modern virus theory - virus chain reaction - (twitter thread)

Steven Avery

Simply give the best proof, and demo, for following theory:


1) inactive ‘virus’ enters passageway
2) pulled through cell membrane
3) virus activates, hijacks cell function
4) cell replicates gazillion viruses
5) cell bursts
6) repeat 2-5 qazillion times
Virus Theory - when did it begin - how is it supposedly demonstrated
Let us start with the beginnings of virus theory applied to human health.
Can you find anybody proposing this theory before, say, 1950?
Who? When?
Try not to dance around.
Please, let us bypass the history of vaccines, like polio and measles, a great topic but only a diversion for finding out how virus theory developed and is supposedly demonstrated. If you really need counterpoint on the vaccines, we can discuss that separately.

A paper that Stephen recommended is essentially worthless to our inquiry.

From the 2008 paper,:

Pathology, Molecular Biology, and Pathogenesis of Avian Influenza A (H5N1) Infection in Humans
Christine Korteweg, M.D. Jiang Gu, M.D., Ph.D.

lots of circularity and equivocation:
"On the molecular level, several viral genes and gene products have been identified that may be responsible for the high pathogenicity of H5N1 influenza viruses. "

", it may be difficult to distinguish diffuse alveolar damage caused by H5N1 virus infections from diffuse alveolar damage caused by other microorganisms such as severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) or by other factors such as aspiration or oxygen toxicity."

" The available studies of human H5N1 autopsies have a number of limitations in terms of pathological findings. "
Why would one small virus be smart enough to infect and hijack the wide variety of cells mentioned?

"human H5N1 influenza. Aside from the respiratory tract, other organs such as the intestines, the brain, and the placenta appear to be infection targets of the virus."

All sorts of vague stuff. Circularity.
No gold standard genome for the 'virus'
Burst cells not even mentioned, nor entrance through cell membrane.

Again and again .. this MAY do that, and POSSIBLY the other. and APPEARS TO BE and, HAVE BEEN SUGGESTED
and requires further exploration and conflicting results

As for the pictures, they prove the existence of some particles, or exosomes, or various somethings, they do not remotely prove the existence of viruses as described in virus theory. That was a humorous claim.

Stephen, if you actually believe the pics prove something about virus theory, please explain why.


Here is the opening back and forth.

Aaron Ginn - Nov 23.
"No study detected live virus beyond day 9 of illness, despite persistently high viral loads. SCoV2 viral load in the upper respiratory tract appeared to peak in the first week of illness, whereas that of SCoV1 peaked at 10–14 and MCoV peaked at 7–10."

And I would read this as an acknowledgement of the falsity of virus theory - that ‘viruses’ are hijacking cell mechanisms to force massive replications, bursting cells, and then being captured by other cells, replication, burst, etc. Never proven, lacking evidence. The virus myth.

That has been determined experimentally. Where’d you get the idea that it hasn’t? It’s also the mechanism that many (successful) vaccines rely on

Specific experiment, please. Thanks.

‘Principles of Viral Pathogenesis’ by Michael B.A Oldstone is a good minireview. Read it, and look at the cited papers, and you’ll find plenty of proof that viruses are not a “myth”. Given that this is readily available and easily accessible, I would hope that you might take.


This beginning was also put on Facebook:

Terrain Model Refutes Germ Theory

Principles of Viral Pathogenesis (1996)
Michael B.A Oldstone, M. D.
Patho is derived from the Greek πάθos, meaning suffering or disease, and genesis from the Greek γέvεσis, which translates “to come into being or origin.” Viral pathogenesis, then, is defined as “how viruses produce disease in the host.” The portrait of viral pathogenesis is the sum of functions through which a virus causes disease (virulence) and the host resists or is susceptible. ... our understanding of how viruses cause disease is scanty. As an example, for poliovirus ... our knowledge of how poliovirus actually causes poliomyelitis is limited. Considering the number of persons infected with the virus, few develop poliomyelitis. ... the determinants that control viral virulence or host susceptibility (or resistance) in the natural host are far from being understood in terms of molecules or genes involved. ... This ignorance of pathogenic mechanisms is not unique to poliovirus. Equally obscure is how HIV causes dementia and immunosuppression and why measles virus promotes generalized immunosuppression, and so on.
Viruses, Plagues, and History: Past, Present, and Future (2020)
Michael B.A Oldstone 2009 2020 2020

