The herpes virus is a viral family shrouded in fear. It was named after the latin word herpein which means “to creep,” and is often reminiscent of uncomfortable grade school health classes.
In fact, there is good reason to be frightful of these all too common bugs: once you contract one, it is very likely to linger for life. Chicken pox and shingles, mononucleosis and oral and genital herpes are all diseases caused by herpes viruses that have evolved the ability to lay dormant in the human nervous system (or sometimes lymphocytes), and become reactivated at random. This dormancy stage is called a lysogenic cycle.
In order to accomplish this waiting game, a virus inserts its DNA into the nucleus of a host cell, which is copied every time that cell divides. This is the cause of reemerging cold sores and late-life shingles rashes: it is impossible to know when the virus will become active again.
Humans are not the only animals that suffer from herpes viruses. Most animals on the planet have associated herpes viruses that plague them; never causing enough harm to compromise their host and persisting steadily within a population. It is an extremely successful evolutionary strategy.
However, because of this close viral-host relationship, each herpes virus can only infect the species it evolved to plague, otherwise they are either completely ineffective or completely lethal.
Herpes B virus is an example of the latter. Albert Sabin, a famed polio researcher, used massive amounts of rhesus macaques in order to test different vaccines.
One of his fellow researchers contracted herpes B, which affects old world monkeys in the same way oral herpes affects humans. However, when physician William Brebner became infected, the virus destroyed his central nervous system and led to his death. Brebner was a dead end host: the virus could neither persist nor be contracted by a new host and thus became an evolutionary dead end.
This example highlights an important fact about the herpes virus family: they are extremely host specific, which is an advantageous characteristic for containment. Diseases that have not become so closely intertwined with human history tend to cause a far more deadly infection - for example, the Ebola virus.
In order to keep up residual infections inside their natural host, herpes viruses have had to come up with some ingenious evolutionary strategies. The immune system, the cells and organs associated with identifying and destroying invading pathogens, is constantly on patrol for infected cells.
Normally, cells that are compromised by a virus initiate apoptosis, a programmed form of cell death. However, a long evolutionary history has allowed the herpes family to invent species-specific ways to persist, avoiding immune detection.
Researchers at the UW-Madison have begun to tease apart the evolutionary arms race that has evolved between cytomegalovirus (a herpes family virus) and the human immune system. Such a relationship is often referred to as the red queen effect. Every time the host evolves a defense against the virus, the virus evolves a way to evade the defense; in other words, you have to keep running to stay in the same place.
Cytomegalovirus is associated with deafness, intellectual disabilities and learning disorders in newborns. New research in this field was conducted by co-lead authors Emily Albright, a graduate student, Song Hee Lee, a former postdoctoral researcher, and Rob Kalejta, professor of molecular virology and oncology. Other members who contributed to the research include Jeong-Hee Lee and Derek Jacobs.
Kalejta et al. have discovered a unique intrinsic immune response of human cells toward this virus, in which the cell secretes proteins that cause dormant virus DNA to become active. This might appear to be counterproductive, as dormant infections are agreeably less problematic than active ones.
However, this process allows the immune system to find infected cells more easily, conferring a significant advantage over the virus.
True to its evolutionary form, human cytomegalovirus has developed a way to block the cell’s signaling. The virus, along with viral DNA, injects a protein into each cell it infects, somehow blocking the cells’ defensive adaptation. Although the mechanism is not yet well understood, the team believes such discoveries are key to developing a cure.