“No phone, no pool, no pets… king of the road,” sang American musician Roger Miller in the song “King of the Road” (1964).
Viruses travel light. While hardy enough to survive the elements, they enjoy the comfort of being indoors.
Viruses evolved from ancient cells, losing inessentials to slim down to fighting trim and vivacious virulence. Some avian and pig viruses get by with just 2 genes. As Roman Emperor Marcus Aurelius noted, “loss is nothing else but change and change is Nature’s delight.”
Each type of virus has its own distinctive size, shape, chemical composition, and host requirements.
Viruses are not even complete single cells. They come in a light coat but little underneath: no nucleus, no mitochondria, no ribosomes.
The vitals of a virus are its virion, comprising the virus’ genome packaged within larger molecules. Some viruses carry other equipment, notably enzymes, to accelerate production once a virus is activated.
A virion is encapsulated within a capsid: a protein protective coat put on when leaving lodgings in a host cell. Despite comprising few building blocks, capsids are intricately complex structures, sometimes with enormous conformational diversity.
“Viral capsids are marvels of biological engineering. They are sturdy enough to withstand pressure exerted by the tightly packed genomes inside yet can come apart or loosen easily to release the viral genome once the virus penetrates the cell. They are also great examples of genetic economy. Because of the limited coding capacity of viruses, capsids are built by using a few proteins over and over,” relates microbiologist Ekaterina Heldwein.
To make it easy on themselves, many viruses evolved capsids that self-assemble. Pakistani virologist Arshan Nasir: “Capsids became more and more sophisticated with time, allowing viruses to become infectious to cells that had previously resisted them. This is the hallmark of parasitism.”
Some viruses, mostly those that infect animals, also sport an overcoat: a lipid envelope derived from the host cell membrane. It helps them travel incognito, evading a host immune system.
Some enveloped viruses have spikes (peplomers): a glycoprotein protrusion out of the envelope but connected to the capsid. These spikes are sensors, essential for host specificity and viral infectivity. A peplomer will only bind to certain receptors on a host cell.
A virus assembles itself within its host’s cell. Hence, all viruses are obligate intracellular parasites.
Viruses are everywhere. Viruses inflict themselves on all life, including their own kind. Every organism is constantly interacting with viruses. “Viruses exist wherever life is found. They are a major cause of mortality, a driver of global geochemical cycles, and a reservoir of the greatest genetic diversity on Earth,” says American biochemist Curtis Suttle.
Viruses need only a genome large enough to invade host cells and redirect their activity to producing viral copies. Meanwhile, cells must carry on complex metabolic processes and maintain a communal existence.
Having minimal needs is why a virus may be only 20–300 nm in diameter, up to an order of magnitude smaller than a prokaryote. Small size facilitates infiltration. But it only works if one can rely upon one’s wiles.
The genetic stuffing of viruses has nothing to do with their ability to lead a furtive life. Viruses are an existence-proof that the intelligence of a mind does not have to be tied to a physical substrate.
Viruses are social: establishing networks of connections among compatriots. Cooperation during infection is common, as the infection process is seldom easy.
The advantage of viral cooperation comes in taking advantage of specialized skill sets. Some viruses are better at certain tasks than others.
Tactical decisions may need to be made. For example, to boost total viral production, viruses may want host cells to live longer. This requires not interfering too much with an infected cell’s self-maintenance.
If a virus is co-infecting with a stranger instead of friends, it may consider this competition. The virus will work its host cell to death as quickly as possible to thwart its rival.
Whether viruses qualify as a life form is a long-standing controversy. Viruses possess several recognized criteria of life. They have a genome. Viruses have enzymes which keep their genome in good working order via self-repair. They evolve. Viruses self-assemble, albeit within a host cell.
The typical virus does not have its own metabolism, nor can it reproduce by itself. The relatively large mimivirus is a known exception, and there may be others.
As to metabolism, many emergent lives – such as spores – start in stasis or kill time in a dormant state. A virus comes most vibrantly alive when it finds a home. A giant virus, thawed out of Siberian permafrost after being frozen for 30,000 years, roared back to being on the hunt once again.
A virus employs its own genes as a guide for assembling viral proteins and reproducing its own genome. Though using hijacked equipment, viruses manage their replication.
A cell with its nuclear DNA destroyed is dead. A virus can inhabit a dead cell, turning it into a viral zombie by activating the cell’s cytoplasm machinery to replicate.
A virus can even bring a cell back to life. Photosynthetic cyanobacteria and algae are often killed by ultraviolet (UV) radiation, which decimates their nuclear DNA. Viruses have in their toolkit enzymes to repair various host molecules, reclaiming the host from the grim reaper.
A cyanobacteria has at its photosynthetic center an enzyme that can be disabled by UV overexposure. Unable to metabolize, the cell dies.
