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1.
J Med Virol ; 94(4): 1734-1737, 2022 04.
Article in English | MEDLINE | ID: covidwho-1568202

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral load dynamics in respiratory samples have been studied, but knowledge about changes in serial serum samples of infected patients in relation to their immunological response is lacking. We investigated the dynamics of SARS-CoV-2 viral load and antibody response in sequential serum of coronavirus disease 2019 (COVID-19) patients and attempted to culture the virus in the serum. A total of 81 sequential serum samples from 10 confirmed COVID-19 patients (5 with mild and 5 with moderate symptoms) were analyzed. Samples were collected during hospitalization and after discharge (median follow-up of 35 days). SARS-CoV-2 ribonucleic acid in the serum was detected by real-time polymerase chain reaction. Total antibody and IgG to SARS-CoV-2 Spike protein were analyzed by Chemiluminescent Immunoassays, and neutralizing antibodies were detected using a Surrogate Virus Neutralization Test. Viremia was observed in all cases at admission, and viral copy gradually dropped to undetectable levels in patients with mild symptoms but fluctuated and remained persistent in moderate cases. The viral culture of samples with the highest viral load for each patient did not show any cytopathic change. The antibody response was faster and higher in moderate cases. This study provides a basic clue for infectious severity-dependent immune response, viremia, and antibody acquisition pattern.


Subject(s)
COVID-19/immunology , COVID-19/virology , Viremia/immunology , Viremia/virology , Adult , Aged , Antibodies, Neutralizing/blood , Antibodies, Viral/blood , Female , Follow-Up Studies , Humans , Immunoglobulin G/blood , Male , Middle Aged , RNA, Viral/blood , RNA, Viral/genetics , SARS-CoV-2/genetics , SARS-CoV-2/immunology , SARS-CoV-2/isolation & purification , Severity of Illness Index , Viral Load
2.
J Autoimmun ; 123: 102703, 2021 09.
Article in English | MEDLINE | ID: covidwho-1322182

ABSTRACT

OBJECTIVES: Durability of the humoral immune response to SARS-CoV-2 has yet to be defined. We longitudinally evaluated during a 12-month period the antibody responses to SARS-CoV-2, and analysed predictors of antibody titres decline and seroreversion. METHODS: Prospective study conducted in a cohort of patients hospitalized for microbiologically-confirmed COVID-19. Blood and nasopharyngeal samples were sequentially obtained during hospital stay and at 1, 2, 6 and 12 months after patients' discharge for measuring anti-spike (S) and anti-nucleocapsid (N) IgG antibody levels and SARS-CoV-2 RNA, respectively. RESULTS: 80 non-vaccinated patients were analysed. At month 12 after discharge, 73 (91.2%) patients exhibited detectable S-IgG and 35 (43.8%) N-IgG antibody titres. A gradual wane was observed in S-IgG and N-IgG antibody titres. Linear regression showed that S-IgG decline was positively associated with peak antibody titres (coefficient [95% CI] 0.059 [0.05-0.067], p < 0.001), inversely with WHO severity score (coefficient [95% CI] -0.042 [-0.079/-0.004], p = 0.033), and there was a trivial positive association with age (coefficient [95% CI] 0.002 [0-0.005], p = 0.10); N-IgG decline was positively associated with peak antibody titres (coefficient [95% CI] 0.091 [0.078-0.105], p < 0.001). Logistic regression showed that seroreversion for S-IgG was inversely associated with peak S-IgG (OR 0.19; 95% CI, 0.04-0.45; p = 0.004); seroreversion for N-IgG was inversely associated with peak N-IgG (OR 0.71; 95% 0.53-0.90; p = 0.009) and positively with cycle threshold of RT-PCR (OR 1.14; 95% CI, 1.00-1.33; p = 0.062). CONCLUSION: Anti-spike IgG antibodies remain detectable one year after hospitalization for COVID-19. Higher peak antibody titres and disease severity were associated with increased durability of detectable antibodies.


