tetano
Editor, Senior Moderator
Infection
. 2024 May 27.
doi: 10.1007/s15010-024-02293-y. Online ahead of print. The roles of the kynurenine pathway in COVID-19 neuropathogenesis
Mona Dehhaghi[SUP] 1 [/SUP], Mostafa Heydari[SUP] 2 [/SUP], Hamed Kazemi Shariat Panahi[SUP] 1 [/SUP], Sharon R Lewin[SUP] 3 4 5 [/SUP], Benjamin Heng[SUP] 6 [/SUP], Bruce J Brew[SUP] 7 8 9 10 [/SUP], Gilles J Guillemin[SUP] 11 12 [/SUP]
Affiliations
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the highly contagious respiratory disease Corona Virus Disease 2019 (COVID-19) that may lead to various neurological and psychological disorders that can be acute, lasting days to weeks or months and possibly longer. The latter is known as long-COVID or more recently post-acute sequelae of COVID (PASC). During acute COVID-19 infection, a strong inflammatory response, known as the cytokine storm, occurs in some patients. The levels of interferon-γ (IFN-γ), interferon-β (IFN-β), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) are particularly increased. These cytokines are known to activate the enzyme indoleamine 2,3-dioxygenase 1 (IDO-1), catalysing the first step of tryptophan (Trp) catabolism through the kynurenine pathway (KP) leading to the production of several neurotoxic and immunosuppressive metabolites. There is already data showing elevation in KP metabolites both acutely and in PASC, especially regarding cognitive impairment. Thus, it is likely that KP involvement is significant in SARS-CoV-2 pathogenesis especially neurologically.
Keywords: COVID-19; Kynurenine pathway; Long COVID; Neurological manifestations; SARS-CoV-2; Tryptophan.
. 2024 May 27.
doi: 10.1007/s15010-024-02293-y. Online ahead of print. The roles of the kynurenine pathway in COVID-19 neuropathogenesis
Mona Dehhaghi[SUP] 1 [/SUP], Mostafa Heydari[SUP] 2 [/SUP], Hamed Kazemi Shariat Panahi[SUP] 1 [/SUP], Sharon R Lewin[SUP] 3 4 5 [/SUP], Benjamin Heng[SUP] 6 [/SUP], Bruce J Brew[SUP] 7 8 9 10 [/SUP], Gilles J Guillemin[SUP] 11 12 [/SUP]
Affiliations
- PMID: 38802702
- DOI: 10.1007/s15010-024-02293-y
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the highly contagious respiratory disease Corona Virus Disease 2019 (COVID-19) that may lead to various neurological and psychological disorders that can be acute, lasting days to weeks or months and possibly longer. The latter is known as long-COVID or more recently post-acute sequelae of COVID (PASC). During acute COVID-19 infection, a strong inflammatory response, known as the cytokine storm, occurs in some patients. The levels of interferon-γ (IFN-γ), interferon-β (IFN-β), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) are particularly increased. These cytokines are known to activate the enzyme indoleamine 2,3-dioxygenase 1 (IDO-1), catalysing the first step of tryptophan (Trp) catabolism through the kynurenine pathway (KP) leading to the production of several neurotoxic and immunosuppressive metabolites. There is already data showing elevation in KP metabolites both acutely and in PASC, especially regarding cognitive impairment. Thus, it is likely that KP involvement is significant in SARS-CoV-2 pathogenesis especially neurologically.
Keywords: COVID-19; Kynurenine pathway; Long COVID; Neurological manifestations; SARS-CoV-2; Tryptophan.