But cyanophage viruses encode their own version of the bacterial photosynthetic enzyme. The viral variant is much more resistant to UV radiation. If a cyanophage infects a recently deceased cell, its photosynthesizer can replace the host’s, and bring the cell back from the dead.
Too much UV can kill even a virally revived cell. But if a cell harbors more than 1 disabled virus, the viral genome sometimes coherently reconstructs from genetic pieces. This self-assembly process is termed multiplicity reactivation.
In complementation, individual genes act in concert to reestablish functionality without fully reforming into a complete virus. Only viruses possess this “phoenix phenotype”: able to bring back the dead or self-resurrect. As Irish playwright George Bernard Shaw said, “Life is nothing but not being stone dead.”
Pathogenic viruses have been a threat to other life for so long that every type of cell has an immune system.
One strategy that many microbes use is to close up shop when viruses are noticed in the neighborhood. Many archaea and bacteria go dormant when they sense a threat. Fear is the most primitive emotion.
Dormancy may not work. Some microbes can only cheat infection by faking their death for a limited time, else the pose becomes a corpse.
Viruses have a counterstrategy: patience. Viruses can commonly wait out microbial dormancies, and so they too hibernate: quietly lurking until they sense nearby prey on the prowl.
Viruses gain entry to animals through the skin and mucosal linings, such as the nose, mouth, lungs, or eye membranes. Some viruses can be passed from an infected host through gametes to offspring.
Having entered a host, a virus attaches to a specific target cell that can promote its activation and reproduction.
Viruses have a selective host range: preferred prey. A virus recognizes its host cell by signature protein markers, called receptors, on the cell surface. (The term receptor here is something of a misnomer, as viruses are most certainly uninvited and unwelcome.) Receptor recognition occurs via subtle molecular bonding. “Pathogen host shifts represent a major source of new infectious diseases,” notes Chinese entomologist Ji Lian Li.
Some viruses specialize in a single cell type. Others, less persnickety, settle for several cell types that originate from the same embryonic germ tissue.
Once a target cell is found, the virus extends fibrous feelers that it normally keeps folded up. The virus roves about until it finds its favored surface receptor.
A virus may perform preparatory work for entry, including changing its structure. It ejects some of its proteins through the cell membrane, creating a path to slide in.
The virus then passes its genetic material in, along with its vitals. After entry, the protein path collapses, and the cell membrane seals.
Despite their delicate subterfuge, most viruses cannot help but leave telltale traces on the cell surface that an immune system may detect. These molecular marks are the makings of an evolutionary race between a virus and its host, to respectively hide and detect infection.
Once inside, a virus sheds its protective coating, freeing its virion to methodically take over the cell.
Some viruses use a host cell’s own mechanisms to gain entry to the cell nucleus.
From a structural standpoint, there are 2 types of viruses: those that comport themselves with either RNA or DNA in their innards. All viruses thoroughly understand genetics, regardless of form.
Most DNA viruses enter the chosen cell’s nucleus before activating. The poxvirus is a notable exception. It carries its own machinery for genome transcription. Thus, the poxvirus can ply its trade in the cytoplasm and thereby replicate quickly.
By contrast to DNA viruses, RNA viruses generally replicate and assemble in the cytoplasm, though there are exceptions.
Activation may not be immediate. Viruses may patiently await certain changes within and around a cell that signal an auspicious status. “Viruses make a ‘decision’ when they infect a cell as to whether or not this is a good time to lyse the cell and make more virus or whether it would be more propitious to integrate their chromosome into the infected cell’s chromosome, turn off their genes and sit there for generations. Then when things look good again they use a different but related pathway to excise their chromosome, in order to make more virus and kill the cell,” explains American molecular biologist Arthur Landy.
To exercise patience, a virus assembles an ensemble of proteins to insert its own genetic code in a precise location in the DNA of the host, thus ensuring that its DNA will persist for many generations of host cells. When the virus decides to activate for replication, it creates another protein ensemble to extract the DNA.
The viral DNA-packing ensemble incorporates key proteins that the cell uses to regulate expression of its own genes. Hence, these proteins reflect the state of the cell. Arthur Landy elaborates: “It makes the system gratuitously dependent on the proteins of the cell which serve as reporters of how well the cell is doing and where it is in its life cycle. This makes it exquisitely sensitive to the physiology of the cell.”
Each virus type exists with variants. One or more strains can become activated upon invading a cell, while other strains await more favorable conditions to activate. Activated viral nucleic acids combine with the necessary host-cell amino acids to replicate.
Enveloped viruses exude offspring through the host cell membrane (lysogeny). A viral nucleocapsid binds to the membrane, which encloses it in a pouch.
Pinching off the pouch sends the virus on its way. Budding of enveloped viruses results in gradual shedding, without immediate sudden cell destruction; nonetheless, accumulated damage from viral intervention hastens cell demise.
