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Acta Biomed ; 91(3): ahead of print, 2020 07 13.
Article in English | MEDLINE | ID: covidwho-761245

ABSTRACT

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.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Killer Cells, Natural/pathology , Lymphoma/complications , Pneumonia, Viral/complications , COVID-19 , Combined Modality Therapy , Coronavirus Infections/diagnosis , Humans , Lymphoma/diagnosis , Lymphoma/therapy , Male , Pandemics , Pneumonia, Viral/diagnosis , SARS-CoV-2 , Tomography, X-Ray Computed , Young Adult
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