The first virus to be discovered was the tobacco mosaic virus (TMV). In the 1880s, researchers figured out that tobacco plants could “catch” what appeared to be a contagious “germ” from other, infected tobacco plants. Subsequent researchers knew enough about bacteria to know how to search for a bacterial pathogen by filtering extracts through special filter paper, etc., but none of those methods worked to find the cause. Someone figured out that it wasn’t just toxins produced by an infected plant, but that there was some agent that was reproducing, and that generation after generation, could still infect tobacco plants. Attempts to grow the pathogen on petri dishes were unsuccessful. Researchers were also puzzled by the fact that, unlike any bacteria (living cells) that were known, this pathogen could not be killed by alcohol, thus they were beginning to suspect some kind of chemical that could only reproduce when inside an appropriate host. Finally in the 1930s, TMV was found by crystalizing it! Indeed, it was a “chemical” that could reproduce like it was alive, yet needed the cells of a host organism to do so, and could be crystalized, but remained “viable” and infectious even then.
The smallest viruses are smaller than ribosomes in cells, and the largest are so big that they’re just barely visible under the highest power of magnification possible with a regular light microscope. A single virus particle is called a virion, and is made of nucleic acid (either single or double-stranded RNA or DNA depending on what kind of virus it is) in a protein shell. The viral nucleic acid (RNA or DNA) is one molecule (one “chromosome”), consisting of from four to several thousand genes in length. Much current DNA technology research is aimed at inserting “good” genes into otherwise harmless viruses, then letting these infect animals/humans as a way of inserting the needed gene into the host’s cells. The surrounding protein coat that encloses the viral nucleic acid is called a capsid, and its shape, its protein structure, is specific to each kind (“species”?) of virus. An isolated virion is inert: it has no metabolic equipment, thus cannot do any chemical reactions on its own. Virions can be separated into separate nucleic acid and protein components, each separately crystallized and stored, and yet if mixed back together, can reassemble and be just as “viable”, as infective, as before.
Viruses are obligate intracellular parasites, that is, they can express their genes, do chemical synthesis of more viral nucleic acid and protein, and replicate only within a living cell of the correct host species. When a virus enters a host cell, it “takes over” the host cell’s metabolic machinery and chemical pathways and uses these to make more virus protein and nucleic acid, which then spontaneously come together to form not two, but MANY new virions. Viruses are capable of replicating many copies of themselves, which then go infect other cells. However, each type of virus has a limited range of host cells. For example, TMV won’t infect humans, but because humans are closely related to gorillas, many human viruses can be transferred from humans to zoo gorillas and make them very sick (hence one of the reasons why people aren’t allowed to feed zoo animals). Viruses use a sort of chemical “lock and key” mechanism to join to receptor sites on the surface of their host cell, thus the host may be only one or or several closely-related species. Some viruses can insert themselves (their DNA) into their host’s genetic material, stay there, and replicate along with host DNA when the host cells do mitosis. Herpes viruses are especially known for this, and it is thought that some forms of cancer may be caused in this way.
Bacterial viruses (viruses that infect bacteria — yes, such things really do exist!) are known as bacteriophages. When these replicate, they then burst out of the host bacterium cell, killing it as many viruses are released. Many plant viruses are passed in the usual way by contamination from another infected plant (don’t work in the garden when the leaves are wet), but some others are passed to the next generation in the seed. Many animal viruses have a slightly different way of entering or leaving their host cells: many have an external membrane “cloaking device” which is derived from the cell membranes of their host cells. This bit of borrowed cell membrane helps the virus to enter/leave a host cell unnoticed, and without “exploding” the host cell. To infect a new cell, the membrane surrounding the virus joins with the cell membrane of a host cell, and the capsid and nucleic acid sneak inside. When the new virions leave, each wraps a bit of cell membrane around itself on the way out. Viruses like Rubella, Rabies, and HIV can also cross the placenta of an infected female mammal and infect her growing baby. If the baby lives, it may be deformed (Rubella) or be born with a viral infection (HIV and Rabies). Interestingly, because Rabies can be transferred transplacentally, many zoos will no longer accept donations of “pet” skunks because there is a question as to how many generations of captive-rearing with no signs of Rabies are necessary to insure that an animal is, indeed, free of Rabies.
One of the biggest questions about viruses is, “Are they alive?” Consider that viruses
Almost all know medicines, such as antibiotics, work by inhibiting some specifically bacterial chemical function, thereby killing the bacteria without harming our cells which don’t do the targeted chemical reaction. Since viruses use our cells to do their work, there is really no antibiotic that can effectively inhibit their growth without messing up the workings of our cells. Thus, despite all the frantic AIDS research, there remains no known cure, no antiviral agent to zap viral infections. Antibiotics do NOT help, and may actually make matters worse. Because antibiotics kill the good bacteria in your system (even if bad bacteria are present), taking them can cause secondary fungus infections. Additionally, if some “bad” bacteria are present in your system, there’s always the chance that there will be just that one mutant one with the chemical machinery to survive the antibiotic, and via natural selection, live to reproduce and pass on its resistant genes when all the others have died. This is how multiple-antibiotic-resistant strains of bacteria develop (multiple-drug-resistant Staphylococcus aureus — “staph infection” — has become such a bad problem in hospitals, etc. that medical people now refer to it by the nickname, “M-D-R-S-A”). Additionally, the more your body is exposed to antibiotics, the greater the chance that you might develop an allergy to one or more, and not be able to take it/them when you really need to. It does no good to take antibiotics for a cold (unless you count the money you just gave to the doctor and drug company as being to their benefit).
The good news is that our immune systems can “learn” to fight off previously-encountered viruses. The first time you are exposed to a virus, your immune system starts to make antibodies against it, so that next time you get an invasion of that virus, you can fight it off without getting sick. Some viruses, like those that cause colds and flu, mutate so quickly (we talk about various strains of flu virus) that they become so different from the last one to which you were exposed that you immune system doesn’t have the right instructions to fight off the new variety. Some viruses, like small pox, mumps, and measles, mutate more slowly, so for these once someone gets the disease, his/her immune system can fight any future exposures and the person doesn’t get sick again. For these viruses, any exposure to even a closely-related strain will trigger an immune reaction, hence vaccination, harmless variants/derivatives of pathogenic viruses, are effective in stimulating the immune system to “learn” how to fight future exposures. As you hopefully recall from our discussion of the immune system, one big problem with the AIDS virus is that it infects and destroys the cells of the immune system that are needed to create immunity to fight off any new pathogens. A person who has been exposed to the AIDS virus does make anti-AIDS antibodies (AIDS testing involves checking for the presence of anti-AIDS antibodies, not the actual virus, itself), but often cannot make antibodies against anything new, thus usually ends up dying of some secondary infection that his/her immune system couldn’t fight.
Copyright © 1997 by J. Stein Carter. All rights reserved.
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