I just stumbled upon Giant Cells in a textbook and thought I'd do a bit of browsing.
I was surprised to find that Giant Cells are poly-nucleated cells. That is, they are several fused cells together:
http://www.online-medical-dictionary.org/P...=Polykaryocytes
Polykaryocytes
Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus.
and, often are T Cells
http://www.ncbi.nlm.nih.gov/pubmed/1312298
What is the significance of this? Apart from in cancer and diseases like arterial disease?
Well, what struck me almost immediately about this is that polykaryocytes look in principle similar to early models of how multi-cellular colonies which led to all higher eukaryotes first form - they are observed to form naturally by cell division that doesn';t complete propperly.
I then thought, what about viral infections? Early viruses wouldn't have hads clever coats to get themselves past the cytoplasm, they would have been vulnerable and thus need a way to traffic about. Logically, social networks of host would be beneficial for ANY parasite therefore, there would be a handy spin off of inducing polykaryocytes in that the continuous cytoplasm would make it easy to infect many cells. If cells could be brought together in this way, they would act as a great vector for an intracellular minute pathogen.
Then I recalled a recent remarkable report I came across on 'blebbinbg' - a rediculously important biological phenomena which demonstrates that the cytoplasm is self managing and organising and can completely detach sections of the cell body to go off and then come back to the master cell by its own power. These 'blebs' are seen in many human cells. The thing that was reported is that macrophages can pass 'blebs' of their own cell, containing viruses to LYMPHOCYTES that flock around the macrophages. This is part of the immune surveilance and communicating system.
I also proposed that red blood cells can actually do the same but that is far from proven, though it could happen through macrophages that naturally eat RBC's as part of biological clearance.
The 'bleb' is part of a smart, networked cytoplasm.The brain itself has a similar network of tubes that cause the cytoplasm to integrate between many cells, something which is central to other hypotheses. What I have wondered is whether cells of the eukaryotic order evolved their smart cytoplasm in response to parasitic invaders. This in fact is a likely situation, because the growth of eukarotes is tied to oxygen, and the emergence of cell nucleus is tied to emergence of the mitochondrion which originated probably from a Rikettsia like organism. Thats important because the smart cytoplasm, and cell size is probably tied to all these features, as larger cells must need a lot of local organisation and not be reliant of central control - something that long nerves demonstrate.
In short, my hunch is that what may have helped trigger this is the need by parasites or viruses to induce cell-cell contact of cytoplasm as a means to transmit the parasite.
Naturally, the parasite becomes embedded in the cell, but by inducing a vector, that may be inherited, infected cells may have a propensity to become networks.
The parasite could minimise its damage merely by switching itrself off and becomming dormant, thereby not killing the enabling vector carring host.
If this was by virus rather than bactia, it would end up in cell code and be inherited as well as transmitted. This means that a species with network forming behavior is encouraged.
Which organisms would be most prone to this?
The predatorial cell that eats other cells, such as bacteria. The origin of all eukaryotes were protists and they seem to have long evolved macrophage like ability to phagocytise (envelop and injest) other cells. This predatorial like behavior gave rise to injestion of cells that would be forced into symbiotic relationships.
The injested bactera would undergo reactions to the stress of injestion, if this process is disrupted it may survive in a number of ways. This can include the observation that isolation from preferred nutrients causes prokaryotes (i.e. bactera) to go into a kind of remarkable dormancy that would in fact potentiate the chances of symbiotic evolution. This dormant state results in metabolic shutdown and the cell actually mutates its own code under this hibinatory setting. Subsequently, mutations that allow the cell to metabolise other nutrients actively results in in reversal of this state, retention and expresion of the mutant code, and cell activity proceeds. This means that prokaryotes evolve in a controlled way whilst alive, similar in some ways to what Lamark had suggested, but also ultimately like the Darwinian process of (enhanced) selection.
As this would allow the injested microbe to adapt to its new setting, whilst temporarily shutting down, the microbe can evolve the ability to use whatever byproducts the Protist has available it does not know what to do with, such as perhaps in some settings, i.e. oxygen and plant polysaccharides.
Now, to assist this, the bacteria that the Protist is injesting would over time get quite fed up with this and evolve by normal selection to 'hide' from protists and avoid injestion, This may mean that they can hide more easily on the inside of the cell, thus facilitatiung symbiotic development rather than being sent off to the corrosive digestion centres of the Protist, or feeding off of byproducts thereby produced..
Since early Eukaryotes would have had new organelles formed from more complete bacteria, they would trhus represent useful environments for those microbes, who would be under selective pressure to exploit this life cycle whilst still capable of independent life - thus a minimally harmful parasite is selected for, whilst it evolves new metabolic pathways compatible with Protist wastes. This couyld already have been potentiated whilst the bacteria were outside the Protist. The parasite woulds also not want to harm the host, so that bacteria living outside a Protist infected with its sibblings would benefit from the Protist surviving, and tend to avoid defensive behaviors against Protist predation, if beneficial to numbers and parasite spread. Note how many parasites excel at using host as transmission vectors rather than terminals, indeed, fruits even do this despite damage to the parent when they are fed on.
