In Fabry disease, the genetically determined deficit of alphagalactosidase A leads to glycosphingolipids accumulation in kidney, heart, vessels and lungs. Glycosphingolipid storage causes impairment of several lysosomal functions including endosomal maturation and autophagy processes (Figure 1B) [5], thus leading to an ‘unfavourable’ host cellular environment that may interfere with infection and propagation of some viruses. We therefore hypothesized that patients with Fabry disease may be less prone to SARS-CoV-2 infection and COVID-19 severe clinical manifestations.
Potential resistance to SARS-CoV-2 infection in lysosomal storage disorders / Pieroni M., Pieruzzi F., Mignani R., Graziani F., Olivotto I., Riccio E., Ciabatti M., Limongelli G., Manna R., Bolognese L., Pisani A.. - In: CLINICAL KIDNEY JOURNAL. - ISSN 2048-8505. - ELETTRONICO. - 14:(2021), pp. 1488-1490. [10.1093/ckj/sfab045]
Potential resistance to SARS-CoV-2 infection in lysosomal storage disorders
Pieroni M.;Mignani R.;Graziani F.;Olivotto I.;Ciabatti M.;Limongelli G.;Manna R.;
2021
Abstract
In Fabry disease, the genetically determined deficit of alphagalactosidase A leads to glycosphingolipids accumulation in kidney, heart, vessels and lungs. Glycosphingolipid storage causes impairment of several lysosomal functions including endosomal maturation and autophagy processes (Figure 1B) [5], thus leading to an ‘unfavourable’ host cellular environment that may interfere with infection and propagation of some viruses. We therefore hypothesized that patients with Fabry disease may be less prone to SARS-CoV-2 infection and COVID-19 severe clinical manifestations.
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