Type 1 Diabetes and Enteroviral Infections - Essay Example

The cause of type 1 diabetes has always been linked to genetic predisposition. However, recent studies suggest that enteroviruses, specifically Coxsackie B enteroviruses (CVB) and an enteroviral capsid protein, vp1, may be contributing to the onset of Type 1 diabetes.

Following up on the said studies, Richardson et al. (2) collected 72 pancreatic autopsy tissues from patients with recent-onset Type 1 diabetes mellitus along with 161 controls.  These samples were immunostained for insulin, glucagon, vp1, double-stranded RNA-activated protein kinase R (PKR), and MHC class 1.  VP1staining was restricted to insulin-containing beta cells (Ibid 1).

The results of the experiment showed the presence of vp1-immunopositive cells in multiple islets, 44 out of 72, from young, recent-onset, Type 1 diabetic patients, compared with just three islets out of 50 specimens from neonatal and pediatric normal controls.  

Dako antiserum in vp1 immunostaining was used because of its specificity in labeling vp1 immunopositive cells, especially when it comes to Islet of Langerhans cells. Another consideration was that polyclonal antisera raised against enteroviruses often cross-react with tyrosine phosphatase (IA-2) and heat shock protein (hsp-60). However, the study results show that cross-reaction does not occur with Dako antiserum as IA-2 is present in both alpha cells and beta cells.  As well, the results showed no minimal alpha cells were stained.

PKR immunostaining was also done since PKR is a protein upregulated in response to enteroviral infections like CVB4. A strong correlation was found between PKR and vp1 immunopositivity which supports the findings that Dako antiserum is indicative of a persistent enteroviral infection.  Two other antisera were used but the results using these were not conclusive.

Results of the experiment have also linked vp1 infection to type 2 diabetes even if there is no autoimmunity. Since PKR production is a response of the infected endocrine cells to the disease, the outcome may be decreased insulin secretion.  Reckoning with obesity as a predisposing factor, one may then expect adult-onset, Type 2 diabetes as a result.

The paper presented a major diagnostic breakthrough that contrasted sharply with the longstanding notion about genetic predisposition being virtually the only explanation for the onset of Type 1 diabetes. The study revolutionizes the way diabetes will henceforth be treated and preventive measures can now be taken. The development of a vaccine for enteroviral infections can lead to a reduction in juvenile diabetes cases worldwide. A breakthrough like this may well be worthy of a Nobel prize.