Last edited:

Steven Avery

Facebook - Terrain Model Refutes Germ Theory

Terrain Model Refutes Germ Theory
Modern Virus Theory

Vaccine Chain Reaction
- (1-8 updated)

1) inactive ‘virus’ enters passageway, fav method is aerosol droplets
2) individual virus is pulled through cell membrane by receptors
3) virus activates
4) virus hijacks cell function
5) cell replicates gazillion viruses
6) cell bursts (lysis)
7) repeat 2-6 gazillion times
8) can result in illness or death

What was the first human (or possibly primate) declaration of this theory?
How is each stage in this symphony demonstrated/proven.
Sebastien Cormier
Yes that is the theory of what viruses do. Of course particles of such size can only be imaged by electron microscopy. Samples prepared for such imaging require a lot of processing steps known as "fixing". There's no way to actually observe viruses doing such things. Sample fixing produces thin slices of resin containing dead and dry material. Retroviruses are said to bud out from the host cell without to kill it. I don't know who first suggested this

Steven Avery
Yes, to look at their electron microscope pics is a funny exercise in circular reasoning. The pics of all dead material show very little, and they try to put the square block in the circular hole. Thomas Cowan also discusses microscopes that might see small items live, Gaston Naessans and Royal Rife.

Ashley Fae
here’s a nice rundown of the history of discovery:
here is a much more succinct and readable rundown if you found that other link to be too in depth/long/boring! (Click download PDF.)
A Short History of the Discovery of Viruses - June 2015
Ed Rybicki
TMV is mentioned several times here. Names and dates of important discoveries in the history of virology:
The History of Virology - Appendix 3 - from Alan Cann - Principles of Molecular Biology
Writing the history of virology in the twentieth century: Discovery, disciplines, and conceptual change
Pierre-Olivier Méthota

Roy Arne Josefsen
Virology theory:
Virology Lectures 2020
Then you can debunk studies found here:
Its all fake
Germ Theory - The New State Religion - Dr. Tim O'Shea

Jim O'Kelly
The Birth of the Living Virus Lie
Jim shreds the early TMV studies

JD Price
you know TMV will not spread unless you manually/ mechanically damage the leaves ? (Won't happen naturally) man's efforts to control are always counterproductive!
Daniel Raymond Fretto also comments on TMV

Michael Bilikas
Someone had a list on here of questions to ask. Might have been infectious myth, but I thought it was here. Thought about revisiting that. Pretty sure it could easily get into the 100s. I'd like to see a MSM answer to all of them. Would probably be very entertaining.... I'll see what I find. I don't think you will find a study which is why I thought about the list. For instance, why do you have to grow virus in a cell culture if it multiples so much that it kills enough cells that it can kill a human being? Why do we use antimicrobials to kill the virus on inert surfaces? You could look into patent applications for these chemicals they claim kill viruses and see what studies they site. Would be interesting. How can they claim ethical concerns when a study has never shown pathogenicity or even caused a death to my knowledge? How many people have died during vaccine trials? I've toyed with tracing backwards, I've seen hundreds of citations in articles. This may be something to hire a researcher off of upwork for😁

Steven Avery Michael Billikens
“For instance, why do you have to grow virus in a cell culture if it multiples so much that it kills enough cells that it can kill a human being?"
A key question. Plus they would have all the burst cells nearby for verification.
Sometimes they make an excuse that the virus is too dangerous to handle!
Some individual came up with the 'gazillion of viruses bursts the cell' idea starting a virus chain reaction. Who, when?
Who commented on that idea?
Before Stefan Lanka and similar scientists. And who has given the most pithy comments about this absurd theory.

