Can Viruses Cause Stuttering, Part 1?

In previous posts, we discussed the dopaminergic hypothesis of stuttering, i.e., that the root cause of stuttering may be excessive dopaminergic activity in the basal ganglia area of the brain. We can now ask what might be the root cause of the abnormal dopaminergic activity. Many think that it may be a genetic cause--through inheritance or through an unlucky throw of the genetic dice, stutterers have a faulty genetic system that expresses itself as excessive dopaminergic activity.

But there may be an alternative explanation. An intriguing article in Discover magazine raises the possibility of a virus being the root cause of other neurological diseases such as schizophrenia, bipolar disorder, and multiple sclerosis. The website for this article can be found at

http://discovermagazine.com/2010/jun/03-the-insanity-virus/article_view?b_start:int=3&-C=

Much like stuttering, imbalances of dopaminergic activity have been observed in the brains of individuals suffering from schizophrenia, but this abnormal activity occurs in a different combination of the brain's anatomical regions. And until recently schizophrenia was also thought to result from bad genes.

The Discover magazine article raises the possibility that schizophrenia begins with an infection. Many schizophrenics show chronic inflammation with respect to their infection-fighting white blood cells. Moreover, they often carry antibodies resulting from viral infections but not the viruses themselves, suggesting that they had been exposed to those infectious agents at some earlier point in their lives.

Viruses are not necessarily passed from person to person by bodily fluids or other contact. Rather, some may live permanently in the human body at the very deepest level intermingled with human DNA. Some researchers now believe that retroviruses, which are types of viruses that convert RNA into DNA, could be the culprits explaining a number of neurological ailments.

Viruses like influenza or measles kill cells when they infect them. But when retroviruses infect a cell, they often let the cell live and splice their genes into its DNA. When the cell divides, the resulting pair of cells carry the retrovirus’s genetic code in their DNA into future generations.

Although it is a rare random event, over the last 100 million years various retroviruses have gotten into human genomes by having infecting one of our animal ancestors in the evolutionary chain. About 100,000 retrovirus sequences appear in human DNA, accounting for more than 40 percent of all DNA. These retroviruses are usually tied up in tight stacks of proteins, but once in a while they slip out, switch on, and start manufacturing proteins beginning the process of infection. About 5 percent of the RNA produced in the brain arises from what appears to be “junk” DNA, which also includes endogenous retroviruses. The presence of RNA could mean that viral proteins are being manufactured in the body more frequently than previously thought since RNA is a step in the path to making proteins.

Although the body tries to keep endogenous retroviruses under control, infections can destabilize this balance. Many infections, such as herpes, toxoplasma, cytomegalovirus, and a dozen others may awaken a retrovirus. The retrovirus contains proteins that activate the immune system during these infections and the white blood cells produce inflammatory molecules called cytokines that attract more immune cells generating a cascading effect.

Whether people develop a specific neurological problem may depend on how their immune system responds to a retrovirus. Several studies implicate immune genes called human leukocyte antigens (HLAs) that are instrumental in the body’s ability to detect invading pathogens. The response to an infectious agent may be why one individual develops a specific neurological ailment and another person does not.

As a concrete example, human DNA has been found to have human endogenous retrovirus W (HERV-W) at specific addresses on chromosomes 6 and 7. Several studies have found active elements of HERV-W in the blood or brain fluids of people with schizophrenia (49% of schizophrenics vs. 4% of healthy people). The more of these active elements they had, the more inflammation they exhibited. In schizophrenia inflammation may overstimulate neurons. The neurons, being excited by these inflammatory signals, discharge neurotransmitters, leading to such symptoms of schizophrenia like hallucinations, delusions, paranoia, and hyper-suicidal tendencies. Some initial infection could have set off a lifelong pattern in which later infections reawaken HERV-W, causing more inflammation and eventually symptoms, explaining why schizophrenia waxes and wanes like a chronic infection.

In summary, genes may lead to a specific neurological problem only in conjunction with certain environmental kicks and a genome’s myriad of parasitical retroviruses might provide part of that kick. Retroviruses can be activated by inflammation resulting from infection and possibly even cigarette smoke or drinking water/food pollutants. In addition, we cannot rule out at this point that a stressor activating a retrovirus might be an emotional trauma affecting the immune system rather than some initial physical invasion. Since stuttering has some parallels to schizophrenia in terms of dopaminergic activity imbalances, a viral cause of this ailment should certainly be considered.