723/
[otherwise known as mRNA]
Viroid is a term exclusive to plants — a viroid associated with human disease is called “viroid-like**”. One particular viroid-like infection known in human disease is Hepatitis D, caused by a so-named “delta agent” that uses the Hepatitis B virus as a “helper virus” to provide it with functional parts –and a demonstration case of the HepB being a ‘host factor’. The Hepatitis D virion below looks like a ‘delta’ viroid (in blue) swallowed by a HepB ‘envelope’ shell (red and tan), or a virus-within-a-virus structure. I’ll post some electron micrograph images of virus-within-virus structures further on.
**Viroid-like particles are also called “virusoids” –here’s a basic explanation of the differences in jargon, including ‘prion’ (infectious protein with no DNA/RNA) . https://courses.lumenlearning.com/microbiology/chapter/viroids-virusoids-and-prions/
Newborns are routinely vaccinated against HepB, a practice begun in 1983 and mandated in the U.S. in 1991.
*
*
So, how did science discover viroids? Accordingly, the credit belongs to Theodor Otto Diener, a Swiss plant pathologist who emigrated to the United States in 1939:
“In 1959, Diener joined the US Department of Agriculture’s Agricultural Research Service Pioneering Laboratory for Plant Virology at the Agricultural Research Center in Beltsville, Maryland,[2] where he investigated the cause of the potato spindle tuber disease. This led to the unexpected discovery of the causative agent, a small RNA molecule, eighty times smaller than the smallest known viruses, for which he proposed the term viroid.[6][7] Later, viroids were characterized as single stranded covalently closed circular RNA molecules occurring as highly base-paired rod-like structures.[8] Viroids, together with viroid-like satellite RNAs have been officially endorsed by the International Committee for Virus Taxonomy (ICTV) as a novel order of subviral agents,[9] which, in its 2014 publication, encompassed 2 families, 8 genera and 32 species.” https://en.wikipedia.org/wiki/Theodor_Otto_Diener
*
Diener himself wrote the following:
Abstract
“The discovery of the viroid in 1971, which initiated the third major expansion of the biosphere towards smaller living entities—after discovery of the “subvisual” microorganisms in 1675 and that of the “submicroscopic” viruses in 1892—has been officially endorsed by the International Committee on Virus Taxonomy as a new order called subviral agents.
“In 1989, I proposed that, based on their respective molecular properties, viroids are more plausible “living fossils” of the hypothetical RNA World (widely assumed to have existed prior to the evolution of DNA or proteins) than are intron-derived RNAs, which were, at that time, suggested as putative survivors. There were few citations of my proposal—and virtually none of viroids—beyond plant virology unil 1994, when Cheles-Flores critically examined the hypothesis and pointed out a serious difficulty, as well as a process by which this difficulty could be overcome. In 2013, when investigations by Koonin and Dolja revealed that of extant RNAs, viroids “strikingly” display some of the molecular properties posited for the earliest evolving, selfish RNAs (primordial RNAs), but, because extant organisms, aside from higher plants, appear not to harbor viroids, they cannot be regarded as primordial fossils, but appear to have evolved post LUCA (the Last Universal Common Ancestor). Here, I review whether some evidence nevertheless is compatible with the original postulate of the 1989 hypothesis. My analysis reveals no unequivocal evidence for an ancient origin of viroids, but suggests, alternatively, that viroids may have evolved de novo more recently, probably by novel processes similar to those suggested by each reviewer.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807594/
*
“…we show that circular RNA replicons analogous to [viroid family] Pospiviroidae emerge if evolution is seeded with minimal circular RNAs that grow through the gradual addition of nucleotides. Further, these rod-like replicons often maintain their structure if independent functional modules are acquired that impose selective constraints. The evolutionary scenario we propose here is consistent with the structural and biochemical properties of viroids described to date.” https://pubmed.ncbi.nlm.nih.gov/31075860/
*
*********************************************************************************************
*
- A) Tobacco Rattle Virus
- B) Tobacco Mosaic Virus
- C) Pepper Mild Mottle Virus
Obtaining viroids (a word not-yet coined) for experimental purposes dates back to the 1955 Tobacco Mosaic Virus publication by Heinz Fraenkel-Conrat and Robley C. Williams from the Virus Laboratory of the University of California (Wendell Stanley’s lab). The men dissolved TMV in a chemical solution, purified and then reconstituted it in solution, obtaining a ratio of infective particles. Their experiment, set to prove the existence of RNA/DNA, caused quite a stir : “Gunther Stent wrote to Sidney Brenner, ‘Frankel-Conrat seems to have done the biggest thing with TMV since Stanley crystalized it. He can add soluble TMV protein to soluble TMV RNA, aggregate the whole mess into rods of which 0.1% are infective!!! Naturally, you don’t believe it–nor did I or anyone else, but unless he has made up the whole thing it seems that it must be true. You can’t beat that for laughs, can you buddy?’ It was true.”
Reference source http://evilutionarybiologist.blogspot.com/2007/10/this-weeks-citation-classic_26.html
*
This electron micrograph image shows their reconstituted virus 
*
*Original document https://www.ncbi.nlm.nih.gov/pmc/articles/PMC528165/pdf/pnas00725-0006.pdf
*
The denaturing and reconstitution of infective TMV at UCBerkeley was paid for by the National Foundation for Infantile Paralysis, NFIP known as the March of Dimes for polio research, and the National Cancer Institute of the NIH. Rosalind Franklin’s “structure group” at Birbeck, University of London, was also paid by NFIP and NCI to study polio (see part two), and these same entities paid for the development of both influenza and polio vaccines from the beginning of World War II forward.
*
When we get to the Common Cold section of this series, we will also see that the ‘discoverer’ of human coronaviruses, Dr. David Tyrell, launched his career as an epidemiologist with the British government following a polio outbreak in his hometown of Sheffield UK, famous for its metal products. Tyrell, however, was notably attached to the WWII U.S. Armed Forces Epidemiological Board (AFEB) during the war and returned to the States in 1951 to work (1951-1954) at the Rockefeller Institute for Medical Research in New York.
Polio is, was, and remains a hub of constancy in nano-bio-tech; structurally identical to the common cold rhinovirus and the cowpea chlorotic mottle virus — its viroid cowpea mosaic virus is mentioned in the citations above as infecting and provoking antibody response in mice –from nature.com: “antibodies to plant viruses have been found in animals, including humans3, and it has also been shown that cowpea mosaic virus can disseminate systemically when orally administered to mice12.” Cowpea mosaic virus has proven more infective than its parent (or descendent, if evolutionary) and is another darling agent of nano-bio-tech, as are all viroids generally. Viroid research opened the way to new RNA technologies of the 1970s forward.
(search clip)
· The unique potency of Cowpea mosaic virus (CPMV) in situ …
pubmed.ncbi.nlm.nih.gov/32914796
[2020] “Our results indicate that CPMV in situ vaccine outperforms Cowpea chlorotic mottle virus (CCMV), Physalis mosaic virus (PhMV), Sesbania mosaic virus (SeMV), bacteriophage Qβ VLPs, or Hepatitis B virus capsids (HBVc). Furthermore, ex vivo and in vitro assays reveal unique features of CPMV that makes it an inherently stronger immune stimulant…”
**************************************************************************
Viroid-type (not showing RNA) protein “disks” of TMV on the left, matched to the UCBerkeley (‘Fig.2) EM graph above, are compared to the assembled TMV rod with the dark RNA coil shown on the right in this illustration.
The next year [1956], Professor Fraenkel-Conrat and his team, which included his wife Beatrice A. Singer, ‘hybrized’ their TMV specimens, mixing the protein disks of one strain type with the purified RNA of another, illustrated below. TMV mutants from these and other experiments were prepared in Berkeley’s particle accelerators by ‘Bea’ Singer and sent to Rosalind Franklin’s group in London for structural study along with ‘Mahoney’ strain polioviruses (crystals in filtrate). The Mahoney poliovirus strain was collected in 1941 from the feces of three siblings who were asymptomatic and considered the most deadly of ‘wild type’ poliovirus.
*
“Tracking the Elusive Viroid”
…”Like a virus, the viroid invades a cell and…forces the cell to duplicate the viroid’s RNA instead of its own. The viroid has no DNA. RNA and DNA are nucleic acids, the molecules of heredity; with the exception of viroids and some viruses, all genes are made of DNA.
“The difference between viroids and RNA viruses is that viroids have no protective protein coat. The scientific dogma in 1971 was that an organism with no protein wasn’t supposed to be able to replicate itself, even with a host cell’s help. And an entity as small as the PSTV (potato spindle tuber viroid)—130,000 daltons—wasn’t supposed to be able to infect anything, even a potato.
“Until that time, scientists believed that the minimum weight necessary for infectivity was about 1 million daltons. (A dalton, also called an atomic mass unit, equals one-twelfth the mass of a carbon-12 atom.) Diener wasn’t much impressed by scientific dogma. He’d seen it turned upside down too many times. But he was very careful to prove that the viroid really existed. In all, it took him 6 painstaking years”… [1965-1971] https://www.ars.usda.gov/oc/timeline/viroid/
- viroids in their two alternate 2D structures of ‘rod’ or ‘ring’
*
“Viruses (Virus particles or virions) are usually units consisting of nucleic acids and coat proteins called capsids. Viroids consist only of RNA, i.e. they contain no protein at all. Except for a few cases, viruses are not surrounded by a membrane. If present, the membrane around a virus particle – as seen in electron microscopic images – stems usually from the host cell (see picture to the left). Viruses have no energy metabolism of their own. Consequently, they cannot perform syntheses and are thus unable to replicate themselves… With plant viruses, the term specificity (or host-specificity) has a very narrow meaning, since no plant virus as such exists. Instead, plant viruses can be grouped in a number of ‘varieties’. The tobacco mosaic-virus (TMV), for example, multiplies within Nicotiana-species, several other solanaceous plants, and a few species of other plant families. The name of a virus is usually derived from the name of its main host plant. Although with viruses, the term ‘species’ may not quite correspond to the way it is defined in biological systematics, it is perfectly reasonable and common to use it for viruses, too, since all viruses and viroids contain an original genome with a species-specific information. Its continuity over generations is [only] guaranteed by replication in the host cells. The genetic information of viruses is either encoded by single-stranded RNA (most plant viruses), double-stranded RNA (wound tumor viruses), single-stranded DNA (gemini-viruses) or double-stranded DNA (cauliflower mosaic-virus: CaMV). Based on the shape of the virus particle, it is distinguished between rod-shaped and icosaedrical viruses with a capsid that seems almost spherical.”
Picture : Viral membranes. Maturation of the virion (Maus-Friend-leukaemia virus) by budding off the host cell’s plasma membrane. Notice the similar structures of the membrane surrounding the virus and the membrane of the host cell (deHARVEN, New York).
*
http://www1.biologie.uni-hamburg.de/b-online/e35/35.htm
**********************************************************************************************************
…making new ‘things’ with TMV:
EASY PIEZY
“The pH affects molecular charge, since it is well known that proteins disaggregate as the charge increases, and they aggregate as the charge decreases. Two often quoted examples are hemoglobin (Fanelli et al., 1964) and tobacco mosaic virus protein (Klug, 1979”)…
https://ecfsapi.fcc.gov/file/10307262054844/3-12%20Attachment%20-%20Blank%2C%20Electromagnetic%20Biology%20%2C%202008.pdf
*
2015– Metal-Based Nanoparticles (MBNPs)
“This review explores the synthesis of inorganic metallic-based nanoparticles (MBNPs) (metals, alloys, metal oxides) using biological and biologically inspired nanoreactors for precipitation/crystallisation. Such nanoparticles exhibit a range of nanoscale properties such as surface plasmon resonance (nobel metals e.g. Au), fluorescence (semiconductor quantum dots e.g. CdSe) and nanomagnetism (magnetic alloys e.g. CoPt and iron oxides e.g. magnetite), which are currently the subject of intensive research… Biological nanoreactors for crystallizing MBNPs within cells (magnetosomes), protein cages (ferritin) and virus capsids (cowpea chlorotic mottle, cowpea mosaic and tobacco mosaic viruses), are discussed along with how these have been modified for applications and for the next generation of new materials. Biomimetic liposome, polymersome and even designed self-assembled proteinosome nanoreactors are also reviewed for MBNP crystallisation and further modification for applications. With the advent of synthetic biology, the research and understanding in this field is growing, with the goal of realising nanoreactor synthesis of MBNPs for biomedical applications within our grasp in the near future.”
https://pubs.rsc.org/en/content/articlehtml/2015/cp/c5cp00375j
*
Display of epitopes on the surface of tobacco mosaic virus: impact of charge and isoelectric point of the epitope on virus-host interactions
M Bendahmane 1, M Koo, E Karrer, R N Beachy
Abstract
The biophysical properties of the tobacco mosaic tobamovirus (TMV) coat protein (CP) make it possible to display foreign peptides on the surface of TMV. The immunogenic epitopes G5-24 from the rabies virus (RV) glycoprotein, and 5B19 from murine hepatitis virus (MHV) S-glycoprotein were successfully displayed on the surface of TMV, and viruses accumulated to high levels in infected leaves of Nicotiana tabacum Xanthi-nn.
https://pubmed.ncbi.nlm.nih.gov/10388554/
*
Rabies virus is in a family called rhabdoviridae
Rhabdoviridae – Wikipedia
https://en.wikipedia.org/wiki/Rhabdoviridae
Rhabdoviridae is a family of negative-strand RNA viruses in the order Mononegavirales. Vertebrates (including mammals and humans), invertebrates, and plants serve as natural hosts. Diseases associated with member viruses include rabies encephalitis caused by the rabies virus, and flu-like symptoms in humans caused by vesiculoviruses.