Ashley Fae
Michael Bilikas I can answer some of these questions for you.
“Why do we use antimicrobials to kill the virus on inert surfaces?”
They don’t die instantly. They can remain infectious for some time, so then when someone touches that surface (or food or whatever touches that surface) then some virions will be reintroduced into a host and can continue replicating etc.
Michael Bilikas “why do you have to grow a virus in cell culture if it multiplies so much that it kills enough cells that it can kill a human being?”
Could probably fill a whole book to properly answer that question but here’s an abbreviated version in my words:
You don’t absolutely have to culture viruses, but it makes them much easier to study and work with. For one thing, the more you have, the more you can experiment (which applies to everything so should not be too controversial.) Say we have a liver biopsy that we want to see if the hepatic cells are infected with a virus and if so we want to characterize it. Well the liver biopsy may be a 2cm x 2cm x 1.5 cm piece of tissue. If we just want to know, “is this infected with hepatitis A, yes or no?” Then that’s fine, that’s plenty of sample. But if it’s negative for Hepatitis A and we want to do more experiments (or it’s positive but we want to know more about it) then we need more sample. Oh wait...we already used the sample for the first test. Shall we open the patient back up and biopsy their liver again? No no that’s quite invasive, we don’t want to do that if we don’t have to. Instead we inoculate a cell culture of hepatocytes with a piece of that biopsy tissue. Then we can make more virus particles. We don’t need more tissue, we just want more virus.
(Please note I’m not trying to make an argument 😊, I’m just trying to briefly explain the practical and logistical reason that cell cultures are done. This is in no way a full explanation - your question is a great one and I can elaborate more or point you in the direction of a more complex and proper answer if you are up for some more reading!)
Pic from Cann and Irving
Virus Isolation
Why Culture Viruses

Jim O'Kelly
Virus has always meant poison. It was clear from the books in the 1800s and early 1900s that virus was the pus of smallpox.

Robert Louw
Yes, it's so laughable and childish actually - and with that rate of replication we would all be changed into the "virus" within minutes - at one moment you are sitting at your desk writing and the next you are a microscopic "virus" nobody can see on your study chair - hilarious... 🤣 🤣

Jill Kirby
Dr. Stefan Lanka 2020 Article Busts the Virus Misconception

Steven Avery
Jill Kirby - among the best articles. Still a bit away from the OP.

Ashley Fae
I understand your question and this is not a perfect answer but here is some info for you’s from a textbook called “Principles of Molecular Virology” so I’m trying to find the relevant parts that answer your question

In the late 1950s, Sydney Brenner and Robert Horne (among others) developed sophisticated techniques that enabled them to use electron microscopy to reveal many of the fine details of the structure of virus particles. One of the most valuable techniques proved to be the use of electron-dense dyes such as phospho- tungstic acid or uranyl acetate to examine virus particles by negative staining.The small metal ions in such dyes are able to penetrate the minute crevices between the protein subunits in a virus capsid to reveal the fine structure of the particle. Using such data, Francis Crick and James Watson (1956) were the first to suggest that virus capsids are composed of numerous identical protein subunits arranged either in helical or cubic (icosahedral) symmetry. In 1962, Donald Caspar and Aaron Klug extended these observations and elucidated the fundamental principles of symmetry, which allow repeated protomers to form virus capsids, based on the principle of quasi-equivalence (see Chapter 2). This combined theoretical and practical approach has resulted in our current understanding of the structure of virus particles.

Ashley Fae
I think there was no one person who made that virus theory. Those things were observed and discovered over the years.
The modern aspects became elucidated with advances in molecular biology in general.

Steven Avery
Ashley Fae - a helpful history, however afaik nothing about the virus chain reaction causing illness.
And this has never been “elucidated.”
Such a theory of a complex, and unlikely, series of steps does not simply come from ether.

Ashley Fae
Steven Avery you described the virus life cycle in the OP but then you mention illness here which is viral pathogenesis. Both of these topics are different subsets of [modern] virology. So maybe I don’t understand exactly what you’re asking, like I thought did.
Is this what you want to know how it was discovered?
Viral Life Cycle Overview
I will do some more research for you but I want make sure I understand your question.