Subject(s)
Antibodies, Neutralizing/immunology , Antibodies, Viral/immunology , COVID-19/immunology , Immunoglobulin G/immunology , SARS-CoV-2/immunology , Viremia/immunology , Adult , Aged , Antigens, Viral/immunology , Convalescence , Coronavirus Nucleocapsid Proteins/immunology , Female , Follow-Up Studies , Hospitalization , Humans , Male , Middle Aged , Phosphoproteins/immunology , Prospective Studies , RNA, Viral/blood , Spike Glycoprotein, Coronavirus/immunology , Time Factors , Viremia/blood
3.
PLoS Pathog ; 17(7): e1009381, 2021 07.
Article in English | MEDLINE | ID: covidwho-1291654

ABSTRACT

Clearance of viral infections, such as SARS-CoV-2 and influenza A virus (IAV), must be fine-tuned to eliminate the pathogen without causing immunopathology. As such, an aggressive initial innate immune response favors the host in contrast to a detrimental prolonged inflammation. The complement pathway bridges innate and adaptive immune system and contributes to the response by directly clearing pathogens or infected cells, as well as recruiting proinflammatory immune cells and regulating inflammation. However, the impact of modulating complement activation in viral infections is still unclear. In this work, we targeted the complement decay-accelerating factor (DAF/CD55), a surface protein that protects cells from non-specific complement attack, and analyzed its role in IAV infections. We found that DAF modulates IAV infection in vivo, via an interplay with the antigenic viral proteins hemagglutinin (HA) and neuraminidase (NA), in a strain specific manner. Our results reveal that, contrary to what could be expected, DAF potentiates complement activation, increasing the recruitment of neutrophils, monocytes and T cells. We also show that viral NA acts on the heavily sialylated DAF and propose that the NA-dependent DAF removal of sialic acids exacerbates complement activation, leading to lung immunopathology. Remarkably, this mechanism has no impact on viral loads, but rather on the host resilience to infection, and may have direct implications in zoonotic influenza transmissions.


Subject(s)
CD55 Antigens/physiology , Influenza A Virus, H1N1 Subtype/isolation & purification , Lung/immunology , Viremia/immunology , Animals , Bronchoalveolar Lavage Fluid/immunology , CD55 Antigens/chemistry , CD55 Antigens/deficiency , Chemotaxis, Leukocyte , Complement Activation , Hemagglutinin Glycoproteins, Influenza Virus/physiology , Host Adaptation , Host Specificity , Host-Pathogen Interactions , Influenza A Virus, H1N1 Subtype/enzymology , Influenza A Virus, H1N1 Subtype/pathogenicity , Influenza A Virus, H1N1 Subtype/physiology , Interferon-gamma/analysis , Lung/pathology , Lung/virology , Mice , Mice, Inbred C57BL , N-Acetylneuraminic Acid , Neuraminidase/physiology , Orthomyxoviridae Infections/immunology , Orthomyxoviridae Infections/pathology , Viral Load , Viral Proteins/physiology , Virulence , Virus Replication , Weight Loss
4.
Mol Neurobiol ; 58(9): 4694-4715, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1281328

ABSTRACT

The unremitting coronavirus disease 2019 (COVID-19) pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) marked a year-long phase of public health adversaries and has severely compromised healthcare globally. Early evidence of COVID-19 noted its impact on the pulmonary and cardiovascular functions, while multiple studies in recent time shed light on its substantial neurological complications, though a comprehensive understanding of the cause(s), the mechanism(s), and their neuropathological outcomes is scarce. In the present review, we conferred evidence of neurological complications in COVID-19 patients and shed light on the SARS-CoV-2 infection routes including the hematogenous, direct/neuronal, lymphatic tissue or cerebrospinal fluid, or infiltration through infected immune cells, while the underlying mechanism of SARS-CoV-2 invasion to the central nervous system (CNS) was also discussed. In an up-to-date manner, we further reviewed the impact of COVID-19 in developing diverse neurologic manifestations associated with CNS, peripheral nervous system (PNS), skeletal muscle, and also pre-existing neurological diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, and myasthenia gravis. Furthermore, we discussed the involvement of key factors including age, sex, comorbidity, and disease severity in exacerbating the neurologic manifestations in COVID-19 patients. An outlook of present therapeutic strategies and state of existing challenges in COVID-19 management was also accessed. Conclusively, the present report provides a comprehensive review of COVID-19-related neurological complications and emphasizes the need for their early clinical management in the ongoing COVID-19 pandemic.


Subject(s)
COVID-19/complications , Nervous System Diseases/etiology , Pandemics , SARS-CoV-2/pathogenicity , Adult , Age Factors , Aged , Aged, 80 and over , Autoimmune Diseases of the Nervous System/epidemiology , Autoimmune Diseases of the Nervous System/etiology , COVID-19/epidemiology , COVID-19/immunology , COVID-19/virology , Central Nervous System/virology , Child , Comorbidity , Female , Humans , Immune System/virology , Inflammation , Male , Middle Aged , Models, Biological , Muscular Diseases/etiology , Nervous System Diseases/drug therapy , Nervous System Diseases/epidemiology , Nervous System Diseases/physiopathology , Neurodegenerative Diseases/complications , Neurons/virology , Organ Specificity , Sex Factors , Viremia/chemically induced , Viremia/immunology , Virus Internalization
5.
J Am Heart Assoc ; 10(9): e019756, 2021 05 04.
Article in English | MEDLINE | ID: covidwho-1088348

