The following points highlight the life cycle of a typical plant virus such as TMV (Tobacco Mosaic Virus) which comprises of four stages. The stages are: 1. Transmission of Virus Particles (Virions) 2. Infection 3. Virus Multiplication 4. Sites of Viral RNA and Viral Protein Synthesis.
Stage # 1. Transmission of Virus Particles (Virions):
The rod-shaped Tobacco Mosaic Virus (TMV) infects only the leaves of tobacco plants. It is transmitted and complete particles introduced into the host cells by insect vectors which are many such as Myzus pseudosolani (false potato aphid), M. circumflexus, Macrosiphum solanifolii and grasshopper.
The virus is also transmitted by mechanical means such as rubbing of virus on the leaves and through handling of tobacco plants at transplanting. The virus is extremely contagious. A person who has handled cigarettes containing infected tobacco leaves may transmit the virus to the healthy plants.
Stage # 2. Infection:
Infection takes place with the whole virus particle. Separately the virus components are not infectious. Fraenkel-Conrat (1956) separated the protein coat from RNA core by delicate chemical procedures.
He found that the protein coat alone is not capable of producing infection. The RNA alone is infectious but much less than that of the intact virus particle. He further placed the protein shells in a solution of viral RNA. The viral particles of TMV were reconstituted.
They were able to reinfect tobacco leaves. It shows that the nucleic acid alone carries full instructions to form new virus particles. Highly interesting and significant were the results of Fraenkel-Conrat and his associates in this connection.
They separated the nucleic acid and protein coats of TMV and another strain of rod-shaped virus HR. They then mixed the protein coats of TMV strain with the RNA cores of HR strain. The result was the reconsitution of virus particles with TMV protein coats and HR core of RNA.
Infections with this new type hybrid virus always yielded the new virus particles in which both the protein coat and RNA belonged to the HR strain which had furnished the infective RNA.
The results of this experiment conclusively prove that the nucleic acid alone is coded with the specific information needed to the host cell for building complete virus particles. Infection may be with viral RNA or with virus particle intact.
Separately both viral RNA and protein are readily attacked by enzymes in host cells and decomposed. Solitary RNA is destroyed quickly by ribonuclease enzyme present in the host cells. Virus particles intact are very resistant to decomposition and thus are stable and viable.
For infection, wounding of the host cell wall is necessary to produce an infectible site. It may be caused by the mouth parts of the insect vector or by wounding epidermal cells or breaking epidermal hairs by abrasion.
Through these infectible sites, the virus particles (virions) intact gain entry into the host and come in contact with the host cell membrane. By the process of pinocytosis, the virions enter the host cell protoplast.
Stage # 3. Virus Multiplication:
After infection, the virus particle disappears from view. It ceases to exist as an organized unit and breaks up into its two component parts in the host cytoplasm. The viral RNA is thus released from the protein coat.
Uncoating of viral RNA is the initial step towards virus multiplication. It takes place within minutes after the virion gains entry into the host cell. This is known as the eclipse stage. Thereafter starts the multiplication process. Viral protein coat remains in the host cell cytoplasm.
The RNA component moves from cell to cell causing the production of new virus components which assemble to form more virus particles. Esau et al. (1966) reported that the virions of beet-yellow virus move intact from cell to cell through plasmodesmata.
Stage # 4. Sites of Viral RNA and Viral Protein Synthesis:
The widely held view is that the virus protein and virus RNA are formed by two separate systems. Entering the host cell the viral RNA takes control of the cell machinery and uses it to produce the viral components instead of the host cell parts.
The viral components are then assembled into new virus particles. The actual mechanism is a mystery. The account of virus multiplication given in books is highly speculative. One view is that the viral nucleic acid combines with or replaces part of that of the host cell. Thereafter the host cell produces the viral components at the expense of its own.
The other commonly held view is that the DNA of the host cell uses viral RNA to elaborate more viral RNA and protein. They are elaborated in the cytoplasm of the host cell, first the viral RNA and then the viral protein.
It is difficult to understand why the host plant DNA which is coded with specific information to build plant RNA and plant protein, starts building the viral components.
There is also a suggestion that the ribosomes in the cytoplasm of the host cell are associated with the elaboration of viral components. This assumption is based on the fact that viral RNA is related to ribosome RNA.
Entering the host cell viral RNA overrides that of the ribosomes and uses the latter to produce viral components. The ribosomes however are considered to have no genetic continuity. It is therefore, difficult to associate them with the replication of specific viral RNA.
Some virologists associate the replication of viral RNA with the chloroplasts in the host cell. The biochemical, cytological and genetic data have proved beyond doubt that chloroplasts are semi-autonomous, self-duplicating organelles of eukaryotic cells.
They thus have a genetic continuity of their own and contain DNA and RNA distinct from analogous nuclear constituents. The replication of chloroplast DNA takes place within the organelle. It is probable, therefore, that the DNA of the chloroplasts codes for the replication of viral RNA and protein.
The widely accepted view is that viral components arc formed by two separate systems. The released viral RNA reaches the nucleus, takes control of the host cell machinery and uses it to produce viral components instead of the host cell pans.
The nucleolus in the nucleus produces the new viral RNA which later escapes to the cytoplasm around the nucleus through channels present in the nuclear membrane. The TMV protein is synthesized in the cytoplasm very near the nucleus on cytoplasmic ribosomes.
The assembly of new TMV particles occurs in the cytoplasm on endoplasmic reticulum. The eclipse stage lasts for about 6 hours. By that time the first progeny of TMV appears in the cytoplasm.
However, the results of experiments with fluorescent microscopy and/or location of labelled anti-bodies and investigations of Reddi (1972) fell a different tale. They are at variance with the majority view. These indicate that TMV protein and RNA both are synthesized within the host cell nucleus.
The assembly of TMV particles also occurs in the nucleus. The assembled TMV virions of particles escape into the host ceil cytoplasm where they accumulate. The attack of TMV causes the leaves to wrinkle and become mottled.
The mottled effect on the leaves gives like the appearance of a mosaic. The disease thus came to be known as Tobacco Mosaic disease (host TMV).
The plant viruses, in general, are not as specific as the bacteriophages and the animal viruses. They have a wide range of hosts. The Tobacco mosaic virus for example also infects tomato. Grant (1934) investigated the host range of this virus and found 29 susceptible species outside the Solanaceae. The lack of host specificity of plant viruses is attributed to the absence of DNA from the plant viruses.