Nonenveloped and complex viruses release their batched brood when the host cell bursts open in its final death throw (lysis). Lysogeny and lysis are the 2 methods of viral offspring release.
Influenza viruses know the dangers of their occupation, so they produce offspring with a wide variety of shapes, maximizing the odds in their favor.
Antiviral measures target proteins on the surface of a viral cell. Knowing this, the flu virus can quickly swap out one set of proteins for another, making the virus notoriously difficult to track and destroy. “Viruses mimic the immune system in order to evade it,” marvels Australian molecular biologist Richard Berry.
Viruses understand their host at the molecular level. One influenza virus mimics a host-cell histone protein, inhibiting the cell’s production of antiviral proteins by repressing gene expression in the host that controls antiviral proteins. Via mimicry, the virus demonstrates its understanding of the epigenetic mechanism by which a host cell mounts its defense against the virus.
Other viruses cloak themselves by fabricating proteins and placing them on the surface of infected cells, deceptively telling the immune system that nothing is wrong. Measles goes further and eradicates host remembrance of infection, thereby robbing the host immune system of any knowledge it may have gained for fighting infection. “The measles virus preferentially infects cells in the immune system that carry the memory of previously experienced infections,” notes Dutch virologist Rik de Swart.
Viruses drive evolution by putting cells on the defensive, prodding cells to tighten their operations. American virologist John Schoggins elaborates: “In the molecular arms race between viruses and their host cells, each side employs multiple strategies to deal with the other. Whereas the host has sophisticated antiviral signaling programs to combat viral infection, viruses use their own proteins to subvert these host defenses. Viruses are often lauded for these clever evasion tactics. However, the host may also have its own brand of molecular chicanery. During infection, a host cell-derived antiviral molecule is packaged inside viral particles. As a stowaway, the antiviral factor is poised to trigger immune defense pathways upon infection of another host cell.”
Bacteriophages are viruses that infect bacteria. It’s a tough business, as bacteria have sophisticated anti-phage defense systems which recognize and target invaders.
Phages counter with genes that encode proteins which stall the bacterial immune system. To implement these anti-defense viral genes, a phage must enter a bacterial host cell and thwart the immune response.
The virus cannot possibly survive this initial assault to reproduce itself. The virus knows this. The initial attack is a sacrifice gambit. The virus’ compeers will carry on to mount the bacteria’s protein-making machinery once its defenses are down. “This cooperation between genetically identical individuals of a viral population is altruism,” explain Israeli geneticists Rotem Sorek & Aude Bernheim.
Some viruses help their hosts, particularly persistent residents. They may serve active duty as a front-line defense against infection of animal mucosal surfaces. Some strains of mammalian herpes virus help their host against bacterial infection.
Viruses provide DNA that can be employed to fight off infection by bacteria or another virus. More generally, viruses help train the host immune system to be more responsive and effective.
Viruses exit a host by discharge: bodily secretions, or even in droplets of moisture exhaled by a host.
Viruses survive outside, passively (inactively) traveling by various means. They may be whisked on the wind or jitneyed by insects. They often attach to particles, organic or inorganic, in water or soil. Waterborne viruses are especially fond of polluted water, where they thrive on bacteria.
Although viruses are commonly portrayed as pathogenic, most are not harmful. Many are beneficial to their hosts: helping provide a better living for their host bacteria, fungi, plants, insects, and animals of most every species.
More than one virus can infect the same cell. Depending upon their social inclinations, different viruses that meet may decide to collaborate, fashioning a new type of virus by mutually contributing apt genetic material.
Viruses intelligently add to their toolkits with infectious enthusiasm. “Viruses are routinely pressured by host reactions to alter their genomes with host nucleic acids or leave parts of viral nucleic acids in the host genome,” explains American paleopathologist Ethne Barnes.
Viruses evolve more than themselves. Viruses have been accelerating the evolutionary adaptivity of all other life since their origination, shortly after prokaryotes arose.
Viruses either invented DNA or appreciated the innovation when they encountered it. They then spread DNA, unifying all life into a compatible genetic regime, thereby providing the illusion of a universal common ancestor.
The most direct way that viruses vector evolution is by injecting genes into host cells. When a host cell manufactures a new virus, some host genes may be incorporated. The new virus carries this genetic material to a new host, effecting gene transfer between hosts.
Viral genes may be added that become a critical part of the host species genome. 8% of the human genome is viral in origin, including the ability of cells to grow into tissues and organs, and to reproduce sexually. Animals would have never evolved beyond blobs of cells without viral innovations. “Most eukaryotic genomes are essentially old battlegrounds between critters and their viruses,” says American entomologist Joe Ballenger.
Viral genic injection is only the beginning of an evolving story. These interlopers provoke cellular genetic innovation to counter them, furthering host evolution.
Ishi Nobu, The Web of Life, BookBaby (2019).