ABSTRACT

Background COVID-19 may present with a variety of cardiovascular manifestations, and elevations of biomarkers reflecting myocardial injury and stress are prevalent. SARS-CoV-2 has been found in cardiac tissue, and myocardial dysfunction post-COVID-19 may occur. However, the association between SARS-CoV-2 RNA in plasma and cardiovascular biomarkers remains unknown. Methods and Results COVID MECH (COVID-19 Mechanisms) was a prospective, observational study enrolling consecutive, hospitalized patients with laboratory-confirmed infection with SARS-CoV-2 and symptoms of COVID-19. Biobank plasma samples used to measure SARS-CoV-2 RNA and cardiovascular and inflammatory biomarkers were collected in 123 patients at baseline, and in 96 patients (78%) at day 3. Patients were aged 60±15 (mean ± SD) years, 71 (58%) were men, 68 (55%) were White, and 31 (25%) received mechanical ventilation during hospitalization. SARS-CoV-2 RNA was detected in plasma from 48 (39%) patients at baseline. Patients with viremia were more frequently men, had more diabetes mellitus, and lower oxygen saturation. Patients with viremia had higher concentrations of interleukin-6, C-reactive protein, procalcitonin, and ferritin (all <0.001), but comparable levels of cTnT (cardiac troponin T; P=0.09), NT-proBNP (N-terminal pro-B-type natriuretic peptide; P=0.27) and D-dimer (P=0.67) to patients without viremia. SARS-CoV-2 RNA was present in plasma at either baseline or day 3 in 50 (52%) patients, and these patients experienced increase from baseline to day 3 in NT-proBNP and D-dimer concentrations, while there was no change in cTnT. Conclusions SARS-CoV-2 viremia was associated with increased concentrations of inflammatory, but not cardiovascular biomarkers. NT-proBNP and D-dimer, but not cTnT, increased from baseline to day 3 in patients with viremia. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT04314232.


Subject(s)
Biomarkers/blood , COVID-19 , Inflammation/blood , SARS-CoV-2/isolation & purification , Viremia , C-Reactive Protein/analysis , COVID-19/blood , COVID-19/diagnosis , COVID-19/epidemiology , Correlation of Data , Female , Ferritins/blood , Fibrin Fibrinogen Degradation Products/analysis , Humans , Inflammation/virology , Interleukin-6/blood , Male , Middle Aged , Natriuretic Peptide, Brain/blood , Norway/epidemiology , Peptide Fragments/blood , Procalcitonin/blood , Troponin T/blood , Viremia/diagnosis , Viremia/etiology , Viremia/immunology
6.
Infect Genet Evol ; 88: 104684, 2021 03.
Article in English | MEDLINE | ID: covidwho-1065474

ABSTRACT

We document two cases of viremic and prolonged active infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) where the viral genome was conserved for two months, but infection was with little or no symptoms. The first infection persisted for 80 days and the second for 62 days. Clearance of infection occurred 40 and 41 days, respectively, after development of detectable antibodies. Both cases were identified incidentally in an investigation of reinfection in a cohort of 133,266 laboratory-confirmed infected persons.


Subject(s)
Antibodies, Viral/blood , COVID-19/immunology , Genome, Viral , RNA, Viral/blood , SARS-CoV-2/genetics , Viremia/immunology , Adult , Asymptomatic Diseases , COVID-19/diagnosis , COVID-19/virology , COVID-19 Testing , Enzyme-Linked Immunosorbent Assay , Female , Humans , Infectious Disease Incubation Period , Male , Reverse Transcriptase Polymerase Chain Reaction , SARS-CoV-2/growth & development , SARS-CoV-2/immunology , Time Factors , Viremia/diagnosis , Viremia/virology
7.
Transplant Proc ; 52(9): 2637-2641, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-813884