Steven Avery
Ashley Fae - outside today 🙂 ipad -
that does elucidate the current theory fairly nicely.

“viral life cycle can be divided into several major stages:
attachment, entry, uncoating, replication, maturation, and release”
Has nothing about the genesis of the chain reaction theory - very thin on any actual attempted proof of key elements.
Last edited:

Steven Avery

On Viruses, Coronaviruses, SARS-CoV-2 and COVID-19, and Pandemics - June 2020
David Chester Buhayo Reyes
What are viruses?

Definition and Description of Viruses
Viruses are among the most mysterious things in biology. Viruses are small particles that are described as obligate intracellular parasites. Obligate intracellular parasites are parasites that have to infect an organism in order to function. This is the reason why viruses cannot affect the host organism unless it enters one of its cells in order to replicate and infect other cells. Viruses are capable of infecting any organism from all three domains of life. Bacteria, Archaea, and Eukarya make up the three primary domains of life. Viruses can even infect other viruses. (Raoult and Forterre, 2008).

Steven Avery

Ashley Fae
There are other tests for COVID but PCR is the gold standard and is the main way. My lab got antigen tests back in March and we could not validate them, I mean they failed our validation studies. We sent them back to the manufacturer and stick to PCR.]-R

Steven Avery
Ashley Fae
- how precisely did you “validate” PCR for covid? Thanks!

Ashley Fae
Steven Avery
We ran negative and positive controls multiple times per shift by various techs (with the bonus of us getting practice performing the test). The negative contains purified inactivated coxsackievirus.
The positive contains purified inactivated SARS-CoV-2. We tested a variety of sample types, different swabs (due to shortages.) We also used made up samples, like just transport fluid with no swab in it, or the positive control diluted with transport fluid. Ran leftover specimens from other tests, some had already tested positive for flu or RSV.
It all gets documented, then, if everything goes ok it gets approved by the pathologist. The documentation would be the exact type of thing an inspector looks for. Instrument printouts, signatures, dates, all that jazz.
Each time we get a new lot of reagents or replace a module on the analyzer, we do another mini-validation, with a few extra runs of QC and by running samples from the former lot and then also running them on the new lot. Some negative, some positive - you want a variety, you know. Also we have these things called CAP surveys. It’s meant for proficiency testing but we use the leftovers for validations.
This is what we did basically:

Xpert® Xpress SARS-CoV-2/Flu/RSV Verification Guide Verification Protocol 10.12.22 AM.pdf

Arora Chance
They use 3 tests the COVID-19 PCR Test, COVID-19 Antibody Test, COVID-19 Antigen Test. These are all options re travelling too. All are believed to be unreliable. Some info here:
Last edited:

Steven Avery

Stephen Moore posted this on twitter (continuation from the 1st post)


I can't believe that I actually set up an account on your exclusive bible forum to try to type up a reply only to not even be able to post, so instead, I will be replying here, free from Twitter's character limits.

First off, you seem to have a lack of understanding of viruses. There is no "virus theory". This is quickly verified by a search of "modern virus theory" into google scholar. I'm not sure if you're confusing it with germ theory, which shares similarities to what you seem to want, but "virus theory" is something that you have seemingly made up. Especially considering that an entire class of viruses - bacteriophages - do not even infect human cells (instead, infecting bacterial cells), and that many viruses behave in different ways. Generally, the germ theory (currently accepted) states that certain (certain in characteristics, numerous in quantity) diseases are caused by the infection of pathogens - microorganisms too small to see without magnification (these microorganisms include fungi, viruses, bacteria, and parasites). It was proposed by Louis Pasteur towards the end of the 19th century (1880s, I believe), and some of his evidence includes the study of silkworms (he found that healthy silkworms became ill when nested with those suffering from disease and that the sterilization of an environment controlled the spread of said disease) - this discovery is what led to the sterilization of surgical equipment between surgeries - and of his cultivation of the anthrax bacillus in a cell culture (from a sheep dying of anthrax) being able to infect other sheep with anthrax (the disease process) upon injection.

