In addition to C5 inhibition, the compstatin-based complement C3 inhibitory drug (AMY-101) has also shown some success [142]

In addition to C5 inhibition, the compstatin-based complement C3 inhibitory drug (AMY-101) has also shown some success [142]. data regarding both the leading pharmacological therapies undergoing clinical trials and vaccine candidates in development to stem the threat of COVID-19. 1.?Introduction Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a positive sense, enveloped RNA beta coronavirus that emerged in Wuhan, China, in December of 2019 [1]. It is the cause of the clinical disease known as COVID-19 that has resulted in more than 50?M infections and more than 1.25?M deaths according to the World Health Organization [2]. COVID-19 is the third respiratory pandemic or epidemic caused by infection with a novel coronavirus. The first, SARS, developed in Hong Kong in the early-2000s, presented an average 6?days after contamination with fever, chills, headache, myalgia, and cough. The principal organs involved were the lungs, which with computerized tomography (CT) imaging exhibited consolidations that evolved within 7C10?days into pulmonary infiltrates. A number of patients required mechanical ventilatory support, and by day 21 following Teglicar initial onset of SARS-CoV, most patients had recovered, with mortality rate of approximately 9.6% [3,4]. The second clinical epidemic caused by a novel coronavirus was dubbed Middle East Respiratory Syndrome (MERS), and arose in 2012 in and near the Arabian Peninsula. This disease was associated primarily with fever, cough, and shortness of breath and it Teglicar had a much higher 35% mortality rate [4,5]. Although SARS-CoV-2 shares sequence similarity with both SARS-CoV (79%) and MERS-CoV (50%), it has been most closely linked to two bat-derived SARS-like viruses (bat-SL-CoVZC45 and bat-SL-CoVZXC21, ~88% similarity) [1]. The novel SARS-CoV-2 virus has been officially classified into the subgenus Sarbecovirus of the Betacoronavirus genus. Although it shares many features with SARS, SARS-CoV-2 contamination is unique in that viral particles are shed during the presymptomatic phase of contamination [6], which has led to significant spread of the virus worldwide. In this article, we will first offer a brief clinical overview of COVID-19, along with an introduction to the biology of the SARS-CoV-2 virus. Then, we will describe in detail the vaccine candidates and various therapeutic strategies, including pharmacologic therapies, convalescent plasma, and monoclonal antibodies, currently undergoing clinical trials. 2.?Clinical overview 2.1. Symptoms Patients Teglicar with COVID-19 most commonly report fever, cough, myalgia, fatigue, dyspnea, anosmia, and ageusia [7,8]. In some cases, there is a presence of increased sputum production, headache, hemoptysis, diarrhea, and Teglicar myalgia [[9], [10], [11], [12], [13], [14]], although roughly 20% percent of patients are thought to be truly asymptomatic (see Disease Course section below) [15]. 2.2. Radiographic findings Typical radiographic obtaining on Neurod1 chest roentgenogram or computerized tomography (CT) imaging demonstrates Teglicar bilateral pulmonary involvement, commonly located in the posterior lung areas. Bilateral ground-glass opacifications are frequent (representing areas of active interstitial inflammation) in subsegmental areas of consolidation, which generally progress following clinical day five into lesions and mass shadows of high density [14,16]. Cavitations, discrete pulmonary nodules, pleural effusions, emphysema, and fibrosis are uncommon [17]. 2.3. Laboratory studies The most widely reported abnormal laboratory assessments with COVID-19 include leucopenia, lymphopenia, and hypoalbuminemia [9,14]. As expected, the presence of elevated cytokines and inflammatory markers, including erythrocyte sedimentation rate, c-reactive protein, and d-dimer are present [11]. These occasionally signal the start of Cytokine Release Syndrome (CRS) in patients, which greatly increases the chances of both mortality and severe acute respiratory distress syndrome (ARDS) [18]. SARS-CoV-2 viral nucleic acid can be detected in the gastrointestinal tract, urine, and saliva [12], and it is not uncommon to encounter abnormal liver function assessments [10] including elevated levels of alanine and aspartate aminotransferases (ALT, AST), creatine kinase, and lactate dehydrogenase [10,11,14]. A few laboratory markers have been noted to be predictive of severe illness. One is an increase in the neutrophil to lymphocyte ratio (NLR), exhibited in patients who required intensive care and/or mechanical ventilation vs. patients with moderate disease [19]. Additionally,.