Pathophysiological Mechanisms Leading to Low Platelet Count in Immune Thrombocytopenia
Paola Roxana Lev1,2, Nora Paula Goette1, Rosana Fernanda Marta1,2*
1Institute of Medical Research A. Lanari, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina
2Department of Hematology Research, Institute of Medical Research (IDIM), National Scientific and Technical Research Council (CONICET), University of Buenos Aires, Buenos Aires, Argentina
Primary immune thrombocytopenia (ITP) is an autoimmune disorder characterized by the decrease in peripheral blood platelet count below 100 x 109/L, and an increased bleeding risk when thrombocytopenia drops below 30 x 109/L. The mechanisms leading to ITP in adults, although not completely elucidated, involves an imbalance between effector and regulatory cells that results in a breakdown of the immune tolerance. Autoantibodies are considered the main responsible for thrombocytopenia, although direct T-cell cytotoxic effect and lysis by Complement attachment and activation could also contribute to platelet elimination from circulation. In addition to increased peripheral clearance, abnormalities in platelet production also favors platelet count reduction. This review is intended to describe some specific knowledge about peripheral and bone marrow mechanisms leading to thrombocytopenia in adult ITP.
DOI: 10.29245/2578-3009/2020/2.1185 View / Download Pdf Children Protection Against COVID-19 at the Pandemic Outbreak
Dana Khdr Sabir1*, Nabaz R. Khwarahm2, Shakhawan M. Ali3, Hayman J Abdoul4, Kochar I. Mahmood5, Rimantas Kodzius6,7*
1Department of Medical Laboratory Sciences, Charmo University, 46023 Chamchamal, Kurdistan Region, Iraq
2Department of Biology, College of Education, University of Sulaimani, Sulaimani, Kurdistan Region, Iraq
3Department of Oral and Maxillofacial Surgery, School of Medicine, Faculty of Dentistry, University of Sulaimani,Sulaimani, Kurdistan Region, Iraq
4Department of Pharmaceutical Chemistry, Charmo University, 46023 Chamchamal, Kurdistan Region, Iraq
5Charmo Centre for Research, Training and Consultancy, Charmo University, 46023 Chamchamal, Kurdistan Region, Iraq
6Kaunas Technology University (KTU), 37164 Panevezys, Lithuania
7Ludwig Maximilian University of Munich (LMU), 80539 Munich, Germany
Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) is a novel strain of coronavirus that is recently identified as an etiological agent for the current pandemic respiratory illness called coronavirus disease 2019 (COVID-19). The disease might have a zoonotic origin and has infected > 19 million people around the globe with > 700,000 deaths. The published data indicate that children are generally less susceptible to contracting COVID-19. Here, we are providing a review on current hypotheses that have tried to explain the low mortality and morbidity rate among children. We believe that understanding the immunological base of children’s protection can prevent further spread of the disease.
DOI: 10.29245/2578-3009/2020/2.1188 View / Download Pdf SARS-CoV-2 Subversion of the Antiviral Interferon Alpha-Response of Lung Macrophages?
Malgorzata Kloc*1,2,3, Rafik M. Ghobrial1,2, Jacek Z Kubiak*4,5
1The Houston Methodist Research Institute, Houston, Texas 77030, USA
2The Houston Methodist Hospital, Department of Surgery, Houston, Texas, USA
3The University of Texas, M.D. Anderson Cancer Center, Department of Genetics, Houston Texas, USA
4Laboratory of Regenerative Medicine and Cell Biology, Military Institute of Hygiene and Epidemiology (WIHE), Warsaw, Poland
5UnivRennes, UMR 6290, CNRS, Institute of Genetics and Development of Rennes, Cell Cycle Group, Faculty of Medicine, Rennes, France
The interferons (IFNs) are the main antiviral immune factors. Currently, various IFNs therapies are used for the treatment of human immunodeficiency virus (HIV), hepatitis B (HBV), and hepatitis C (HCV), cancer, and autoimmune diseases. Recently, it has been suggested that IFN-α therapy should be used to lessen the respiratory symptoms in the SARS-CoV-2 virus- infected (COVID-19) patients. The SARS-CoV-2 enters the cells by binding to the Angiotensin-converting enzyme 2 (ACE2), which by recognizing the spike S1 protein of the virus, acts as a virus receptor. Because the expression of ACE2 is induced by IFN-α, the SARS-CoV-2 virus may exploit the anti-viral response by subverting the IFN functions to further its own propagation and infectability. We discuss here how the SARS-CoV-2 may also subvert the immune response of the lung macrophages, which also express ACE2, to exacerbate the severity of the COVID-19 respiratory symptoms.
DOI: 10.29245/2578-3009/2020/2.1189 View / Download Pdf