SARS-CoV-2-infection in the setting of autotransplants for multiple sclerosis

The severe adult respiratory syndrome virus type 2 (SARS-CoV-2) related acute respiratory distress syndrome (ARDS) has a strong immunological and inflammatory component; accordingly investigators are employing monoclonal antibodies to ameliorate the virus-induced cytokine storm such as antibodies ag...

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Published in:Hematology (Luxembourg) 2023-12, Vol.28 (1), p.2164443-2164443
Main Authors: Olivares-Gazca, Juan Carlos, Gale, Robert Peter, Sánchez-Bonilla, Daniela, Gallardo-Pérez, Moisés Manuel, Soto-Olvera, Silvia, Ruiz-Delgado, Guillermo J., Ruiz-Argüelles, Guillermo José
Format: Article
Language:English
Subjects:
Adult
Autografts
autoimmune disease
autologous hematopoietic stem cell transplantation
COVID-19
Cyclophosphamide
Humans
multiple sclerosis
Multiple Sclerosis - therapy
Respiratory distress syndrome
SARS-CoV-2
SARS-CoV2
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Summary:The severe adult respiratory syndrome virus type 2 (SARS-CoV-2) related acute respiratory distress syndrome (ARDS) has a strong immunological and inflammatory component; accordingly investigators are employing monoclonal antibodies to ameliorate the virus-induced cytokine storm such as antibodies against interleukin 6 (IL-6), tumor necrosis factors alpha (TNF-alpha) and CC chemokine receptor 5 (CCR5) (1). Cyclophosphamide (Cy) has proven its role in various settings including autoimmune diseases, and in the post-haploidentical stem cell transplant setting; Cy depletes cytotoxic and effector T cell populations while relatively sparing the regulatory T cells (Tregs) and could tip the balance away from the overtly pro-inflammatory setting (1). We present here the cases of three persons who were infected by the SARS-CoV-2 virus during the Cy-induced pancytopenia of an autologous hematopoietic stem cell transplantation (HSCT), aimed to down-regulate the immune response in multiple sclerosis (MS) (2). The surprisingly benign course of the COVID-19 in the three cases suggest that the Cy could have had a role in abrogating the inflammatory response in these persons.
ISSN:1607-8454
1607-8454
DOI:10.1080/16078454.2022.2164443