Second off, your demand for "proof" demonstrates that you are lacking in the understanding of scientific philosophy. Science is largely based on falsifiability - the capacity for a hypothesis to be contradicted by evidence. It's why scientific inquiry begins with a null hypothesis before moving on to an experimental hypothesis (if the null hypothesis fails). This is relevant for our discussion because 1) nothing in science can be proven with universal truth (however, this is NOT to say that science should be ignored - when sufficient evidence for a concept is available, it becomes scientific truth, but to state otherwise would be incorrect). So no, I will not be able to "prove" that viruses are real - only that there is over a century of evidence (yes, over a century, began with Pasteur) to support their existence with strong experimental evidence. 2) Falsifiability, though, is designed so that hypothesis can be rejected. If viruses are in fact a myth, there should be evidence (strong, extensive, and peer-reviewed evidence) that contradicts either germ theory (in its modern form, specifically addressing pathogens' causative effect on disease) or the existence of viruses altogether. I've yet to find any research that accomplishes this but would invite you to try to find it yourself - however, given that you haven't provided any such evidence thus far, I doubt you have it on hand now. Which brings me to my next point: that your entire argument is based upon a burden of truth fallacy. You made the initial claim that viruses are a myth, and yet it is solely my duty to prove otherwise. In proper logic, you should be providing the evidence for viruses being a myth, something which I readily await. You (incorrectly - I'll get to that later) rejecting the evidence that I have provided (again - incorrectly - I'll discuss that later on) without presenting any evidence of your own when you made the initial claim is not debating in any sort of academic (or frankly, good-natured) way.

Now, I'll address your "rejections":

First, your dismissal of vaccines as part of the virus discussion is not justified. The early vaccines, including those of Jenner and Pasteur (18th/19th century), were based upon the observation that those subjected to some diseases or a weakened form of some disease resulted in immunity to some disease (obviously, though, this is just medical history). What was notable, though, is that they didn't know viruses existed at the time - it was the success of these vaccines that helped spur the development of virology - people sought to understand why they worked (and vaccines being effective is something you'll find incredibly hard to refute - just look at the success of the Polio vaccine, Measles vaccine, etc.). I would love to hear your counterpoints to the effectiveness of vaccines - there is strong empirical evidence for their effectiveness.
Second, I'll acknowledge that " Pathology, Molecular Biology, and Pathogenesis of Avian Influenza A (H5N1) Infection in HumansChristine Korteweg, M.D. Jiang Gu, M.D., Ph.D. " was not the best example to use - mainly because it is a relatively poorly studied virus (at least this specific strain). However, your (arrogant) dismissals are flawed:
" lots of circularity and equivocation:
"On the molecular level, several viral genes and gene products have been identified that may be responsible for the high pathogenicity of H5N1 influenza viruses. "", it may be difficult to distinguish diffuse alveolar damage caused by H5N1 virus infections from diffuse alveolar damage caused by other microorganisms such as severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) or by other factors such as aspiration or oxygen toxicity."" The available studies of human H5N1 autopsies have a number of limitations in terms of pathological findings. "
"- First, you may want to refresh yourself on both circularity and equivocation - equivocation implies ambiguity, and I think that you would be one of very few - regardless of whether you "believed" in it or not - to say that these examples are open to more than one interpretation. It is literally a review that is recapping what has been studied about H5N1. And regarding circularity, I'll use a quote of yours: "That was a humorous claim ".
- Second, because while my first point is true, it doesn't address what was actually being discussed, is that you have a knack for cherry-picking SINGLE SENTENCES, OUT OF CONTEXT, and using them to dismiss a much larger work.

For your first quote ("on the molecular level..."), I will first pull the preceding sentences from the very paragraph where you found it:
" H5N1 influenza is still a relatively novel disease with poorly understood pathology and pathogenesis. During the period from the first known outbreak nearly a decade ago until the present, only a limited number of reports describing pathological findings in human H5N1 cases has been published. Nevertheless, recent studies combined with early findings have gradually resulted in a better understanding of the cell and organ pathology caused by the H5N1 virus, as well as the viral tissue tropism. These findings together with animal and in vitro experiments have also contributed to a basic understanding of the pathogenesis of this disease. "

This is a review. It sums up what is known based on research done up until that point. This is partially my fault, though - I should've found a different, more well studied virus as an example.

