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SARS-CoV2 Covid-19 NK lymphoma EBV DNA Remission
Covid-19 infection was a possible causal factor in the exhaustion and decrease number of NK clonal cells, resulting in a evident improvement of signs, symptoms and clinical features related to NK lymphoma refractory to previous immuno-chemiotherapy.
It has been shown that SARS-CoV2 binds to ACE2. Covid-19 may infect NK cells to suppress their functions, as NK cells express angiotensin converting enzyme 2 (ACE2). The excessive production of proinflammatory cytokines in Covid-19 infection may have played a crucial role in lymphodepletion. Although not published in Covid-19, other RNA viruses that cause acute pulmonary infections promote NK cell apoptosis.
In NK/T-cell lymphoma plasma EBV-DNA is a sensitive surrogate biomarker of lymphoma load. In this case, we also notice a dramatic transient reduction in plasmatic EBV-DNA viral copies during Covid-19 pneumonia other than NK clonal cells reduction, and after the infection resolution we described a lymphoma relapse as well as EBV-DNA increase and the rising in NK clonal cells count.
Although the mechanism leading to spontaneous remission remain uncharacterized, we hypothezised that a favorable adaptive immunity against concurrent viral infection could render an enhanced anti-tumor effect. We suppose COVID-19 infection have induced a transient remission in this patient affected with NK neoplasm.
2.Zheng M, Gao Y, Wang G, et al. Functional exhaustion of antiviral lymphocytes in COVID-19 patients. Cell Mol Immunol 2020 Mar 17. [Epub ahead of print]
3.Santos JM, Cervera-Carrascon V, Havunen R, et al. Adenovirus Coding for Interleukin-2 and Tumor Necrosis Factor AlphaReplaces Lymphodepleting Chemotherapy in Adoptive T Cell Therapy. Mol Ther 2018 Sep 5;26(9):2243-2254.
4.Snijder J, Mihyawi N, Frolov A, et al. Spontaneous remission in diffuse large cell lymphoma: a case report. J of Med Case Reports. 2019 13:28.
5.Musto P et al. Spontaneus remission in Acute Myeloid Leukaemia: A role for endogenous production of Tumour necrosis factor and Interleukin-2? Br J Haematol. 1994 Aug;87(4): 879-80.