virus cell replication theory history

Steven Avery

Viruses (1962)
Kenneth Manley Smith (1892-1981)

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Steven Avery

In considering how viruses multiply or replicate themselves it is
best to avoid any comparison with the growth of an organism. From
a survey of what is known of replication in the viruses of plants and
the higher animals a general picture of biosynthesis emerges, an
assembly rather than a multiplication. Luria puts it like this—4 virus
multiplication belongs on the level of the replication of sub-
cellular elements’, or according to Pirie 4it is the exploitation
and diversion of the pre-existing synthetic capacities of the host

In the replication of many viruses, especially the smaller ones,
a dual process is involved in which the protein and nucleic acid are
formed separately and then polymerized into the infectious particle.
The new advances in the techniques of electron microscopy and
X-ray diffraction studies (described in chapter 4) have given us a greater
knowledge of the ultrastructure of virus particles. Using this, it is
possible, to a certain extent, to visualize the process of its construction
or replication.

It was shown by Markham and Smith that the purified virus of
turnip yellow mosaic would separate, after centrifuging, into two
portions called the ‘top and bottom components’. On the electron
microscope the two kinds of particles looked similar, but the top
component was of lower density and contained no nucleic acid.
Moreover, infectivity was confined to the bottom component which
did contain the nucleic acid. This was the first definite proof that the
infectivity of a plant virus was centred in the nucleic acid of the virus
particle and that the nucleic acid was inside the protein coat. Since
then a number of other viruses has been shown to have top and
bottom components, and empty shells similar to the ‘ top component ’
have also been observed in several animal viruses.

Tobacco mosaic virus
A great step forward was made by Gierer and Schramm and
when they showed independently in 1956 that the
RNA of tobacco mosaic virus (TMV) could initiate infection in the
absence of the protein part of the virus particle. It has since been
,,,about 60 per cent of the infectivity of normal TMV. The whole
process has been carried out in vitro by Takahashi, whereby infectious

Bacterial viruses
,,,. 1). Anderson first
showed how the phage-particle infects the cell. Contrary to what
might be expected, the virus attaches itself tail first to the bacterial
cell wall which it then penetrates, allowing the DNA contents of the
head to pass down into the bacterium. ...
Kellenberger and his co-workers have shown that the breakdown of
the bacterial nucleus is accompanied by the formation of marginal
vacuoles containing DNA, from which the pool of phage DNA
develops some minutes later. The phage DNA starts to increase

Fowl-plague virus
This belongs to the myxovirus group and seems morphologically
similar to influenza A virus; the multiplication cycle has been
studied by Werner Schafer from whose work this account is taken.
... The cycle of replication is thought to be somewhat as follows

Steven Avery

Viruses "hijack the host cells' replication machinery"?


Thanks for the article!

"They must rely on a host so must invade the cells of living things and hijack the host cells’ replication machinery to make new copies of themselves."

However, there is no replicable science experiment that ever proved or demonstrated this theory. It should have taken place c. 1950-55, when the idea started to come into scientific lingo by scholastic osmosis.

Without a scientific base, there is no virology science.
The discussion could properly end right there.

On top of that, this is truly an extraordinary claim, (normally simply assumed by circularity, assumption to conclusion) and an extraordinary claim needs powerful evidence to be accepted. Inactive/dead RNA/DNA snippets somehow getting into cells, drifting over to the right spot for the incredible hijacking, even of multiple types of cells, and then the lysis or budding to get out. Absolutely incredible!

So where is the non-circular science establishing this as a fact, rather than a theory only by scholastic osmosis?

Steven Avery
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Steven Avery

Did Thomas M. Rivers in 1937 work with the hijacking of cell replication theory?

"The distinguished American virologist, Thomas Rivers, introduced a lot more flexibility to Koch’s original postulates to take into account the vagaries of viruses, their requirement for very specific host cells and conditions, and the fact that disease doesn’t always manifest as a result of infection."

This seems to imply that Rivers even in 1937 there was acceptance of the theory of viruses hijacking cell replication.

You will see quotes like this as part of the Rivers exposition.
"The virus can be cultivated in host cells."
However, that is quite ambiguous.

So we go to the key 1937 paper.
From The Rockefeller Institute for Medical Research, New York

"How does one go about proving that a virus is the cause of a disease? Viruses, regardless of whether they are parasites or the fabrications of autocatalytic processes, are intimately associated with host cells and, therefore, should always be found at the proper time in specific lesions. In addition, viruses, as is the case with bacteria, may be found also in the blood stream, not necessarily multiplying there but appearing frequently only as a phenomenon of overflow from lesions in the tissues."

So it should be clear that the theory of viruses hijacking cell replication was not part of "science" so-called until the 1950s. And never had an experimental base.

It would be fascinating to attempt to document how this theory became accepted, without any experimental base of replicable experiments.

Steven Avery
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Steven Avery

Still an sv4o /carlsmythecells/status/1701234241298726965?s=61&t=CN7Xq1azV7DXPhFnIj20TA

https://x. com/carlsmythecells/status/1703794945595719713?s=61&t=CN7Xq1azV7DXPhFnIj20TA

Have you tried using Scopus to find the subsequent papers that cite this one?

The work of Stillman and colleagues identified all of the proteins required for SV40 replication. You were provided with this information before.

“Not late on the day at all, for SV40.”

earlier you said that SV40 gave the first indications of trying to show this theory of ‘viruses’ hijacking cell replication function


Steven Avery

The steps in replication, the viral initiator, the host proteins, and their mechanisms of action were initially defined using a cell-free SV40 replication reaction. Although our understanding of the vastly more complex host replication fork is advancing, no eukaryotic replisome has yet been reconstituted and the SV40 paradigm remains a point of reference.