A brief analysis and hypotheses about the risk of COVID-19 for people with type 1 and type 2 diabetes mellitus

© Springer Nature Switzerland AG 2020..

COVID-19 is an infectious respiratory disease which firstly occurred in Wuhan, China and evolved rapidly around the globe. The causative pathogen is a novel coronavirus called SARS-CoV-2 with genomic similarities with SARS-CoV and MERS-CoV. The disease is transmitted among humans either through direct contact or via droplets from sneeze or cough. Most infected persons remain asymptomatic or mildly symptomatic, but some patients may develop severe clinical features, including pneumonia, respiratory failure, sepsis and even death. People of advanced age and/or with underlying diseases (including diabetes mellitus) are at greater risk. The innate and adaptive immune system are responsible for protecting the body against viral infection. Nevertheless, it is assumed that SARS-CoV-2 interferes with the immune system through immunomodulating mechanisms which intensify its pathogenesis. A delayed or reduced response of the innate immune system is critical for the development of pathogenesis of the virus. People with diabetes are more likely to develop severe symptoms of COVID-19. The present article speculates that special aspects of the immune dysfunction caused by chronic hyperglycaemia is the main reason for this susceptibility.

Medienart:

E-Artikel

Erscheinungsjahr:

2020

Erschienen:

2020

Enthalten in:

Zur Gesamtaufnahme - volume:19

Enthalten in:

Journal of diabetes and metabolic disorders - 19(2020), 2 vom: 23. Dez., Seite 2035-2039

Sprache:

Englisch

Beteiligte Personen:

Milionis, Charalampos [VerfasserIn]
Milioni, Stella Olga [VerfasserIn]

Links:

Volltext

Themen:

COVID-19
Diabetes mellitus
Diabetic complications
Editorial
Hyperglycaemia

Anmerkungen:

Date Revised 10.11.2023

published: Electronic-eCollection

Citation Status PubMed-not-MEDLINE

doi:

10.1007/s40200-020-00592-3

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM314113983