Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
1.
Int J Mol Sci ; 22(11)2021 May 21.
Article in English | MEDLINE | ID: covidwho-1244037

ABSTRACT

COVID-19 is a respiratory disease caused by newly discovered severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease at first was identified in the city of Wuhan, China in December 2019. Being a human infectious disease, it causes high fever, cough, breathing problems. In some cases it can be fatal, especially in people with comorbidities like heart or kidney problems and diabetes. The current COVID-19 treatment is based on symptomatic therapy, so finding an appropriate drug against COVID-19 remains an immediate and crucial target for the global scientific community. Two main processes are thought to be responsible for the COVID-19 pathogenesis. In the early stages of infection, disease is determined mainly by virus replication. In the later stages of infection, by an excessive immune/inflammatory response, leading to tissue damage. Therefore, the main treatment options are antiviral and immunomodulatory/anti-inflammatory agents. Many clinical trials have been conducted concerning the use of various drugs in COVID-19 therapy, and many are still ongoing. The majority of trials examine drug reposition (repurposing), which seems to be a good and effective option. Many drugs have been repurposed in COVID-19 therapy including remdesivir, favipiravir, tocilizumab and baricitinib. The aim of this review is to highlight (based on existing and accessible clinical evidence on ongoing trials) the current and available promising drugs for COVID-19 and outline their characteristics.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Antiviral Agents/therapeutic use , COVID-19 Drug Treatment , Drug Repositioning/methods , SARS-CoV-2/drug effects , Anti-Inflammatory Agents/chemistry , Anti-Inflammatory Agents/pharmacology , Antiviral Agents/chemistry , Antiviral Agents/pharmacology , COVID-19/physiopathology , Humans , Pharmaceutical Preparations/administration & dosage , Pharmaceutical Preparations/chemistry , Virus Replication/drug effects
2.
Int J Mol Sci ; 22(4)2021 Feb 11.
Article in English | MEDLINE | ID: covidwho-1079664

ABSTRACT

The novel coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a global challenge. Currently, there is some information on the consequences of COVID-19 infection in multiple sclerosis (MS) patients, as it is a newly discovered coronavirus, but its far-reaching effects on participation in neurodegenerative diseases seem to be significant. Recent cases reports showed that SARS-CoV-2 may be responsible for initiating the demyelination process in people who previously had no symptoms associated with any nervous system disorders. It is presently known that infection of SARS-CoV-2 evokes cytokine storm syndrome, which may be one of the factors leading to the acute cerebrovascular disease. One of the substantial problems is the coexistence of cerebrovascular disease and MS in an individual's life span. Epidemiological studies showed an enhanced risk of death rate from vascular disabilities in MS patients of approximately 30%. It has been demonstrated that patients with severe SARS-CoV-2 infection usually show increased levels of D-dimer, fibrinogen, C-reactive protein (CRP), and overactivation of blood platelets, which are essential elements of prothrombotic events. In this review, the latest knowledge gathered during an ongoing pandemic of SARS-CoV-2 infection on the neurodegeneration processes in MS is discussed.


Subject(s)
COVID-19/complications , Multiple Sclerosis/complications , Neurodegenerative Diseases/etiology , Animals , COVID-19/pathology , COVID-19/virology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/pathology , Cytokine Release Syndrome/virology , Humans , Multiple Sclerosis/pathology , Multiple Sclerosis/virology , Neurodegenerative Diseases/pathology , Neurodegenerative Diseases/virology , SARS-CoV-2/isolation & purification , Thrombosis/etiology , Thrombosis/pathology
3.
J Clin Med ; 9(9)2020 Aug 19.
Article in English | MEDLINE | ID: covidwho-721506

ABSTRACT

The 2019 global pandemic of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been declared a public health emergency of international concern by the World Health Organization (WHO). The WHO recognized the spread of COVID-19 as a pandemic on 11 March 2020. Based on statistics from 10 August 2020, more than 20.2 million cases of COVID-19 have been reported resulting in more than 738,000 deaths. This completely new coronavirus has spread worldwide in a short period, causing economic crises and healthcare system failures worldwide. Initially, it was thought that the main health threat was associated with respiratory system failures, but since then, SARS-CoV-2 has been linked to a broad spectrum of symptoms indicating neurological manifestations, including ischemic stroke. Current knowledge about SARS-CoV-2 and its complications is very limited because of its rapidly evolving character. However, further research is undoubtedly necessary to understand the causes of neurological abnormalities, including acute cerebrovascular disease. The viral infection is inextricably associated with the activation of the immune system and the release of pro-inflammatory factors, that can stimulate the host organism to defend itself. However, the body's immune response is a double-edged sword that on one hand, destroys the virus but also disrupts the homeostasis leading to serious complications, including thrombosis. Numerous studies have linked coagulopathies with COVID-19, however, there is great uncertainty regarding it functions on the molecular level. In this review, a detailed insight into the biological processes associated with ischemic stroke in COVID-19 patients and suggest a possible explanation for this phenomenon is provided.

SELECTION OF CITATIONS
SEARCH DETAIL