SARS-CoV-2-infection in the setting of autotransplants for multiple sclerosis.
Juan Carlos Olivares-GazcaRobert Peter GaleDaniela Sánchez-BonillaMoisés Manuel Gallardo-PérezSilvia Soto-OlveraGuillermo J Ruiz-DelgadoGuillermo José Ruiz-ArguellesPublished in: Hematology (Amsterdam, Netherlands) (2023)
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.
Keyphrases
- sars cov
- regulatory t cells
- multiple sclerosis
- acute respiratory distress syndrome
- respiratory syndrome coronavirus
- dendritic cells
- extracorporeal membrane oxygenation
- inflammatory response
- immune response
- stem cells
- mechanical ventilation
- high glucose
- diabetic rats
- drug induced
- bone marrow
- coronavirus disease
- white matter
- rheumatoid arthritis
- acute myeloid leukemia
- lipopolysaccharide induced
- endothelial cells
- high dose
- stem cell transplantation
- toll like receptor
- intensive care unit
- cell therapy
- peripheral blood
- binding protein
- stress induced