What early eukaryotic colonies demonstrate, in the Sponge, is a very early innate immune system based on self / non self recognition, and cruciually, are able to reject other sponges whose cells are able to invade. The early immune system looks very much like the system of auto-immunity and cell policing / rejection seen in all higher eukaryotes and in many human diseases. The immune system goes even further in the sponge, which could tell us a lot, and this is that bacteria are preferencially grown and defended by the Sponge that attack other invading spongfes and their bacteria. This means that early symbiotic relationships with 'freindly' bacteria' like those of the gut, are part of the immune system, as you would expect. SA defensive shield of microbes has always been employed.
What I suspect is that colocation of Protists and bacteria/archea results in a pattern of selection that shows mutual tollerence and non predation of those microbes that have poarasitic life cycles. These eventually evolve into stripped down, minimal organelles that are dependent on the host, like mitochondria, but the process may have helped Protists coexist with related species, thus they had a tendency to colocate (sharing similar chemistry inside and outside the protist due to efluent of byproducts) and mutually defend the relationship against others.
multitasking
Since cells can evolve multiple energy pathways, which is especially true in eukaryotes, they are not forced into defensive evolution by the loss of one pathway - they can switch. This means that evolutionary conflicts are avoided and thus symbiotic relationships can more readily evolve. For example, early algae almost certainly already had mitochondria, and then copted independently several times cyanobacteria which became chloroplasts. Protists with different stages of this chloroplast development ranging to more cyanobacterial forms in their cells have been found.
The development of different metabolic pathways favours Protists with an ability to accomodate more than one symbiont. There seems to be many different symbionts each forming different animal cells organelles. Thus the host favours size, whilst symbiont favours smallness, so Protists naturally form from the larger cells, and end up with more symbionts. As we speculated above, parasites and early symbiants would favour protists that could fuse at least temporarily, or exchange 'body fluid' like Blebs, over Protists that couldn't do this. In turn, fused cells are under selective presure and this favours the smartest, best self organising cytoplasm so that the network has some chance of organisation as a group and surviving the fusing process.
So, I think it plausible that parasites would tranbsfer genes and tend to inflence behaviors that would favour growth of cell host and cell cytoplasm connection, and they would favour a pattern that made them dormant when nutrient sources are unavailable. This in turn, provided that this situation is not potentiated, would favour symbiotic relationships that are not harmful to host growth, whilst the m,acrophage like feeding of the Protist host leads to other parasites and symbionts that would feed the cell when the other symbionts were starved and dormant, thus allowing the host to survive changing environment and spread throughout the sea and eventually the land and sky.
This greatly iuncreases dispersal and survivability of these adapting parasites. For example, in the pro-algal Protist, infection with mitochondria and cyanobacteria would allow it to survive different environments and disperse across the ocean, exactly as many algea do, somer of which can swim due to these multiple power sources that they can use.
Finally, it would make sense that predation on given microbes will force parasitism, enhanced by remarkable processes of adaptation, and by a pressure to make eukarotes with cytoplasm large enough and manageable enough to tollerate infection which seems to have resulted in the evolution of a more independant cell nucleus, another key feature of eukaryotes, it would also tend to favour in the early stages external co-association of the parasite relatives which may have been intrumental in the evolution of microbial tollerence and relationships such as those seen in the gut, which modulate immune responses to them and other microbes (sometimes in a hodstile way to bacterial competitors) and this will select for Eukarotes that benefit from parasites to not attack parasite relatives or kin outside of the cell, and infection would tend to push towards whatever was the best thing for it. The Protist can only survive this by managing nutrient supply and 'regionalising' infection to maintain a grip of evolutionary direction of the parasite towards a symbiotic one bgy controilling its activity metabolically or by destroying it. The host will always tend to evolve such balancing powers, and will have interbnal infection defenses anyway as a result of its predation of microbes which have all sorts of hostile capabilities.
The parasite, I think, will evolve to 'implant' a vector enhancement as it infects any host as a general riule of thumb. Thus viruses may evolve to implant behaviors that cause infected cells to traffic more from their surface and admit more viruses. Vuiruses in turn would evolve to transfer things of benefit. In turn, thius may create the mechanisms of transfer responsible for sideways gene transfer, which the organism can use to innovate new abilities, and are in the interest both of the host DNA and the transferred material. The exciting possibility is that an 'economics' emerges in which trafficking results in prokaryotes (and the prokaryotic ancester of Eukaryotes) to have the ability to traffic and turn to their advantage trafficked genes, thus ensuring greater spread and survaival of trafficked code (i.e. the ability of prokaryotes to control gene expression following mutation in low metabolic states may itself be trafficked by a kind of self serving parasite, rather than be viewed as host evolved defense against parasites, although both probably happen to the same exact end. There is possibly here a remarkable cross stimulation of effects on evolutionary pressures). This in turn accelerates evolution of the infected, and their ability to further evolve may be inherited in this way and enhanced. And, in Protists, it may have led towards the cytoplasm that can be healthily infected and/or the cytoplasm that connects?
What may be transferred may be benerficial, and from many kinds of infection, viral maybe, in which viriuses are merely the pathogenic variation of another machinery that is healthily and proffitably traficked, whilst other infections can control host behavior and also traffic genes with it. There are probably a multitude of processes responsible, and they are horizontal, with various vertical effects (i.e. inheritence of parasites in the cytoplasm or host genetic code additions from viruses / parasite.