Plant cells, while superficially similar to animal cells in basic construction as far as all organelles except chloroplasts and often extensive vacuoles are concerned (see here), have one large and fundamental difference to animal cells, which profoundly affects the way in which they are infected by viruses, and how viruses move between them.
This is their possession of thick, rigid, cellulose-based cell walls.
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| Plant cell section, showing nucleus, chloroplasts and vacuole | Detail of cellulose and chloroplast |
copyright Russell Kightley
Every cell is
separated from every other cell by thick cell walls, whose dimensions are far
larger than
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| Plasmodesmata |
the size of the average virion (ie: >1
micron, cf. TMV = 300
nm). This means that plant cells are effectively inaccessible to viruses,
even given mechanisms of injection similar to the T-even phages. Live
plant cells interconnect only via specific discontinuities in the cellulose
walls: the most numerous of these are plasmodesmata, which are
complex structures filled with membrane-derived processes continuous with the
endoplasmic reticulum. These are "gated" intercellular channels,
which limit the passage of molecules between cells, and certainly do not
admit particles as large as virions. Plant viruses have therefore evolved
specific movement functions, mediated by one or more virus-specified
proteins, which interact with the plasmosdesmatal machinery so as to increase
the "pore" size, and allow specific transport of viral nucleoprotein
complexes. All plant-infecting viruses possess one or more movement-related protein (MP) genes: these are
very varied, although there are distinct groups of them, and they appear to
largely derive from host plant genes for chaperonins and plasmodesmata-associated
proteins.
Plant viruses, therefore - which
are almost overwhelmingly ssRNA +ve sense and non-enveloped -
do not appear to specifically interact with host cell membranes or cell
walls, as do bacterial and animal viruses; even when the
plant-infecting virus also infects an animal (eg: plant rhabdoviruses and
bunyaviruses) and presumably behaves normally in the other host, and even
though apparently plant cells are capable of phagocytosis /
endocytosis. The mechanisms employed to enter cells rather appear
to be passive carriage through breaches in the cell wall in the first
instance, followed by later cell-to-cell spread in a plant by means of
specifically-evolved "movement" functions, and perhaps spread via
conductive tissue as whole virions.
See here for a new model of plant virus movement
The "passive carriage" referred to above could mean:
The mode of transmission of viruses affects their concentration and
localisation in plants. For example, mechanically transmitted viruses
(eg: bromoviruses,
tobamoviruses) tend to reach very high
concentrations in most tissues of a plant (up to 4g / kg plant): this is
necessary for survival, as it guarantees that a large number of virions will be
present for onward transmission by whatever non-specific means presents itself.
Viruses which are introduced into plants via insect vectors with piercing
mouthparts, on the other hand, tend to be limited in their multiplication to
phloem elements, which are preferred target tissues for insect feeding.
Consequently, these viruses (eg:
luteoviruses,
geminiviruses)
reach only very low concentrations (mg / kg) in whole plants.
See also here for insect transmission:
An EXCEPTION to the above rules are some of the PHYCODNAVIRIDAE, which infect marine and aquatic algae and some protozoans, which have large (>300 kb) dsDNA genomes, and very large (130 - 200 nm), complex virions. Exemplars which infect algae appear to have specific enzymes at the surface of virions which may degrade the CHITIN cell wall of the alga, to allow interaction of the particle with the cell membrane directly. Some of these viruses also appear to be able to "inject" their DNA, much as phages do, and to enter a lysogenic state.
A useful Web page describing phycodnaviruses and other large-genome DNA viruses - though dated - is GiantVirus.Org.
See also these posts in MicrobiologyBytes:
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Fungal hyphae - of Penicillium sp. |
There are certain superficial similarities between plants and FUNGI with respect to the cell wall; however, in the latter case, cell walls are composed of CHITIN, a different complex polysaccharide, and fungal hyphae are often effectively "tubes" with no cross-walls.
No fungal viruses appear to have any specific mechanisms for gaining entry to fungal cells; indeed, it is extremely difficult to demonstrate the infectivity of virus-like particles, and it is only since the advent of the GENE GUN or biolistic transformation apparatus, that many viruses have been shown to be infectious at all - by being "shot" into fungal cells adsorbed onto metal particles.
It is probable that most fungal viruses - like the plant-infecting CRYPTOVIRUS genus of the mainly fungus-infecting Partitiviridae - are only transmitted by "grafting", or the physical connection of infected to healthy cells by anastomosis. Thus, fungal mating is a good means of transmission, as it results in the mixing of cell contents of different hyphae. Otherwise, transmission would be vertical, or to progeny via spore formation.
It is claimed - in the ICTV 8th Report article on Narnaviridae, which include the chestnut blight fungus-infecting mitoviruses - that most fungal viruses have no extracellular stage. Indeed, narnaviruses do not even make particles.
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Plant&Fungal |
Copyright Ed Rybicki, August 1997, October 2000; September 2003,
April 2008
(Unless
otherwise stated)
