A REVIEW OF EPSTEIN BARR VIRUS COINFECTION IN COVID-19 PATIENTS
DOI:
https://doi.org/10.53555/nnpbs.v8i6.1364Keywords:
Corona virus, EBV, Autoimmune, CoinfectionAbstract
Epstein–Barr virus (EBV) could tip an already compromised system into a self-perpetuating metabolic-oxidative stress-inflammatory spiral that could underly many of the symptoms of long COVID.
References
Dotan A, Muller S, Kanduc D, David P, Halpert G, Shoenfeld Y. The SARS-CoV-2 as an instrumental trigger of autoimmunity. Autoimmun Rev. 2021 Apr;20(4):102792.
Ying K, Zhai R, Pyrkov TV, Shindyapina AV, Mariotti M, Fedichev PO, et al. Genetic and phenotypic analysis of the causal relationship between aging and COVID-19. Commun Med. 2021;1(1):35.
Tiku V, Tan MW, Dikic I. Mitochondrial functions in infection and immunity. Trends Cell Biol. 2020;30(4):263–75.
Nunn AVW, Guy GW, Brysch W, Botchway SW, Frasch W, Calabrese EJ, et al. SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing. Immun Ageing. 2020;17(1):33.
Ajaz S, McPhail MJ, Singh KK, Mujib S, Trovato FM, Napoli S, et al. Mitochondrial metabolic manipulation by SARS-CoV-2 in peripheral blood mononuclear cells of patients with COVID-19. Am J Physiol Cell Physiol. 2021;320(1):C57-65.
Gold JE, Okyay RA, Licht WE, Hurley DJ. Investigation of long COVID prevalence and its relationship to Epstein-Barr virus reactivation. Pathogens. 2021;10(6):763
Paolucci S, Cassaniti I, Novazzi F, Fiorina L, Piralla A, Comolli G, et al. EBV DNA increase in COVID-19 patients with impaired lymphocyte subpopulation count. Int J Infect Dis. 2021;104:315–9.
Verma D, Church TM, Swaminathan S. Epstein-Barr virus lytic replication induces ACE2 expression and enhances SARS-CoV-2 Pseudotyped virus entry in epithelial cells. J Virol. 2021;95(13):e0019221.
Groff D, Sun A, Ssentongo AE, Ba DM, Parsons N, Poudel GR, et al. Short-term and long-term rates of Postacute Sequelae of SARS-CoV-2 infection: a systematic review. JAMA Netw Open. 2021;4(10):e2128568.
Vernon SD, Whistler T, Cameron B, Hickie IB, Reeves WC, Lloyd A. Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr virus. BMC Infect Dis. 2006;6:15.
Lisci M, Barton PR, Randzavola LO, Ma CY, Marchingo JM, Cantrell DA, et al. Mitochondrial translation is required for sustained killing by cytotoxic T cells. Science.
Thompson EA, Cascino K, Ordonez AA, Zhou W, Vaghasia A, Hamacher-Brady A, et al. Metabolic programs define dysfunctional immune responses in severe COVID-19 patients. Cell Rep. 2021;34(11):108863.
LaJeunesse DR, Brooks K, Adamson AL. Epstein-Barr virus immediate-early proteins BZLF1 and BRLF1 alter mitochondrial morphology during lytic replication. Biochem Biophys Res Commun. 2005;333(2):438–42.
Wiedmer A, Wang P, Zhou J, Rennekamp AJ, Tiranti V, Zeviani M, et al. Epstein-Barr virus immediate-early protein Zta co-opts mitochondrial single-stranded DNA binding protein to promote viral and inhibit mitochondrial DNA replication. J Virol. 2008;82(9):4647–55.
Vichaya EG, Chiu GS, Krukowski K, Lacourt TE, Kavelaars A, Dantzer R, et al. Mechanisms of chemotherapy-induced behavioral toxicities. Front Neurosci. 2015;9:131.
Gold JE, Okyay RA, Licht WE, Hurley DJ. Investigation of long COVID prevalence and its relationship to Epstein–Barr virus reactivation. Pathogens. 2021;10(6):763.
Shafiee, A., Aghajanian, S., Athar, M.M.T. and Gargari, O.K. (2022), Epstein–Barr virus and COVID-19. J Med Virol, 94: 4040-4042.
Steven NM, Annels NE, Kumar A, Leese AM, Kurilla MG, Rickinson AB. Immediate early and early lytic cycle proteins are frequent targets of the Epstein–Barr virus-induced cytotoxic T cell response. J Exp Med. 1997;185(9):1605-1617.
Chen T, Song J, Liu H, Zheng H, Chen C. Positive Epstein–Barr virus detection in coronavirus disease 2019 (COVID-19) patients. Sci Rep. 2021;11(1):10902.
Paolucci S, Cassaniti I, Novazzi F, et al. EBV DNA increase in COVID-19 patients with impaired lymphocyte subpopulation count. Int J Infect Dis. 2021;104:315-319.
Chen J, Dai L, Kendrick S, Post SR, Qin Z. The anti-COVID-19 drug remdesivir promotes oncogenic herpesviruses reactivation through regulation of intracellular signaling pathways. Antimicrob Agents Chemother. 2022;66:e0239521.
Meng M, Zhang S, Dong X, Sun W, Deng Y, Li W, Li R, Annane D, Wu Z, Chen D. COVID-19 associated EBV reactivation and effects of ganciclovir treatment. Immun Inflamm Dis. 2022 Apr;10(4):e597. doi: 10.1002/iid3.597. PMID: 35349757; PMCID: PMC8959425.
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