In 1898, Friedrich Loeffler and Paul Frosch discovered that the cause of foot-and-mouth disease in livestock was an infectious particle smaller than any bacteria. This was the first clue to the nature of viruses.
Viruses are responsible for some of the worst diseases inflicting mankind: smallpox, the common cold, chickenpox, measles, influenza, shingles, herpes, polio, rabies, Ebola, hanta fever, and AIDS are just a few examples of viral diseases.
Fortunately, most of the 500 different varieties of viruses from 80 different families do not affect humans but do affect other animals and cause blights on plants.
Viruses are genetic entities that lie in the gray area between the living and nonliving.
On their own, viruses are either DNA or RNA, which carries the genetic code for the virus, surrounded by a protein coat. While isolated outside a host cell, the virus is metabolically inert and cannot replicate.
A virus infects a host cell by attaching to a specific site on the surface of the cell via an amino acid sequence on the protein coat of the virus, which is “tuned” to attack certain kinds of cells.
Some viruses enter the cell, while others only inject their genetic material into the cell. In either case, the virus takes control of the cell’s factory and uses it to assemble many copies of the original virus, which it then ejects to infect new cells. In the process the host cell dies.
Some viruses may remain dormant inside host cells for long periods, causing no obvious changes, but when stimulated it activates, manufactures new viruses that self-assemble and burst out of the host cell, killing the cell and going on to infect other cells.
This is the case with the varicella virus that causes chickenpox. It reappears as shingles in more than 10% of adults who had chickenpox as children.
The human immune system is normally very efficient in identifying and destroying invading microbes.
The immune system learns to recognize and then remembers certain proteins, called antigens, on the invading microbes and builds specific antibodies that will attack them upon subsequent invasions.
Immunization works for some kinds of viral diseases such as smallpox, measles, and polio, but not for others.
The influenza-A virus is especially adept at fooling the immune system because of two types of changes that take place on the protein coat of the virus.
‘Antigenic drift point mutations’ that result in changes in as few as two amino acids may allow the virus to sneak unrecognized past the antibodies acquired from previous influenza infections, thereby fooling the immune system.
The other mechanism of antigenic variation is ‘antigenic shift,’ which occurs either when viruses bearing unique combinations of two types of proteins enter human populations from an animal host, typically birds or pigs, or by a re-assortment of proteins between animal and human influenza-A viruses.
From 5% to 40% of the general population gets the flu annually, depending on the severity of the influenza strains in a flu season.
With all of the complexities of the information in the human genome, it is surprisingly easy for an invading virus to subvert it.
The great mystery is how the relatively simple genome of the virus is capable of commandeering the host cell’s own DNA to manufacture viruses instead of assembling the proteins that it normally builds.
The information carried in the genome of the virus is minuscule compared with that of the host cell. Each cell uses only certain parts of its entire DNA sequence, depending on what type of cell it is; yet, viruses are able to thwart the process and take over the cell completely.
A virus may incorporate genetic material from its host as it is replicating and transfer genetic information to a new host, even one unrelated to the original host.
Some researchers suspect that this may serve as a means of evolutionary change, although it is not clear how important an evolutionary mechanism it is.
Richard Brill is a retired professor of science at Honolulu Community College. His column runs on the first and third Fridays of the month. Email questions and comments to brill@hawaii.edu.
