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Sisay Getu,1 Tegenaw Tiruneh,1 Henok Andualem,2 Wasihun Hailemichael,2 Teklehayimanot Kiros,3 Demeke Mesfin Belay,4 Mulugeta Kiros3 1Hematology and Immuno-hematology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia; 2Immunology and Molecular Biology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia; 3Microbiology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia; 4Pediatrics and Child Health Nursing, College of Health Sciences, Debre Tabor University, Debre Tabor, EthiopiaCorrespondence: Sisay GetuHematology and Immuno-hematology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, EthiopiaEmail sis.gtu@gmail.comAbstract: COVID-19 disease has led to an extraordinary inclusive health crisis globally. Elevation of D-dimer is the major remarkable abnormal coagulation test in seriously ill COVID-19 patients. In nearly 50% of COVID-19 patients, the value of D-dimer was significantly enhancing. Recent literature indicated that COVID-19 patients were at higher risk of developing disseminated intravascular coagulation. Pro-inflammatory cytokines and chemokines are some of the factors leading to these conditions. The majority of COVID-19 patients showed a higher profile of pro-inflammatory cytokines and chemokines in severe clinical conditions. Tumor necrosis factor-α (TNF-α) and interleukins (ILs) elevated in COVID-19 infected patients. TNF-α, IL-6, and IL-1 are major cytokines vital for the inhibition of intrinsic anticoagulant pathways. COVID-19 becomes a higher complication with a significant effect on blood cell production and hemostasis cascades. Deep vein thrombosis and arterial thrombosis are common complications. Changes in hematological parameters are also frequently observed in COVID-19 patients. Especially, thrombocytopenia is an indicator for poor prognosis of the disease and is highly expected and aggravates the likelihood of death of SARS-CoV-2 infected individuals. Thrombopoiesis reduction in COVID-19 patients might be due to viral abuse of the bone marrow/the viral load may affect thrombopoietin production and function. In other ways, immune-inflammation-mediated destruction and increased consumption of platelets are also the possible proposed mechanisms for thrombocytopenia. Therefore, the counting of platelet cells is an easily accessible biomarker for disease monitoring. All SARS-CoV-2 infected patients should be admitted and identifying potential higher-risk patients. It is also obligatory to provide appropriate treatments with intensive care and strict follow-up. In addition, considerations of chronic diseases are essential for better prognosis and recovery. The current review discusses coagulopathy among SARS-CoV-2 infected individuals and its complication for the management of the disease.Keywords: COVID-19, SARS-CoV-2, coagulopathy, DIC

Wasihun Hailemichael,1 Mulugeta Kiros,2 Yibeltal Akelew,3 Sisay Getu,4 Henok Andualem1 1Immunology and Molecular Biology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia; 2Medical Microbiology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, Ethiopia; 3Immunology and Molecular Biology, Medical Laboratory Sciences, College of Health Sciences, Debre Markos University, Debre Markos, Ethiopia; 4Hematology and Immuno-Hematology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, EthiopiaCorrespondence: Wasihun HailemichaelImmunology and Molecular Biology, Medical Laboratory Science, College of Health Sciences, Debre Tabor University, Debre Tabor, EthiopiaTel +251 946111414Email wasihunh383@gmail.comAbstract: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has rapidly spread across the world since its first emergence in China in late 2019. It is a major public health concern with no effective treatct 3ments. The immunopathology of SARS-CoV-2 is associated with an excessive inflammatory response. Macrophage activation syndrome (MAS) is also associated with the severity of the disease in SARS-CoV-2-infected patients. Neopterin is a macrophage activation marker produced by monocytes and macrophages upon activation by interferon-gamma (IFN-γ). Neopterin is a well-established marker in a variety of diseases, and recent evidence indicates that it could be helpful in early prediction of the severity of COVID-19 disease and serve as a prognostic marker. Here, we outline the role of macrophage activation syndrome in the pathogenesis of SARS-CoV-2 and suggest that neopterin could be used as a biomarker for progression of COVID-19.Keywords: neopterin, biomarker, MAS, SARS-CoV-2, COVID-19

Henok Andualem,1 Mulugeta Kiros,2 Sisay Getu,3 Wasihun Hailemichael1 1Immunology and Molecular Biology, Department of Medical Laboratory Science, College of Health Science, Debre Tabor University, Debre Tabor, Ethiopia; 2Medical Microbiology, Department of Medical Laboratory Science, College of Health Science, Debre Tabor University, Debre Tabor, Ethiopia; 3Clinical Hematology and Immunohematology, Department of Medical Laboratory Science, College of Health Science, Debre Tabor University, Debre Tabor, EthiopiaCorrespondence: Henok AndualemImmunology and Molecular Biology, Department of Medical Laboratory Science, College of Health Science, Debre Tabor University, Debre Tabor, EthiopiaTel +251923251524Email henokyaa@yahoo.comAbstract: The global threat of COVID-19 is continued with no commercially available vaccine or drug yet. While the application of convalescent therapy is usually beneficial, for critically ill patients, the detrimental effect associated with some antibodies is also reported. The immunoglobulin G (IgG) antibody in response to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is described, albeit the lack of defining whether the difference in subclasses has a beneficial or detrimental role. IgG2 has limited ability to activate innate immune cells and complement-mediated inflammation, which have been inversely described in SARS-CoV-2 pathogenesis. The expansion of IgG2 is promoted by interferon γ (IFN-γ); however, there is a low level of IFN-γ in COVID-19 patients. Therefore, this review describes the importance of targeting IgG2, with IFN-γ in minimizing the SARS-CoV-2 associated inflammation, and may provide insight into the design of vaccine or antibody-based therapies to COVID-19 disease.Keywords: IgG2, IFN-γ, antibody therapy, COVID-19 vaccine

The global threat of COVID-19 is continued with no commercially available vaccine or drug yet. While the application of convalescent therapy is usually beneficial, for critically ill patients, the detrimental effect associated with some antibodies is also reported. The immunoglobulin G (IgG) antibody in response to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is described, albeit the lack of defining whether the difference in subclasses has a beneficial or detrimental role. IgG2 has limited ability to activate innate immune cells and complement-mediated inflammation, which have been inversely described in SARS-CoV-2 pathogenesis. The expansion of IgG2 is promoted by interferon γ (IFN-γ); however, there is a low level of IFN-γ in COVID-19 patients. Therefore, this review describes the importance of targeting IgG2, with IFN-γ in minimizing the SARS-CoV-2 associated inflammation, and may provide insight into the design of vaccine or antibody-based therapies to COVID-19 disease.