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SARS-CoV-2: a storm is raging
Open accessAbstract
A rapidly expanding pandemicIn early December 2019, several local health facilities first reported pneumonia cases of unknown origin in Wuhan, China.This new coronavirus infectious disease (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was first reported on December 1, 2020 and identified as a previously unknown betacoronavirus (1, 2).Since then, studies have increasingly demonstrated that SARS-CoV-2 can be transmitted effectively among humans through aerosol or fomites (3-5).With transmission capabilities even before symptom onset (6, 7), this pandemic is rapidly evolving and expanding.As of April 2, 2020, a total of 962,977 confirmed cases of COVID-19 and 49,180 deaths have been reported across 180 countries and regions.Recent models indicated that as much as 86% of all infections early in the spread were undocumented, suggesting the real number of infections is likely much greater (8).As a public health emergency of international concern, COVID-19 was declared a pandemic by the World Health Organization.Public health authorities around the globe are now racing to contain the spread.
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“Patients infected with SARS-CoV-2 present elevated levels of IL-6, IL-10, IL-1β, INF-γ, CCL2, TNF-α, CXCL10, CCL7, IL-1 receptor antagonist and IL-2 receptor, supposedly associated with disease severity [9, 98–105].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [100]
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“Patients with severe disease exhibit profound inflammatory responses and immunopathology (10).”
BackgroundThe mechanistic basis linking cytokine storm to thrombosis in COVID-19
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“Significant upregulation of eicosanoids in COVID-19, perhaps creating an “eicosanoid storm”, may create an amplification effect that potentiates CSS [83].”
InfluentialNon-classical HLA class I molecules and their potential role in viral infections
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“The world’s apex health organization, WHO declared this as pandemic because of rapid spread in almost every part of the world [8, 9].”
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“This cross-sectional study was conducted in the COVID-19 high care unit (HCU) and intensive care unit (ICU) from June 2020 to February 2021.”
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Purbey, P. K., Roy, K., Gupta, S., & Paul, M. K. (2023) · Molecular Immunology · doi:10.1016/j.molimm.2023.03.009 · Cited by 19
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“Most adults infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develop minimal symptoms.(1) However, following an approximately 8-day interval, a subset of individuals with mild to moderate symptoms advance to severe/critical coronavirus disease 2019 (COVID-19).”
T cell receptor β repertoires in patients with COVID-19 reveal disease severity signatures
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“T cells, also known as T lymphocytes, are integral components of the immune response against coronaviruses (12 – 14).”
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NSAIDs for early management of acute respiratory infections
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“suggests that a cytokine cascade or “storm” may play a pathophysiological role in severe illness with increases in interleukin-2, interleukin-6, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumor necrosis factor-α…”
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Sex differences in immune responses to SARS-CoV-2 in patients with COVID-19
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“Critical patients were characterized with higher levels of IL-6, IL-10, TNFα [17], meanwhile, although the counts of CD4+ and CD8+ T lymphocytes decreased [17], they were overactive and Table 1 Baseline characteristics of COVID-19 patients at admission”
BackgroundA narrative review of COVID-19: magnesium isoglycyrrhizinate as a potential adjuvant treatment
Tang, C., Ding, H., Sun, Y., Han, Z., & Kong, L. (2021) · Annals of Palliative Medicine · doi:10.21037/apm-20-1971 · Cited by 18
“SARS-CoV-2 infects the human body, first characterized by increased secretion of early response cytokines such as IL-1, and TNF-α, further promoting the secretion of antiinflammatory cytokines to adjust the degree of inflammatory response and maintain immune homeostasis (139).”
BackgroundAdipose tissue dysfunction and MAFLD in obesity on the scene of COVID-19
Cordeiro, A., Ribamar, A., & Ramalho, A. (2021) · Clinics and Research in Hepatology and Gastroenterology · doi:10.1016/j.clinre.2021.101807 · Cited by 19
“Recent studies suggest that the virus may bind to ACE-2 receptors located on cells liver diseases, especially in cholangiocytes where their expression is more abundant [74,75].”
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Immunological Interfaces: The COVID-19 Pandemic and Depression
Perlmutter, A. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.657004 · Cited by 18
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“state, the massive cytokine release, which begins within the first 24–48 h of disease onset, causes a worsening of disease progression and severity that becomes evident after 7 to 10 days of infection [48].”
