Review of studies on SARS-CoV-2 infection inhibitors

Abstract

Introduction and objective. COVID-19 is a human infectious disease manifested by acute respiratory syndrome. On 30 January, 2020, the Word Heath Organization (WHO) declared a COVID-19 pandemic. The purpose of this article is to review publications on the search for substances that show inhibitory activity against SARS-CoV-2 infectivity, paying particular attention to the effect on different stages of the life cycle of the virus. Review methods. The review was based on an analysis of the latest available scientific literature and international databases. The data collected relate to the years 2020-2021. Brief description of the state of knowledge. Extremely intensive research is underway to find compounds that inhibit infection with the SARS-CoV-2 virus. Promising areas of research among the many current endeavours are antiviral compounds that stimulate the immune system, counter proliferation or affect individual viral replication cycles. These include, among others, interferons, monoclonal antibodies, natural compounds, peptides, aptamers, metal salts, and anti-inflammatory agents, inhibitors of viral enzymem, such as the RNA-dependent RNA polymerase. Preparations that help the body to combat the effects of infection have also assumed much importance. Conclusions. The ongoing research is focused on the development of new antiviral agents, as well as the use of the existing drugs on the market. The results of clinical trials are promising and give hope for the development of effective therapies against SARS-CoV-2 and emerging variants of this virus.

Outcome of Remdesivir on Mortality in Patients with COVID-19 Pneumonia

“…Remdesivir is administered as an intravenous infusion after reconstitution and further dilution. The starting dose on the rst day is 200 mg once a day and then 100 mg once a day for a total of ve days [19].…”

“…Coronavirus disease 2019 (COVID- 19) is an infectious disease caused by SARS-CoV-2; it originated in China at the end of 2019 and then spread worldwide within a short period, leading to an unprecedented pandemic. The main symptoms of COVID-19 pneumonia are fever and cough [1], which may be accompanied by increased in ammation, lymphopenia, and elevated lactate dehydrogenase (LDH) levels [1,2].…”

Safety of Repeated Administration of Xenogeneic Human Apoptotic State (Allocetra-OTS) in Sprague Dawley Rats

“…The immunomodulatory mechanisms associated with physiological apoptotic cell removal (called efferocytosis) were reported in different experimental models of inflammatory diseases or transplantation settings using apoptotic cell infusion [ 19 , 20 , 21 , 22 , 23 , 24 ]. Apoptotic cells have been suggested as a clinical therapeutic modality in a variety of immune-mediated disorders [ 10 , 25 , 26 , 27 , 28 ], including autoimmune and autoinflammatory conditions (e.g., arthritis [ 29 ], colitis [ 15 ]), graft rejection [ 23 ], post-ischemic injury, and conditions characterized by a cytokine storm, such as septic shock [ 30 ] and COVID-19 [ 31 ]. The properties of apoptotic cells may promote an immunogenic response and anti-tumor activity by restoring organ macrophage homeostasis [ 32 ].…”

Safety of Repeated Administration of Xenogeneic Human Apoptotic State (Allocetra-Ots) in Sprague Dawley Rats

“…The immunomodulatory mechanisms associated with physiological apoptotic cell removal (called efferocytosis) were reported in different experimental models of inflammatory diseases or transplantation settings using apoptotic cell infusion [21][22][23][24][25][26]. Apoptotic cells have been suggested as a clinical therapeutic modality in a variety of immune-mediated disorders [27][28][29][30][31], including autoimmune and autoinflammatory conditions (e.g., arthritis [32], colitis [33]), graft rejection [34], post-ischemic injury and conditions characterized by a cytokine storm such as septic shock [35] and COVID-19 [36]. The properties of apoptotic cells may promote an immunogenic response and anti-tumor activity by restoring organ macrophage homeostasis [37].…”