Corona Virus Disease 2019 (COVID-19) is caused by the novel coronavirus SARS-CoV-2. Emerging genetic and clinical evidence suggests similarities between COVID-19 patients and those with severe acute respiratory syndrome and Middle East respiratory syndrome. Hematological changes such as lymphopenia and thrombocytopenia are not rare in COVID-19 patients, and a smaller population of these patients had leukopenia. Thrombocytopenia was detected in 5-41.7% of the patients with COVID-19. Analyzing the dynamic decrease in platelet counts may be useful in the prognosis of patients with COVID-19. However, the mechanisms underlying the development of thrombocytopenia remain to be elucidated. This review summarizes the hematological changes in patients infected with SARS-CoV-2 and possible underlying mechanisms of thrombocytopenia development. Coronavirus types and their receptorsSix types of human CoVs have been identified till date: HCoV-NL63 and HCoV-229E are Alphacoronaviruses and HCoV-OC43, HCoVHKU1, SARS-CoV, and Middle East respiratory syndrome coronavirus (MERS-CoV) are Betacoronaviruses (Table I) [6-10]. SARS-CoV-2 is the seventh member of the RNA-containing enveloped CoV family. SARS-CoV-2 and SARS-CoV reside on different branches of the phylogenetic tree, but the genome of SARS-CoV-2 shares more than 85% homology with that of SARS-CoV [7]. HCoV-229E, OC43, NL63, and HKU1 cause mild respiratory diseases. The last two decades have seen fatal infections caused by SARS-CoV and MERS-CoV [8].CoVs use cell surface receptors to enter host cells [9]. SARS-CoV primarily binds to the angiotensin-converting enzyme 2 (ACE2) [10], whereas MERS-CoV interacts with dipeptidyl peptidase 4 (DPP4; also known as CD26; Table I). Similar to SARS-CoV, COVID-19 develops upon binding of SARS-CoV-2 viral particles to ACE2, but not to other CoV receptors, such as aminopeptidase N and DPP4 [7]. SARS-CoV has similar antigenic characteristics as human 12]. HCoV-229E enters monocytes and macrophages via CD13 and induces cell apoptosis [13]. In addition, Betacoronaviruses can utilize CEACAMla (CD66a) as receptors [4,14]. Clinical manifestations and treatment of COVID-19Patients with COVID-19 can be divided into four categories based on their clinical manifestations: light, common, severe, and critical. Guan et al. performed a retrospective study (n = 1099) demonstrated that COVID-19 is associated with a wide range of symptoms [1]. Fever
Severe acute respiratory syndrome (SARS), caused by infection with a novel coronavirus (SARS-CoV), was the first major novel infectious disease at the beginning of the 21st century, with China especially affected. SARS was characterized by high infectivity, morbidity and mortality, and the confined pattern of the disease spreading among the countries of South-East and East Asia suggested the existence of susceptible factor(s) in these populations. Studies in the populations of Hong Kong and Taiwan showed an association of human leucocyte antigen (HLA) polymorphisms with the development and/or severity of SARS, respectively. The aim of the present study was to define the genotypic patterns of HLA-A, -B and -DRB1 loci in SARS patients and a co-resident population of Guangdong province, southern China, where the first SARS case was reported. The samples comprised 95 cases of recovered SARS patients and 403 unrelated healthy controls. HLA -A, -B and -DRB1 alleles were genotyped using polymerase chain reaction with sequence-specific primers. The severity of the disease was assessed according to the history of lung infiltration, usage of assisted ventilation and occurrence of lymphocytopenia. Although the allelic frequencies of A23, A34, B60, DRB1*12 in the SARS group were slightly higher, and A33, -B58 and -B61 were lower than in the controls, no statistical significance was found when the Pc value was considered. Similarly, no association of HLA alleles with the severity of the disease was detected. Thus, variations in the major histocompatibility complex are unlikely to have contributed significantly to either the susceptibility or the severity of SARS in the population of Guangdong.
Acute lung injury (ALI) caused by sepsis occurs early and the condition is severe, and is also an important reason for accelerating the death of patients. Increasing evidence has identified long non‐coding RNA (lncRNA) metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) as a regulator of ALI. However, the potential mechanism underlying MALAT1 on ALI still needs further identification. To explore the mechanisms of gene regulation expression mediated by MALAT1 through miR‐149/MyD88 in lung injury inflammation, we constructed a lung injury inflammatory model using the lipopolysaccharides (LPS)‐induced method and quantificated the cytokines and signaling cascade molecules as well as miR‐149. The MALAT1, myeloid differentiation factor 88 (MyD88), tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and IL‐6 levels were significantly increased, and the nuclear factor‐κB (NF‐κB) pathway was activated, but the miR‐149 level was decreased in the LPS‐induced ALI model. miR‐149 directly targeted both lncRNA MALAT1 and the MyD88 gene. Knockdown of MALAT1 down‐regulated the levels of MyD88, TNF‐α, IL‐1β, and IL‐6, and inhibited the NF‐κB pathway. However, MALAT1 knockdown up‐regulated the expression of miR‐149. Overexpression of miR‐149 down‐regulated MyD88, TNF‐α, IL‐1β, and IL‐6 levels, and inhibited the NF‐κB pathway. MALAT1 acts as a pro‐inflammatory factor in ALI via the miR‐149/MyD88/NF‐κB axis and is therefore a potential novel therapeutic target for ALI treatment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.