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Hypothesis: inflammatory acid-base disruption underpins Long Covid

van der Togt, Vicky, Rossman, Jeremy S. (2023) Hypothesis: inflammatory acid-base disruption underpins Long Covid. Frontiers in Immunology, 14 . Article Number 1150105. ISSN 1664-3224. (doi:10.3389/fimmu.2023.1150105) (KAR id:101099)


The mechanism of Long Covid (Post-Acute Sequelae of COVID-19; PASC) is currently unknown, with no validated diagnostics or therapeutics. SARS-CoV-2 can cause disseminated infections that result in multi-system tissue damage, dysregulated inflammation, and cellular metabolic disruptions. The tissue damage and inflammation has been shown to impair microvascular circulation, resulting in hypoxia, which coupled with virally-induced metabolic reprogramming, increases cellular anaerobic respiration. Both acute and PASC patients show systemic dysregulation of multiple markers of the acid-base balance. Based on these data, we hypothesize that the shift to anaerobic respiration causes an acid-base disruption that can affect every organ system and underpins the symptoms of PASC. This hypothesis can be tested by longitudinally evaluating acid-base markers in PASC patients and controls over the course of a month. If our hypothesis is correct, this could have significant implications for our understanding of PASC and our ability to develop effective diagnostic and therapeutic approaches.

Item Type: Article
DOI/Identification number: 10.3389/fimmu.2023.1150105
Uncontrolled keywords: Immunology, Long Covid, PASC, COVID-19, SARS-CoV-2, inflammation, acid-base, acidosis
Subjects: Q Science > QH Natural history > QH301 Biology
Q Science > QR Microbiology
Divisions: Divisions > Division of Natural Sciences > Biosciences
Funders: University of Kent (
SWORD Depositor: JISC Publications Router
Depositing User: JISC Publications Router
Date Deposited: 02 May 2023 13:11 UTC
Last Modified: 16 May 2023 13:06 UTC
Resource URI: (The current URI for this page, for reference purposes)

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