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Pacritinib Inhibition of IRAK1 Blocks Aberrant TLR8 Signalling by SARS-CoV-2 and HIV-1-Derived RNA
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“…[1, 2], impaired interferon (IFN) response [3–5] and T cell function [6–9], the production of autoantibodies [10], and the uncontrolled release and high circulating levels of pro-inflammatory cytokines including interleukin (IL) 1β (IL-1β), IL-6, and tumour necrosis factor (TNF) [5, 11–13].”
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Exploring the Potential of GANs in Biological Sequence Analysis
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“I. INTRODUCTION Biological sequences usually refer to nucleotides or amino acids-based sequences and their analysis can provide detailed information about the functional and structural behaviors of the corresponding viruses which are usually responsible for causing diseases, for example, Flu [1], Covid-19 [2], etc.”
BackgroundWu, H.-B., Wang, C., Chung, Y., Shan, Y.-S., Lin, Y.-J., Tsai, H., & Lee, G. (2023) · Analytica Chimica Acta · doi:10.1016/j.aca.2023.341531 · Cited by 16
“virus, which belongs to the betacoronavirus subfamily of the coronaviridae family; the viral genome is around 30 kb [1,2].”
Immunomodulating Phytochemicals: An Insight into their Potential Use in Cytokine Storm Situations.
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Acute necrotizing encephalopathy in children with COVID-19: a retrospective study of 12 cases
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Potential Use of Alpha-1 Anti-trypsin in the Covid-19 Treatment
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“In COVID-19 patients, disease severity and high mortality are associated to respiratory failure from ARDS and multiple organ dysfunctions due to an impressive cytokine storm, with significant increased levels of several inflammatory mediators, including IL-6, interferon gamma (INFγ), TNFα, interleukin 17 (IL-17), IL-8…”
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“Serum levels of IL family members are elevated in patients experiencing a cytokine storm, including IL-6, IL-1, IL-1β, tumor necrosis factor (TNF), and C-C chemokine ligand 2 (CCL2) [39, 40].”
BackgroundStroke increases the expression of ACE2, the SARS-CoV-2 binding receptor, in murine lungs
Singh, V., Beer, A., Kraus, A., Mang, F., Zhang, X., Xue, J., Hagemann, N., Hermann, D. M., & Gunzer, M. (2021) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2021.01.039 · Cited by 16
“The ensuing infection is accompanied by inflammatory lung injury and death and has caused a worldwide epidemic since its start at the end of 2019 (Pedersen and Ho, 2020).”
SARS-CoV-2 infection: molecular mechanisms of severe outcomes to suggest therapeutics
Hartog, N., Faber, W., Frisch, A., Bauss, J. M., Bupp, C. P., Rajasekaran, S., & Prokop, J. W. (2021) · Expert Review of Proteomics · doi:10.1080/14789450.2021.1908894 · Cited by 14
“Notable cytokines IL6, IL10, IL2, IL7, G-CSF, IP10, MCP1, MIP1A, and TNFα are produced as a result of severe COVID19, with a suppression of type I interferon [53,54].”
BackgroundPham, T. L., He, J., Kakazu, A. H., Calandria, J. M., Do, K. V., Nshimiyimana, R., Lam, T. F., Petasis, N. A., Bazán, H. E. P., & Bazan, N. G. (2021) · Scientific Reports · doi:10.1038/s41598-021-92293-x · Cited by 25
Cardiovascular Disease Complicating COVID-19 in the Elderly
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“Another key potential link between COVID-19 and hypertension is IL-6, a pleiotropic cytokine found at high levels in cytokine storms, which are responsible for stimulating the production of acute-phase proteins [46,47].”