Full context for quote #2:
Because the above histopathological features are not unique to H5N1 influenza, it may be difficult to distinguish diffuse alveolar damage caused by H5N1 virus infections from diffuse alveolar damage caused by other microorganisms such as severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) or by other factors such as aspiration or oxygen toxicity. More specific tests such as in situ hybridization, reverse transcription-polymerase chain reaction (RT-PCR), and virus isolation are required to confirm H5N1 infection.

Simply acknowledging that the symptom is shared by other diseases (after which they list two other viruses, among other things). They then clarify - in good scientific practice, as no specific research has been done specifically on this histopathological feature - that further inquiry is needed to make the connection. Also, this part simply discusses many of the symptoms (you see those in the tables) shared during the autopsies of those deceased from the virus (no, this is NOT circular reasoning - the review is not arguing for the existence of viruses - that is assumed (assumed based on literature - it's how science works), it is just reviewing what is known, so no circular reasoning).

" Why would one small virus be smart enough to infect and hijack the wide variety of cells mentioned?
"human H5N1 influenza. Aside from the respiratory tract, other organs such as the intestines, the brain, and the placenta appear to be infection targets of the virus." "

- You're not going to believe this, but organs are different from cells. While those are, in fact, organs listed, they all share epithelial cells. Influenza A viruses mostly express tropism for respiratory epithelial cells, but can also infect epithelial cells of other organs. Influenza viruses surface proteins bind to sialic acid receptors on human cells.
"No gold standard genome for the 'virus'Burst cells not even mentioned, nor entrance through cell membrane."
- Genome discussed in the section "Viral Genes and Gene Products Involved in the Pathogenesis of H5N1 Influenza", here is another linkm though: H5N1 highly pathogenic avian,about 13.5 kb in total.

No, "burst" cells (the process is referred to as lysis, but I'll let that one go) are not discussed in this particular review. My apologies, for this means that my statement that it covers of 1-6 of your list was incorrect. Entrance through cell membranes is discussed in section "Receptor Specificity and Transmissibility of the H5N1 Virus" - once receptor bonding occurs, fusion occurs.

Your analysis of that review is an insult to the scientists that wrote it.
Electron microscope visualizations shows the structure, x-ray crystallography gives the atomic structure (which are used in the development of therapeutics), where DNA/RNA sequence, along with proteins and structure are identified.
Here's a collection that I believe will cover off what you are looking for (the chosen virus is HIV) HIV genome consists of,core of the virus particle.

100% Upvoted
Comment as purebible

Steven Avery


Hi Stephen,

Here is a slightly updated summary of modern virus theory, the virus chain reaction.

Modern Virus Theory

Virus Chain Reaction
- (1-8 updated)
  1. inactive ‘virus’ enters passageway, fav theoretical method today is aerosol droplets
  2. individual virus (or viruses) is pulled through cell membrane by receptors
  3. virus uncoats and activates
  4. virus hijacks cell function
  5. cell replicates gazillion viruses
  6. cell bursts (lysis), releasing huge numbers of viruses
  7. repeat steps 2-6 gazillion times
  8. may result in illness or death (why is unclear)
What was the first human (or possibly primate) declaration of this theory?

How is each stage in this symphony demonstrated/proven?


Now, if you know virus history, it is clear that
* this theory did not exist in the 1800s or the first half of the 1900s. *

And if you are not sure of it being properly characterized as modern virus theory, here you have most of the cycle indicated:

Viral Life Cycle Overview
“viral life cycle can be divided into several major stages: attachment, entry, uncoating, replication, maturation, and release”
So this is the modern theory. Today this is the "life cycle" of all viruses.
No identification of a virus can be outside this life cycle.


Let us start with the simple question.

Who first expressed this theory?
And when and where.

Or .. who first put forth this "life cycle" of a "virus".


