the onset of t1d. the biobreeding diabetes-prone (bb) rat is another widely used spontaneous experimental model for t1d. the onset of diabetes occurs, in up to 90% of individuals (regardless of sex) at 8–16 weeks of age. during insulitis, the pancreatic islets are infiltrated by t lymphocytes, b lymphocytes, macrophages, and nk cells, with the difference from the human course of insulitis being that cd4 + t lymphocytes are markedly reduced and cd8 + t lymphocytes are almost absent. the aforementioned lymphopenia is the major drawback of this model. the disease is characterized by hyperglycemia, hypoinsulinemia, weight loss, ketonuria, and the need for insulin therapy for survival. bb rats are used to study the genetic aspects of t1d and are also used for interventional studies and diabetic nephropathy studies. lew-1ar1 / -iddm rats are derived from congenital lewis rats and represent a rarer spontaneous model for t1d. these rats develop diabetes at about 8–9 weeks of age with no sex differences unlike nod mice. in lew mice, diabetes presents with hyperglycemia, glycosuria, ketonuria, and polyuria. the advantage of the model is the progression of the prediabetic phase, which is very similar to human disease, with infiltration of islet by immune cells about a week before hyperglycemia is observed. this model is suitable for intervention studies or for the search for predictive biomarkers. it is also possible to observe individual phases of pancreatic infiltration by immune cells. the advantage of congenic lew mice is also the good viability after the manifestation of t1d (compared to nod mice and bb rats). chemically induced the chemical compounds aloxan and streptozotocin (stz) are commonly used to induce diabetes and destroy β-cells in mouse/rat animal models. in both cases, it is a cytotoxic analog of glucose that passes glut2 transport and accumulates in β-cells, causing their destruction. the chemically induced destruction of β-cells leads to decreased insulin production, hyperglycemia and weight loss in the experimental animal. the animal models prepared in this way are suitable for research into blood sugar-lowering drugs and therapies (e.g. for testing new insulin preparations). they are also the most commonly used genetically induced t1d model is the so-called akita mouse (originally c57bl/6nsic mouse). the development of diabetes in akita mice is caused by a spontaneous point mutation in the ins2 gene, which is responsible for the correct composition of insulin in the endoplasmic reticulum. decreased insulin production is then associated with hyperglycemia, polydipsia and polyuria. if severe diabetes develops within 3–4 weeks, akita mice survive no longer than 12 weeks without treatment intervention. the description of the etiology of the disease shows that, unlike spontaneous models, the early stages of the disease are not accompanied by insulitis. akita mice are used to test drugs targeting endoplasmic reticulum stress reduction, to test islet transplants, and to study diabetes-related complications such as nephropathy, sympathetic autonomic neuropathy, and vascular disease. for testing transplantation therapies. their advantage is mainly the low cost, the disadvantage is the cytotoxicity of the chemical compounds. virally induced viral infections play a role in the development of a number of autoimmune diseases, including human type 1 diabetes. however, the mechanisms by which viruses are involved in the induction of type 1 dm are not fully understood. virus-induced models are used to study the etiology and pathogenesis of the disease, in particular the mechanisms by which environmental factors contribute to or protect against the occurrence of type 1 dm. among the most commonly used are coxsackie virus, lymphocytic choriomeningitis virus, encephalomyocarditis virus, and kilham rat virus. examples of virus-induced animals include nod mice infected with coxsackie b4 that developed type 1 dm within two weeks.