Student guest post by Andrew Behan
Type I Diabetes Mellitus (T1DM) is a disease most affecting children (previously named juvenile-onset diabetes). However, adults can still develop this life-threatening illness. Research in the genetic arena has provided evidence this disease is partially due to inheritance, leaving a portion of causality yet to be determined. More specifically, a look at certain viruses which attack the beta cells of the pancreas, the cells responsible for producing insulin, have provided new information regarding etiology of T1DM. Some recent research aimed at enteroviruses as pathogens for triggering T1DM has sparked the interest of scientists and general public alike.
First, a quick overview of enteroviruses. Enteroviruses are second only to rhinovirus in terms of incidence worldwide (2). When a susceptible falls victim to an enterovirus, most will never know they contracted the virus. A minority will experience influenza-like illness (ILI), presenting with symptoms such as headache, malaise, stomach cramps, diarrhea, vomiting, or fever. A small percentage of that minority will have major complications, such as pericarditis or myocarditis, and possibly sudden death (1). Interestingly, the CDC reports enteroviruses are responsible for almost 50% of sudden deaths in the U.S. In regards to cost of healthcare and loss of productivity due to enteroviruses, the CDC states $132 billion dollars is spent yearly as a result of enteroviruses, with about $90 billion due to direct healthcare costs and the remaining $42 billion lost as a result of loss in productivity (2). With this point in mind, it is no wonder research has been targeted at this nasty group of viruses in hopes of finding vaccines to prevent premature death.
Enteroviruses have only recently been studied in relation to T1DM, due to improvements in diagnostics. The technology to detect enteroviruses enabled researchers in England to study its possible link to T1DM, especially in children. One such study, "Enteroviruses May Play Role in Type 1 Diabetes," appeared in the March issue of the leading European Diabetes journal, Diabetologia. The team, funded by the Juvenile Diabetes Research Foundation (JDRF), studied the pancreases from 72 people under age 18 who died after recently being diagnosed with T1DM. The team found evidence of enterovirus infection in the beta cells of over 60% of pancreases (3). The collaborators also studied pancreases of 50 individuals without T1DM and found that hardly any of the beta cells had any signs of an enterovirus infection (3).
Keep in mind these findings do not suggest T1DM is caused by enterovirus infection alone. The study aforementioned merely points out children who already have genetic predisposition to T1DM when infected with enterovirus "may start the process where the immune system identifies beta cells as 'foreign' and rejects them" (3).
The study did have a second component, whereby researchers found infection of enteroviruses in over 40% of pancreases of adults, compared to 13% of the non-diabetics of the same age group (3). The evidence for linkage of enteroviruses to type 2 diabetes mellitus is not as strong, but a possible conclusion suggests infection of beta cells causes them to be less able to produce insulin. This factor, combined with obesity and, subsequently, a much larger demand for insulin, could contribute to progression of the disease.
These findings could cause one to think proactively; i.e. vaccination. However, there are over 100 different strains of enteroviruses (2), and researchers have not narrowed exactly which of the 100 strains are more likely associated with the development of diabetes, either type 1 or 2. The only strain named to date is the coxsackievirus B4 (4), but, like similar studies, did not find an absolute causal relationship between the infection and development of T1DM. Instead, the study did solidify the argument enterovirus infection does cause beta-cell lysis, molecular mimicry, 'bystander activation' and viral persistence (4).
Having not yet found the cause and, more importantly, the cure for this life-threatening chronic disease, JDRF and the rest of the scientific world remain hopeful future research into enteroviruses and their role in T1DM development may eventually provided definitive answers. When asked about the study, "Enteroviruses May Play Role in Type 1 Diabetes" Karen Addington, Chief Executive for JDRF, commented "JDRF passionately believes that research such as this brings us a step closer to improving treatment and eventually curing this condition" (3). Hopefully, research may continue to make large strides, as diabetes diagnosis continues to rise on a global scale at an alarming rate.
(1)Maze, S. S.; R. J. Adolph (February 1990). "Myocarditis: unresolved issues in diagnosis and treatment". Clinical Cardiology 13 (2): 69-79.
(2)CDC. Feb 2010.
(3)"Enteroviruses May Play Role in Type 1 Diabetes." Feb 2010.
(4)Enterovirus and Type 1 Diabetes. "Role of Coxsackievirus B4 in the Pathogenesis of Type 1 Diabetes." Retrieved from PubMed Feb 2010.
this was my thought all along. A virus that attacks the beta cells and causes a mutation that is repeated into all future cells when they devide. This mutation allarms the ammune system and causes the white blood cells to attack in order to protect the body. Because the cell its self is changed and every cell is a replica of the previous the mutation will never go away. However the virus is only short time before it dyes, is killed by the body, or leaves the body...
I am little bit shocked to see the results and certain studies which are favoured the Enteroviruses which are responsible for the juvenile diabetes in small children just creating high problems.From this disease,Certain Metabolic activities and immune power lowers down as result many more such disorders faced in the body.There are two types of diabetes found from which Type 1 is more harmful compared to other one.
That's another pan of going into the success path,enteroviruses with ignores were able to even lead science to the wrong way,by sticking on inheritance factor.May financial means should be added for the new detection to bring new ways of seeing the diabetes in it generality
I honestly believe until we get a better handle on how we process our food and water we will continue to have problems like Type 1 diabetes. When you see how most of the livestock are raised and then slaughtered, you would see why we not only have to contend with bacteria, but viruses as well.
Then you have runoff from these feed yards that now infect the produce. Then not to mention the fact that a large majority of corn and soybeans are genetically modified. It was shown in the book, genetic roulette THE DOCUMENTED HEALTH RISKS of GENETICALLY ENGINEERED FOODS, that mice made to eat Roundup Ready soy had problems with the pancreas. It also showed an atrophy in testicles and was very effective at killing the offspring of rats.
I find the work (for Myocarditis) of Nora Chapman interesting in this context, on how deletions on the 5' end can lead to persistent Coxsackie infections. The viruses are no longer infectious (if I understand the work correctly), they no longer produce lots of virons and no longer lyse cells, but still "linger" in cells (where the white blood cells can't reach them) producing some viral proteins (and causing disease). Not all methods to look for the virus work in this circumstance, with histologic staining for the VP1 protein being the best (as far as I understand it) and neutralizing assays being better than antibody assays (as far as I understand it).
John Chia is doing some work on this with regards to Enterovirus infections and ME/CFS, and his work is a follow up to the work of British scientists from the 70/80/90ties - but I have the feeling there is very little research currently being targeted there.