Note that if this theory were true, huge numbers of viruses, and burst cells, would be available in abundance in tissue cultures from those ill, or in autopsies. And it would be the actual virus, the genome would be at hand, without large computer simulation guesses.
Last edited:

Steven Avery

A 1949 paper (the full theory was not yet developed).

Facebook - Terrain

Note: this was removed by a Terrain mod on Dec 4, 2020.
And I think they do not really understand the topic of searching out the history of the Modern Virus Theory.
Granted, I did not add any comments, as I first wanted you to see the main text extracts.

Steven Avery
Somewhere in here there is
"in virus production in a chain reaction of some sort within the complex."

From 1949:

The Reactions of Bacterial Viruses with Their Host Cells (1949)
Thomas F. Anderson
p. 465

By themselves the virus particles seem to be quite inert; like the seeds and spores of higher forms, whose regularity in size and shape they resemble, they become active only in a suitable environment—the host cell. Attempts to study their mode of reproduction by grinding up host cells at intervals after infection have yielded only debris, and in some cases a few finished virus particles. Direct observation of their mode of reproduction is impossible, since, on the one hand, the particles themselves are smaller than the wave lengths of visible light, and, on the other, most cells are too thick for convenient observation of internal structure with the electron microscope. Investigators of the mode of virus reproduction are therefore forced to employ the more indirect methods of genetics, biophysics and biochemistry.

p. 466
Then, too, the short generation time of the host makes it possible to complete in 24 hours experiments on growth and heredity which involve huge clones of individual cells (10-to11th or more) or of virus particles. For these and other reasons it is mainly in the bacterial viruses that we have the type of information on virus reproduction which will be discussed in this review.

p. 468
Life Cycle and Morphology.
The life cycle of these bacterial viruses consists of three easily recognizable stages (23) :
o) Adsorption of the virus on the host cell.
b) A process of proliferation on the virus within the host.
c) Lysis of the host with simultaneous liberation of new virus.

... Following adsorption, no change in the morphol-
ogy of the host is to be seen, nor does the number of visible virus particles increase. The intracellular events leading to virus liberation are not visible. However, beginning 21 minutes after adsorption, bacteria may be seen which have burst, as in Fig. 3, to liberate a hundred or so phage particles. These are quite like the infecting one in structure.

Fig 1-3 pictures of tadpole viriuses!

p. 471
Multiplicity of Infection. In many types of experiment it is important to have reliable information on the distribution of virus particles among the infected bacteria. If a number of virus particles, s, is adsorbed on a number of bacteria, t, the ratio s/t is termed the “multiplicity of infection,” m.

p. 476
Since a bacterial cell is capable of supporting the growth of 100 or so different viruses, it is supposed that its surface contains a corresponding number of different types of receptor spots, one for each type of virus to which it is sensitive. (more on p. 480-483)

p. 485
Killing of the Host by Damaged Virus Particles.

p. 494
So far we have discussed the virus particle, its adsorption on the host and the manner in which the biological composition of the resulting complex affects the virus products which are ultimately formed.... As yet the confusing multitude of clues gives only a vague picture of the developmental processes.

p. 500-501
Free virus particles can be studied directly; they have remarkably uniform morphologies within a given strain or group of serologically related strains. Alone the virus particles are inert. They display biological activity only when adsorbed on their host cells, or, of course, when injected into animals where they elicit antibody formation. Some bacterial viruses need to take up substances (co-factors) from the medium before they are adsorbed on their hosts. Some are not adsorbed in violently agitated media. In quiet media the adsorption rate can be accounted for by diffusion of the virus to the cell surface when a large proportion of the collisions results in irreversible adsorption. Mutation of bacteria to resistance occurs in the absence of virus, and results in the loss of the adsorption mechanism for the virus in question. (continues)

Bibliography p. 502-505


Bacterial viruses- a virus that infects and replicates within bacteria and archaea



maybe here

When a drop of solution containing a single virus is placed on a “lawn” of bacteria spread on a petri dish, achain reaction is initiated. The virus infects a nearby host and a short time later a large cohort of virus progeny emerge from the lysed cell and adsorb to nearby hosts.

Last edited: