I think there were some early reports of an uptick in T1D when COVID hit but don't think that has panned out with time? I'm not certain about other novel viruses.

The only firm statistical correlation that I am aware of is CVB.

I find the idea of dsRNA being causative a compelling idea. Yuval Dor's data helps with this idea. However, CVB and SARS-Cov-2 both produce dsRNA during its replication, as I understand, so idk how to separate them in this context.

Very good question, but I don't have a good answer for you. Simply - I don't know.

We put a proposal into the NIH to investigate this question but were not selected for funding. If funders won't fund this work, I can't say for certain.

This is what I am going to get to protect my sequencing data

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Overall, CVB3 sparks diverse, cell type-specific stress pathways in islets, with MIR7-3HG emerging as a regulator of infection + survival. These insights could help unravel viral contributions to T1D.

We also identified the lncRNA MIR7-3HG as a key player. Knockdown in stem cell-derived islets ↓ viral genome levels, ↓ apoptosis, and altered autophagy, suggesting new therapeutic angles.

CVB3 disrupted mitochondria differently across cell types. Beta cells had increased mitochondrial size but lose efficiency. Alpha cells had shrunken mitochondria. These are potentially protective acclimations.

Beta, alpha, and duct cells had the strongest responses. Beta and alpha cells demonstrated mitochondrial dysfunction. Duct had the strongest interferon & HLA responses. All cells had unique stress and immune signatures.