BackgroundHypercoagulability of COVID-19 and Neurological Complications: A Review
MOORE, P. J., Esmail, F., Qin, S., Nand, S., & Berg, S. A. (2021) · Journal of Stroke and Cerebrovascular Diseases · doi:10.1016/j.jstrokecerebrovasdis.2021.106163 · Cited by 17
“Clinically, fever, multiple organ dysfunction and a CRS-like syndrome characterize CRS that may develop due to a severe viral infection, including COVID-19.(9)”
Pregnancy-specific responses to COVID-19 revealed by high-throughput proteomics of human plasma
Gomez‐Lopez, N., Romero, R. J., Escobar, M. F., Carvajal, J. A., Echavarría, M. P., Albornóz, L. L., Nasner, D., Miller, D., Gallo, D. M., Galaz, J., et al. (2023) · Communications Medicine · doi:10.1038/s43856-023-00268-y · Cited by 17
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Do COVID-19 Infections Result in a Different Form of Secondary Hemophagocytic Lymphohistiocytosis
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“COVID-19 patients display high levels of both inflammatory cytokines and chemokines (IL-1a/β, IP-10, MCP-1), with severe cases showing elevation in TNFα, IL-1, IL-6, IL-18, IL-8, IL-10, MCP-1 and MIP-1A [119,124,127,131,132].”
BackgroundPotential Prophylactic Treatments for COVID-19
Ben-Zuk, N., Dechtman, I.-D., Henn, I., Weiss, L., Afriat, A., Krasner, E., & Gal, Y. (2021) · Viruses · doi:10.3390/v13071292 · Cited by 15
“This upregulation of inflammatory mediators progresses in some patients to a “cytokine storm” [4].”
Backgroundde Paula, H. D. S. C., Santiago, S. B., de Araújo, L. A., Pedroso, C. F., Marinho, T. A., Gonçalves, I. A. D. J., Santos, T. A. P., Pinheiro, R. S., de Oliveira, G. A., & Batista, K. D. A. (2021) · Brazilian Journal of Medical and Biological Research · doi:10.1590/1414-431x2021e11631 · Cited by 14
“Patients with severe COVID19 present lower levels of CD4 and CD8 lymphocytes, decreased interferon-gamma expression by CD4 cells, and a higher level of pro- and anti-inflammatory cytokines, which may predispose them to superinfections (78,79).”
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“These cytokines are released upon SARS–CoV-2–induced alveolar tissue damage, mount systemic adaptive immunity to the virus, and trigger inflammation and tissue damage (19).”
BackgroundCOVID-19: влияние на иммунитет, систему гемостаза и возможные пути коррекции
Bi, K., Хавинсон, В. Х., & Линькова, Н. С. (2020) · Успехи физиологических наук · doi:10.31857/s0301179820040037 · Cited by 16
Time evolution of cytokine profiles associated with mortality in COVID-19 hospitalized patients
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“In fact, it has been observed that the reduction in IFN‐γ expression in CD4+ T cells is related to disease severity in patients with COVID‐19 (61).”
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Karina, K., Rosliana, I., Rosadi, I., Sobariah, S., Christoffel, L. M., Novariani, R., Rosidah, S., Fatkhurohman, N., Hertati, Y., Puspitaningrum, N., et al. (2021) · International Journal of Inflammation · doi:10.1155/2021/5531873 · Cited by 15
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“This finding supported the hypothesis that patients with severe COVID-19 exhibited strong inflammatory activation [5,6,8], and it confirmed previous findings from Abers et al.”
ResultDeciphering the immunoboosting potential of macro and micronutrients in COVID support therapy
Batiha, G. E., Al-Gareeb, A. I., Qusti, S. Y., Alshammari, E. M., Kaushik, D. K., Verma, R., & Al-Kuraishy, H. M. (2022) · Environmental Science and Pollution Research · doi:10.1007/s11356-022-20075-7 · Cited by 17
“This will be crucial to the so-known cytokine storm observed amid severe COVID-19 with the presentation of unsuppressed inflammation (Pedersen and Ho 2020; Gao et al. 2017).”
BackgroundApplying polypharmacology approach for drug repurposing for SARS-CoV2
Jamir, E., Sarma, H., Priyadarsinee, L., Nagamani, S., Kiewhuo, K., Gaur, A. S., Rawal, R. K., Murugan, N. A., Subramanian, V., & Sastry, G. N. (2022) · Journal of Chemical Sciences · doi:10.1007/s12039-022-02046-0 · Cited by 14
Raghavan, P. R. (2020) · BioMed Research International · doi:10.1155/2022/1558860 · Cited by 14
“Therefore, cytokine storms [85] result in ARDS.”
