Antioxidant Genetic Profile Modifies Probability of Developing Neurological Sequelae in Long-COVID

Understanding the sequelae of COVID-19 is of utmost importance. Neuroinflammation and disturbed redox homeostasis are suggested as prevailing underlying mechanisms in neurological sequelae propagation in long-COVID. We aimed to investigate whether variations in antioxidant genetic profile might be a...

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Veröffentlicht in:Antioxidants 2022-05, Vol.11 (5), p.954
Hauptverfasser: Ercegovac, Marko, Asanin, Milika, Savic-Radojevic, Ana, Ranin, Jovan, Matic, Marija, Djukic, Tatjana, Coric, Vesna, Jerotic, Djurdja, Todorovic, Nevena, Milosevic, Ivana, Stevanovic, Goran, Simic, Tatjana, Bukumiric, Zoran, Pljesa-Ercegovac, Marija
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Sprache:eng
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Zusammenfassung:Understanding the sequelae of COVID-19 is of utmost importance. Neuroinflammation and disturbed redox homeostasis are suggested as prevailing underlying mechanisms in neurological sequelae propagation in long-COVID. We aimed to investigate whether variations in antioxidant genetic profile might be associated with neurological sequelae in long-COVID. Neurological examination and antioxidant genetic profile (SOD2, GPXs and GSTs) determination, as well as, genotype analysis of Nrf2 and ACE2, were conducted on 167 COVID-19 patients. Polymorphisms were determined by the appropriate PCR methods. Only polymorphisms in GSTP1AB and GSTO1 were independently associated with long-COVID manifestations. Indeed, individuals carrying or allele exhibited lower odds of long-COVID myalgia development, both independently and in combination. Furthermore, the combined presence of and alleles exhibited cumulative risk regarding long-COVID myalgia in carriers of the combined genotype. Moreover, individuals carrying combined genotype were more prone to developing long-COVID "brain fog", while this probability further enlarged if the allele was also present. The fact that certain genetic variants of antioxidant enzymes, independently or in combination, affect the probability of long-COVID manifestations, further emphasizes the involvement of genetic susceptibility when SARS-CoV-2 infection is initiated in the host cells, and also months after.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox11050954