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. 2022 Aug 12;65(12):2108–2120. doi: 10.1007/s00125-022-05779-2

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Immunofluorescence staining of cultured cell monolayers infected with EV strains (green) isolated from the diabetic DiViD cases and the pancreatic adenocarcinoma cases without diabetes. Counterstaining with Evans blue (red). (a–i) Cytoplasmic staining of the enteroviral capsid protein using mAb 6-E9/2: (a) negative control: uninfected AV3 cell monolayer. DiViD cases: DiViD-1 (b; inset shows the granular pattern of cytoplasmic staining); DiViD-2 (c); DiViD-5 (d); DiViD-6 [(e) infection before filtration; (f) second passage after filtration through 100 nm membrane]. LPN cases without diabetes: LPN-01 [(g) infection before filtration; (h) second passage after filtration through 100 nm membrane]; LPN-15 (i). (l–n) Staining by mAb 3D-05 to the enteroviral RNA polymerase enzyme (speckled nuclear staining): DiViD-1 (j), DiViD-2 (k), DiViD-6 (l). Scale bars represent 100 μm or 50 μm in the higher-magnification picture (b, inset)