Dificultades para la regulación emocional del profesorado chileno en tiempos de SARS-CoV-2
Fuentes-Vilugrón, G., Lagos-Hernández, R., & Fuentes-Merino, P. (2022) · Bordón. Revista de pedagogía · doi:10.13042/bordon.2022.89794 · Cited by 20
Chen, K., Huang, Y., Wu, W.-S., Chang, L., Chu, C., & Kuo, H. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.995886 · Cited by 15
Li, L., Wang, X., Guo, X., Li, Y., Song, Q., & Li, A. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1013428 · Cited by 15
“According to clinical studies, an abnormal concentration of various cytokines (such as TNF-α , IL-6, IL-8) and an excessive release of reactive oxygen species in COVID-19 could cause an overactive immune response in COVID-19 (Behrens & Koretzky, 2017; Huang et al., 2020; Pedersen & Ho, 2020).”
BackgroundAnderson, C. F., Wang, Q., Stern, D., Leonard, E. K., Sun, B., Fergie, K. J., Choi, C.-Y., Spangler, J. B., Villano, J., Pekosz, A. S., et al. (2022) · Matter · doi:10.1016/j.matt.2022.11.027 · Cited by 14
Ahluwalia, P. K., Ahluwalia, M., Vaibhav, K., Mondal, A. K., Sahajpal, N., Islam, S. U., Fulzele, S., Kota, V. K., Dhandapani, K. M., Baban, B., et al. (2020) · The EPMA Journal · doi:10.1007/s13167-020-00230-1 · Cited by 14
“Given this progression, the swift pathological release of excessive amount of cytokines, termed as “cytokine storm” and is concomitant to high fever, respiratory distress, multi-organ failure, and increased mortality in COVID-19 patients [129, 130, 137].”
BackgroundMechanisms of COVID-19 thrombosis in an inflammatory environment and new anticoagulant targets.
Liu, H., Hu, T., Zhang, C., Chen, X., Zhang, S., Li, M., Jing, H., Wang, C., Hu, T., & Shi, J. (2021) · PubMed Central · Cited by 14
Nguee, S. Y. T., Júnior, J. W. B. D., Epiphânio, S., Rénia, L., & Claser, C. (2022) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2022.899581 · Cited by 14
“When this response becomes excessive, it may have deleterious effects on the lung tissue resulting in injury (Tutkun et al., 2019;West, 2019; Pedersen and Ho, 2020; Ragab et al., 2020).”
BackgroundPolypharmacology guided drug repositioning approach for SARS-CoV2
Jamir, E., Sarma, H., Priyadarsinee, L., Kiewhuo, K., Nagamani, S., & Sastry, G. N. (2023) · PLoS ONE · doi:10.1371/journal.pone.0289890 · Cited by 13
The neutrophil extracellular traps in neurological diseases: an update
Yu, X., Chen, Z., Bao, W., Jiang, Y., Ruan, F., Wu, D., & Le, K. (2024) · Clinical & Experimental Immunology · doi:10.1093/cei/uxae057 · Cited by 15
Bao, Y., Ma, Q., Chen, L., Feng, K., Guo, W., Huang, T., & Cai, Y. (2024) · Molecular Immunology · doi:10.1016/j.molimm.2024.12.004 · Cited by 14
Mechanisms Underlying Potential Therapeutic Approaches for COVID-19
Benani, A., & Mkaddem, S. B. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01841 · Cited by 15
Abnormal liver-related biomarkers in COVID-19 patients and the role of prealbumin
Wei, F., Li, T., Guo, Y., Zhuang, X., Huang, L., Zhang, X., & Yang, B. (2020) · Saudi Journal of Gastroenterology · doi:10.4103/sjg.sjg_239_20 · Cited by 14
“[6,7,12] Second, the cytokine storm ensuing the infection with SARS‐CoV‐2 leads to increased release of inflammatory factors and decreased CD4+ and CD8+ T lymphocyte counts.[13,14] Moreover, over‐activation of the inflammatory response, which is common in septic patients, may cause dysfunction of multiple organs, incl…”
BackgroundPredictive role of clinical features in patients with coronavirus disease 2019 for severe disease.
