The mechanisms of SARS-COV-2 injury have been proposed, including: (1) infecting target cells expressing ACE-2, such as immune cells; (2) inhibiting IFN response and promoting virus replication; (3) increasing the activation of neutrophils and macrophages and the release of proinflammatory cytokines, leading lung injury; and (4) activating specific Th1/Th17 and B cells, leading to a series of inflammatory responses associated with SARS-CoV-2 antibodies [34]. the overactivated inflammation response, and other therapies such as herbal medicine and mesenchymal stem cells. Besides, the ongoing development of inventing prophylactic interventions such as various vaccines by companies and institutions worldwide is crucial to decline morbidity and mortality. This review mainly focused on promising candidates for the treatment of COVID-19 and collected recently updated evidence relevant to its feasibility in clinical practice in the near future. strong class=”kwd-title” Keywords: SARS-CoV-2, COVID-19, Antiviral drugs, Immunotherapy, Vaccines Introduction Coronavirus disease 2019 (COVID-19) is a severe acute respiratory syndrome that has infected more than 23,300,000 patients and caused 806,410 deaths from 216 countries and territories so far. delta-Valerobetaine The pathogen of COVID-19 is severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new member of the coronaviridae family that also includes severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) [1C3]. Bats, the natural reservoirs of SARS-CoV and MERS-CoV, might also be the source of COVID-19 due to the similarity of RaTG13 from the short RNA-dependent RNA polymerase (RdRp) region between bat coronavirus and SARS-CoV-2 [1, 4, 5]. The main mode Rabbit Polyclonal to TMEM101 of transmission is airborne, contact transmission and respiratory droplets and the median incubation period from exposure to onset for COVID-19 was about 3.0?days [6]. The majority of confirmed cases are between 30 and 79?years of age and that patients older than 60 tend to develop more serious symptoms or even die [7, 8]. Approximately 25.2C50.5% of patients with SARS-CoV-2 infection have one or more underlying diseases, including hypertension, diabetes, chronic obstructive pulmonary disease, cardiovascular disease, and malignancy [9, 10]. The clinical manifestations of patients with SARS-CoV-2 infection range from mild non-specific symptoms to severe pneumonia with organ function damage. The main clinical symptoms of COVID-19 are fever (83C98%), cough (59C82%), shortness of breath (19C55%), weakness (38.1C69.6%), sputum production (28.2C56.5%), headache (6.5C33.9%) and muscle aches (11C44%), which are similar to severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) [11]. For COVID-19, chest computed tomography (CT) plays a very important role in detecting infected individuals, with imaging showing mainly ground-glass opacity, interstitial abnormalities, patchy shadowing, crazy-paving pattern and septal thickening [12C14]. Therefore, the CT images of COVID-19 change in a variety of forms rapidly [15]. Besides, the changing levels of C-reactive protein (CRP), erythrocyte sedimentation rate, serum ferritin and interleukin-6 (IL-6), d-dimer, lactate dehydrogenase and creatine kinase might also indicate the disease progression [16]. Confirmation of SARS-CoV-2 infection mainly relies on the positive results of high-throughput sequencing or real-time reverse transcriptase-polymerase chain reaction (RT-PCR) test results [17]. Additionally, chest CT with its high sensitivity to COVID-19, has been given more value in the diagnosis [18]. The current treatment of COVID-19 depends on existing antiviral drugs and immunotherapy [19]. The delta-Valerobetaine mechanism of antiviral drugs is targeting various stages of the viral invasion pathway including virus recognition, fusion, entry and genome proliferation. Currently the main targets are the angiotensin-converting enzyme 2 delta-Valerobetaine (ACE2) receptor and the transmembrane protease/ serine subfamily member 2 (TMPRSS2) delta-Valerobetaine and common types of drugs are protease inhibitors, RNA polymerase inhibitors and interferons [20]. SARS-CoV-2 induces a hyper-inflammatory state characterized by an excessive immune response and cytokine dysregulation, which eventually leads to cytokine storms and fatal complications [21]. Thus, in addition to antiviral drugs and symptomatic treatment, immunomodulatory therapy is another critical measure. Common treatment options include corticosteroids, anti-cytokine drugs, Janus kinase (JAK) inhibitors, chloroquine (CQ), hydroxychloroquine (HCQ), convalescent plasma, Intravenous immunoglobulin (IVIG) and interferon (IFN). In addition to these two broad categories of treatment options, stem cell therapy and traditional herbal treatments could also be promising medication [22, 23]. For the prevention of COVID-19, a large number of vaccines are already in the development process, mainly including mRNA vaccine, DNA vaccine, recombinant vaccine Ad5-nCoV [24, 25]. In this review we collected updated evidence regarding the usage of various therapies for COVID-19 in clinical practice and its feasibility, hoping to offer helpful instructions for clinical management and strategies. Introduction of SARS-CoV-2 SARS-CoV-2 is tightly associated with SARS-CoV, both originating from bat [26C29]. For SARS-CoV, the intermediate hosts for zoonotic transmission of SARS-CoV between bats and humans are palm civets and raccoon dogs, while for SARS-CoV-2, the intermediate hosts have not.