*
RHABDOVIRIDAE – Stanford University
https://web.stanford.edu/group/virus/rhabdo/2004bischoffchang/Rhabdo.htm
Rhabdoviridae is a virus family within the Mononegavirales order, which also contains the Bornaviridae, Filoviridae, and Paramyxoviridae families. Rhabdoviridae contains six genera: vesiculovirus, lyssavirus, ephemerovirus, norvirhabdovirus, cytorhabdovirus, and nucleorabdovirus.
*
Abstract
“Classical plant rhabdoviruses infect monocot and dicot plants, have unsegmented negative-sense RNA genomes and have been taxonomically classified in the genera Cytorhabdovirus and Nucleorhabdovirus. These viruses replicate in their hemipteran vectors and are transmitted in a circulative-propagative mode and virus infection persists for the life of the insect. Based on the discovery of numerous novel rhabdoviruses in arthropods during metagenomic studies and extensive phylogenetic analyses of the family Rhabdoviridae, it is hypothesized that plant-infecting rhabdoviruses are derived from insect viruses. Analyses of viral gene function in plants and insects is beginning to reveal conserved and unique biology for these plant viruses in the two diverse hosts. New tools for insect molecular biology and infectious clones for plant rhabdoviruses are increasing our understanding of the lifestyles of these viruses.”
https://pubmed.ncbi.nlm.nih.gov/30500682/
*
“The Hemiptera /hɛˈmɪptərə/ or true bugs are an order of insects comprising some 50,000 to 80,000 species[3] of groups such as the cicadas, aphids, planthoppers, leafhoppers, bed bugs and shield bugs. They range in size from 1 mm (0.04 in) to around 15 cm (6 in), and share a common arrangement of sucking mouthparts.[4] The name “true bugs” is often limited to the suborder Heteroptera…Most hemipterans feed on plants, using their sucking and piercing mouthparts to extract plant sap.” https://en.wikipedia.org/wiki/Hemiptera
Plants — “Monocots, as the name implies, are defined by having seeds that contain a single (mono-) embryonic leaf known as a cotyledon. This is a monophyletic group that constitutes a majority of our agricultural biomass and include many important crop staples including, but not limited to, rice, wheat, corn, sugar cane, bamboo, onion, and garlic… the biggest difference of all between monocots and dicots, is the seed… Often incorrectly thought of as a tree, the banana plant is actually a monocot and is closely related to the grass family… https://biologydictionary.net/monocot/
Murine Hepatitis Virus (MHV) is a coronavirus
2001, Abstract “Inoculation of mice with most neurotropic strains of the coronavirus mouse hepatitis virus results in an immune response-mediated demyelinating disease that serves as an excellent animal model for the human disease multiple sclerosis. Recent work has shown that either virus-specific CD4(+) or CD8(+) T cells are able to mediate demyelination and also that the antibody response is crucial for clearing infectious virus. Another exciting advance is the development of recombinant coronaviruses, which, for the first time, will allow genetic manipulation of the entire viral genome.” https://pubmed.ncbi.nlm.nih.gov/11495812/
*
*
1999, “Hybrids of tobacco mosaic virus (TMV) were constructed with the use of fusion to the coat protein peptides…containing the…epitope from the spike protein of murine hepatitis virus (MHV, [coronavirus])… The TMV hybrids were propagated in tobacco plants, and the virus particles were purified. Immunogold labeling, with the use of the monoclonal MAb5B19 antibody, showed specific decoration of hybrid TMV particles, confirming the expression and display of the MHV [coronavirus spike protein] epitope on the surface of the TMV… Mice were immunized with purified hybrid viruses after several regimens of immunization. Mice that received TMV-5B19L intranasally developed serum IgG and IgA specific for the 5B19 epitope and for the TMV coat protein. Hybrid TMV-5B19, administered by subcutaneous injections, elicited high titers of serum IgG that was specific for the 5B19 epitope and for coat protein, but IgA that was specific against 5B19 was not observed. Mice that were immunized with hybrid virus by subcutaneous or intranasal routes of administration survived challenge with a lethal dose (10 x LD50) of MHV strain JHM, whereas mice administered wild-type TMV died 10 d[days] post challenge. …These studies show that TMV can be an effective vaccine delivery vehicle for parenteral and mucosal immunization and for protection from challenge with [corona] viral infection.” https://pubmed.ncbi.nlm.nih.gov/10393897/
Jennifer Lake's Blog 