ABSTRACT

Here we report a single-center cohort of 6 patients (4 kidney only, and 2 simultaneous liver/kidney transplants) diagnosed with COVID-19 at a median of 1.9 years (range = 0.2-9.3 years) post transplant. Five (of 6) patients required inpatient admission, 2 patients (mortality = 33%) died. Among those with mortality, an increased concentration of inflammatory biomarkers (interleukin-6 and C-reactive protein) was noted with a lack of response to interleukin-6 blockade, remdesivir, and/or convalescent plasma. None of the kidney-only transplants (4/6; 67%) had elevation in plasma donor-derived cell-free DNA above the previously published cut-off of 1%, suggesting absence of significant allo-immune injury. Four (of 5) admitted patients had detectable SARS-CoV-2 (severe acute respiratory syndrome-coronavirus 2) in blood on samples obtained at/during hospitalization. Of the 4 discharged patients, 2 patients with undetectable virus on repeat nasopharyngeal swabs had seroconversion with positive SARS-CoV-2 IgG formation at 30 to 48 days post infection. One patient had prolonged shedding of virus on nasopharyngeal swab at 28 days post discharge despite lack of symptoms. In this preliminary report, we find that immunocompromised transplant patients had higher rates of RNAemia (67%) than reported in the general population (15%), seeming absence of allo-immune injury despite systemic inflammation, and formation of IgG overtime after recovery from infection.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/immunology , Immunocompromised Host/immunology , Kidney Transplantation/adverse effects , Pneumonia, Viral/immunology , Postoperative Complications/immunology , Adult , COVID-19 , Coronavirus Infections/mortality , Coronavirus Infections/therapy , Coronavirus Infections/virology , Female , Hospitalization/statistics & numerical data , Humans , Immunization, Passive , Male , Middle Aged , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Postoperative Complications/mortality , Postoperative Complications/virology , SARS-CoV-2 , Viremia/immunology , Viremia/mortality , Viremia/virology
8.
Transpl Infect Dis ; 22(6): e13367, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-596059

ABSTRACT

The clinical course and outcomes of immunocompromised patients, such as transplant recipients, with COVID-19 remain unclear. It has been postulated that a substantial portion of the disease burden seems to be mediated by the host immune activation to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Herein, we present a simultaneous heart-kidney transplant (SHKT) recipient who was hospitalized for the management of respiratory failure from volume overload complicated by failure to thrive, multiple opportunistic infections, and open non-healing wounds in the setting of worsening renal dysfunction weeks prior to the first case of SARS-CoV-2 being detected in the state of Connecticut. After his third endotracheal intubation, routine nucleic acid testing (NAT) for SARS-CoV-2, in anticipation of a planned tracheostomy, was positive. His hemodynamics, respiratory status, and ventilator requirements remained stable without any worsening for 4 weeks until he had a negative NAT test. It is possible that the immunocompromised status of our patient may have prevented significant immune activation leading up to clinically significant cytokine storm that could have resulted in acute respiratory distress syndrome and multisystem organ failure.


Subject(s)
COVID-19/immunology , Cardiomyopathy, Dilated/surgery , Heart Transplantation , Immunocompromised Host/immunology , Immunosuppressive Agents/therapeutic use , Kidney Failure, Chronic/surgery , Kidney Transplantation , Malnutrition/immunology , Opportunistic Infections/immunology , Antibiotics, Antineoplastic/adverse effects , BK Virus , Bacteremia/complications , Bacteremia/immunology , COVID-19/complications , COVID-19 Nucleic Acid Testing , Cardiomyopathy, Dilated/chemically induced , Cardiomyopathy, Dilated/complications , Cardiotoxicity , Doxorubicin/adverse effects , Graft Rejection/prevention & control , Gram-Positive Bacterial Infections/complications , Gram-Positive Bacterial Infections/immunology , Humans , Incidental Findings , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/therapy , Male , Malnutrition/complications , Methicillin-Resistant Staphylococcus aureus , Middle Aged , Mycophenolic Acid/therapeutic use , Opportunistic Infections/complications , Polyomavirus Infections/complications , Polyomavirus Infections/immunology , Postoperative Complications/therapy , Prednisone/therapeutic use , Renal Dialysis , SARS-CoV-2 , Staphylococcal Infections/complications , Staphylococcal Infections/immunology , Surgical Wound Infection/complications , Surgical Wound Infection/immunology , Tacrolimus/therapeutic use , Tracheostomy , Tumor Virus Infections/complications , Tumor Virus Infections/immunology , Vancomycin-Resistant Enterococci , Viremia/complications , Viremia/immunology , Water-Electrolyte Imbalance/complications , Water-Electrolyte Imbalance/therapy
9.
Int Immunopharmacol ; 85: 106683, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-548979

