Research Article

Elevated levels of IL-1 and IL-12 in type 1 diabetic patients infected with Coxsackievirus

Abstract

It is generally accepted that Coxsackievirus B (CVB) infections are a major factor in initiating or hastening the development of type 1 diabetes (T1D) and islet autoimmunity, especially in people with genetic predispositions. These viruses have the ability to directly destroy cells and release beta-cell antigens by infecting beta cells in the pancreas. Both the innate and adaptive immune systems are activated in response to this viral invasion, as seen by the activation of T lymphocytes, B cells, dendritic cells, and macrophages. Initially designed to eradicate the virus, the immune system may inadvertently attack the body’s own insulin-producing cells, triggering or exacerbating autoimmune reactions that aid in the pathophysiology of type 1 diabetes and beta-cell loss. During the period from November 1, 2024, to February 1, 2025, blood samples were collected from 60 patients (40 males and 20 females) diagnosed with type 1 diabetes, as well as 30 healthy individuals who were visiting private laboratories in Al-Najaf Governorate. The diagnosis was confirmed through molecular detection using Real Time -qPCR to detect CVB infection. Positive results were seen in 20 (33.3%) of suspected patients in compared with 40 (66.7%) were negative. While all healthy control subjects 30 (100.0%) were have negative results of Real-time PCR, and the difference was significant, (P= 0.001). The effect of Coxsackievirus infection on the immune response was evaluated by analyzing the immunological parameters (IL-1, 12) in 60 individuals with type 1 diabetes. The purpose of this assessment was to ascertain whether the virus may be involved in initiating or intensifying inflammatory processes that lead to the death of beta cells. Gaining knowledge of the immunological processes connected to CVB infection could help explain how viral infections and autoimmune disorders, especially type 1 diabetes, are related. The comparison of Interleukin-1β (IL-1β) level between DM with CVB, DM without CVB and control groups has been carried out. Mean levels of IL-1β were 18.69 ± 4.3, 16.33 ± 2.31 and 11.01 ± 1.06, in DM with CVB, DM without CVB and control groups respectively; the mean levels were higher in both groups of patients in compared to healthy control and the difference was significant (P < 0.05). But the mean levels was non-significant difference between patients groups themselves (DM with CVB and DM without CVB) themselves (P < 0.05). The comparison of Interleukin-12 (IL-12) level between DM patients and control groups has been carried out. Mean levels of IL-12 were 26.89 ± 5.4, 21.77 ± 3.86 and 10.68 ± 2.26, in DM with CVB, DM without CVB and control groups respectively; the mean levels were higher in both groups of patients in compared to healthy control and the difference was significant (P < 0.05). But the mean levels was non-significant difference between patients groups themselves (DM with CVB and DM without CVB) themselves (P < 0.05). The current study recorded the week correlation between each of interleukin 1 levels and Type 1 diabetes patients with CVB (r= 0.61); and were acceptable correlation between each of IL-12 and Type 1 diabetes patients with CVB (r = 0.77).