Mo, J., Liu, J., Wu, S., Lü, A., Xiao, L., Chen, D., Zhou, Y., Liang, L., Liu, X., & Zhao, J. (2020) · PubMed · doi:10.11817/j.issn.1672-7347.2020.200384 · Cited by 14
Efficacy and safety of tocilizumab in COVID-19 patients
Zheng, K., Xu, Y., Guo, Y., Diao, L., Kong, X., Wan, X., Zhao, F., Ning, F., Wang, L., Qiao, F., et al. (2020) · Aging · doi:10.18632/aging.103988 · Cited by 14
Coagulopathy as a Prodrome of Cytokine Storm in COVID-19-Infected Patients
Guo, H., Sheng, Y., Li, W., Li, F., Xie, Z., Li, J., Zhu, Y., Geng, J., Liu, G., Wang, L., et al. (2020) · Frontiers in Medicine · doi:10.3389/fmed.2020.572989 · Cited by 14
Perspectives on Targeting IL-6 as a Potential Therapeutic Strategy for COVID-19
Khaedir, Y., & Kartika, R. (2021) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2020.0135 · Cited by 13
“Increased levels of cytokines, such as tumor necrosis factor-a (TNF-a ), interleukin-6 (IL-6), and IL-10, lymphopenia, and decreased interferon-g (IFN-g ) expression are associated with severe COVID-19 (Pedersen and Ho 2020).”
Tocilizumab: From Rheumatic Diseases to COVID-19
Raiteri, A., Piscaglia, F., Granito, A., & Tovoli, F. (2021) · Current Pharmaceutical Design · doi:10.2174/1381612827666210311141512 · Cited by 14
Abreu-Hernández, L. F., Valdez-García, J. E., Hernández, R. I. E., & Olivares, S. L. O. (2020) · Gaceta Médica de México · doi:10.24875/gmm.20000306 · Cited by 14
Ferreira, G., Blasina, F., Rey, M. R., Anesetti, G., Sapiro, R., Chavarría, L., Cardozo, R., Rey, G., Sobrevía, L., & Nicolson, G. L. (2021) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2021.166285 · Cited by 15
“development of ARDS, leading to the development of the most severe cases of COVID-19 disease during the first and third trimester, or immediately after delivery [149,150].”
Kocherlakota, C., Banda, N., Narala, A., Srinath, A., Kothapalli, K. S. D., & Brenna, J. T. (2022) · Prostaglandins Leukotrienes and Essential Fatty Acids · doi:10.1016/j.plefa.2022.102426 · Cited by 16
“of COVID-19) [2], asthma [3,4], cystic fibrosis (CF) [5], chronic obstructive pulmonary disease (COPD) [6], interstitial lung disease (ILD) [7] or other lung disorders [8,9] are commonly accompanied by pulmonary inflammation.”
The relationship between human coronaviruses, asthma and allergy—An unresolved dilemma
Chałubiński, M., Gajewski, A., & Kowalski, M. L. (2020) · Clinical & Experimental Allergy · doi:10.1111/cea.13718 · Cited by 14
Current and New Drugs for COVID-19 Treatment and Its Effects on the Liver
Satsangi, S., Gupta, N. R., & Kodan, P. (2021) · Journal of Clinical and Translational Hepatology · doi:10.14218/jcth.2020.00174 · Cited by 14
Liver disorders in COVID-19, nutritional approaches and the use of phytochemicals
Vargas-Mendoza, N., García‐Machorro, J., Ángeles-Valencia, M., Martínez‐Archundia, M., Madrigal‐Santillán, E., Morales‐González, Á., Anguiano‐Robledo, L., & Morales‐González, J. A. (2021) · World Journal of Gastroenterology · doi:10.3748/wjg.v27.i34.5630 · Cited by 14
Role of Polypeptide Inflammatory Biomarkers in the Diagnosis and Monitoring of COVID-19
Sen, A., Nigam, A., & Vachher, M. (2022) · International Journal of Peptide Research and Therapeutics · doi:10.1007/s10989-022-10366-5 · Cited by 16
Ruiz‐Rodríguez, J. C., Chiscano‐Camón, L., Ruiz‐Sanmartín, A., Palmada, C., Plata-Menchaca, E. P., Franco‐Jarava, C., Pérez-Carrasco, M., Hernández-González, M., & Ferrer, R. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2021.779038 · Cited by 14
Geographic components of SARS-CoV-2 expansion: a hypothesis
Joyce, K. E., Weaver, S. R., & Lucas, S. J. E. (2020) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00362.2020 · Cited by 13
Mono/polyclonal free light chains as challenging biomarkers for immunological abnormalities
Napodano, C., Pocino, K., Gulli, F., Rossi, E. G., Rapaccini, G. L., Marino, M., & Basile, U. (2022) · Advances in clinical chemistry · doi:10.1016/bs.acc.2021.08.002 · Cited by 13
Adamescu, A.-I., Tilişcan, C., Stratan, L. M., Mihai, N., Ganea, O. A., Ciobanu, S., Marinescu, A. G., Aramă, V., & Aramă, Ș. S. (2025) · Medicina · doi:10.3390/medicina61040634 · Cited by 14
The Cross-Talk between Age, Hypertension and Inflammation in COVID-19 Patients: Therapeutic Targets
Casucci, G., Acanfora, D., & Incalzi, R. A. (2020) · Drugs & Aging · doi:10.1007/s40266-020-00808-4 · Cited by 14
Severe Acute Respiratory Syndrome Coronavirus 2-Induced Neurological Complications
Yu, S., & Yu, M. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.605972 · Cited by 15
“” Mononuclear phagocytes are over proliferated with accumulated interleukin (IL)6, IL-7, tumor necrosis factor (TNF), inflammatory chemokines CCL2, CCL3, and CXCL10 (Pedersen and Ho, 2020).”
BackgroundCardiovascular Complications of COVID-19 and Associated Concerns: A Review.
Yu, W.-L., Toh, H. S., Liao, C.-T., & Chang, W. (2021) · Europe PMC (PubMed Central) · doi:10.6515/acs.202101_37(1).20200913a · Cited by 13
“Although the exact mechanism has not been elucidated, the possible explanations include direct and indirect impacts on the cardiovascular system, such as SARS-CoV-2 infection per se, hypoxic injury, subsequent cytokine storm, coronary spasm, microthrombi, and an overactive immune system.(16,17) These series of reactio…”
BackgroundDravid, A. N., Kashiva, R., Khan, Z. A., Memon, D., Kodre, A., Potdar, P., Mane, M., Borse, R., Pawar, V., Patil, D. H., et al. (2021) · Medicine · doi:10.1097/md.0000000000026705 · Cited by 12
Use of Anti-Cytokine Therapy in Kidney Transplant Recipients with COVID-19
Bodro, M., Cofán, F., Ríos, J., Herrera, S., Linares, L., Marcos, M. Á., Soriano, À., Moreno, A., & Diekmann, F. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10081551 · Cited by 13
Update on Immunology of COVID-19 Disease and Potential Strategy for Controlling.
Dezfuli, N. K., Adcock, I. M., Montazami, N., Mortaz, E., & Velayati, A. A. (2020) · PubMed · Cited by 12
Metadata
- Authors
- Pedersen, S. F., & Ho, Y.-C.
- Affiliations
- Yale University (US)
- Corresponding author
- Ho, Ya-Chi
- ORCID
- Ho, Ya-Chi
- Venue
- Journal of Clinical Investigation
- Published
- 2020-04-13
- Volume
- 130
- Issue
- 5
- Pages
- 2202-2205
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC7190904
- OpenAlex
- W3014001472
- Cited by
- 1,137
- References
- 23
- Citations by year
- 2026: 11 · 2025: 34 · 2024: 60 · 2023: 113 · 2022: 183 · 2021: 341 · 2020: 395
- FWCI
- 33.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- amfAR, The Foundation for AIDS Research
- Yale University
- Gilead Sciences
- National Institutes of Health (AI150464, DA047037, UL1TR001863)
- National Institute on Drug Abuse (R61DA047037)
- National Institute of Allergy and Infectious Diseases (UM1AI126620, P50AI150464, R01AI047868, R01AI141009, R37AI147868)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Physical Sciences › Mathematics › Modeling and Simulation › COVID-19 epidemiological studies
- Keywords
- SARS-CoV-2, COVID-19 pandemic, pandemic, Betacoronavirus, airborne transmission, fomite transmission, pre-symptomatic transmission, undetected infections, WHO pandemic declaration
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Age Factors, Humans, Lymphocytes, Pneumonia, Viral, Respiratory Distress Syndrome, Severity of Illness Index, Cytokines, Coronavirus Infections, Disease Progression, Pandemics
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