ABSTRACT

BACKGROUND: Since December 2019, novel coronavirus (SARS-CoV-2)-infected pneumonia (COVID-19) occurred in Wuhan, and rapidly spread throughout China. Our study aimed to evaluate the robustness of neutrophil to CD4+ lymphocyte ratio (NCD4LR) in predicting the negative conversion time (NCT) of SARS-CoV-2 in COVID-19 patients. METHODS: Univariate and multivariate analysis were conducted to evaluate the independency of NCD4LR in predicting NCT. Receiver operating characteristic (ROC) curve analysis and area under the curve (AUC) were used to assess the diagnostic accuracy. RESULTS: Compared with low NCD4LR patients, patients with high NCD4LR had an older age; higher incidence of fever, fatigue, chest distress/breath shortness, severer disease assessment on admission; higher levels of inflammatory indicators; low levels of lymphocyte subsets, and a longer NCT. Multivariate analysis also identified NCD4LR as an independent risk factor for delayed NCT. ROC analysis showed that NCD4LR had a better performance than neutrophil to lymphocyte ratio in predicting the virus negative conversion within 2 weeks (AUC = 0.772), 3 weeks (AUC = 0.710), 4 weeks (AUC = 0.728), or 5 weeks (AUC = 0.815). CONCLUSION: This study suggests that NCD4LR is a potential and useful biomarker for predicting the virus negative conversion time in COVID-19 patients. Furthermore, due to the NCDLR value is easily calculated, it can be widely used as a clinical biomarker for disease progression and clinical outcomes in COVID-19 patients.


Subject(s)
Antibodies, Viral/blood , Betacoronavirus/isolation & purification , CD4-Positive T-Lymphocytes , Clinical Laboratory Techniques , Coronavirus Infections/immunology , Leukocyte Count , Neutrophils , Pneumonia, Viral/immunology , Viral Load , Viremia/immunology , Adult , Age Factors , Aged , Area Under Curve , Betacoronavirus/immunology , Biomarkers , COVID-19 , COVID-19 Testing , Convalescence , Coronavirus Infections/blood , Coronavirus Infections/diagnosis , Coronavirus Infections/virology , Female , Humans , Inflammation , Inpatients , Lymphocyte Count , Male , Middle Aged , Multivariate Analysis , Nasopharynx/virology , Pandemics , Patient Discharge , Pneumonia, Viral/blood , Pneumonia, Viral/virology , ROC Curve , Retrospective Studies , Risk Factors , SARS-CoV-2 , Symptom Assessment , Time Factors
10.
J Immunol ; 205(1): 12-19, 2020 07 01.
Article in English | MEDLINE | ID: covidwho-306037

ABSTRACT

The 2019 coronavirus disease (COVID-19) pandemic caused by the virus severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has created an unprecedented global crisis for the infrastructure sectors, including economic, political, healthcare, education, and research systems. Although over 90% of infected individuals are asymptomatic or manifest noncritical symptoms and will recover from the infection, those individuals presenting with critical symptoms are in urgent need of effective treatment options. Emerging data related to mechanism of severity and potential therapies for patients presenting with severe symptoms are scattered and therefore require a comprehensive analysis to focus research on developing effective therapeutics. A critical literature review suggests that the severity of SARS-CoV-2 infection is associated with dysregulation of inflammatory immune responses, which in turn inhibits the development of protective immunity to the infection. Therefore, the use of therapeutics that modulate inflammation without compromising the adaptive immune response could be the most effective therapeutic strategy.


Subject(s)
Coronavirus Infections/immunology , Coronavirus Infections/pathology , Cytokine Release Syndrome/immunology , Pneumonia, Viral/immunology , Pneumonia, Viral/pathology , Adaptive Immunity , Age Factors , Animals , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/therapy , Cytokine Release Syndrome/pathology , Health Status Disparities , Humans , Pandemics , Pneumonia, Viral/epidemiology , Pneumonia, Viral/therapy , Sex Factors , Viremia/immunology , Viremia/pathology
11.
Clin Immunol ; 215: 108410, 2020 06.
Article in English | MEDLINE | ID: covidwho-38673

ABSTRACT

Infection caused by SARS-CoV-2 can result in severe respiratory complications and death. Patients with a compromised immune system are expected to be more susceptible to a severe disease course. In this report we suggest that patients with systemic lupus erythematous might be especially prone to severe COVID-19 independent of their immunosuppressed state from lupus treatment. Specifically, we provide evidence in lupus to suggest hypomethylation and overexpression of ACE2, which is located on the X chromosome and encodes a functional receptor for the SARS-CoV-2 spike glycoprotein. Oxidative stress induced by viral infections exacerbates the DNA methylation defect in lupus, possibly resulting in further ACE2 hypomethylation and enhanced viremia. In addition, demethylation of interferon-regulated genes, NFκB, and key cytokine genes in lupus patients might exacerbate the immune response to SARS-CoV-2 and increase the likelihood of cytokine storm. These arguments suggest that inherent epigenetic dysregulation in lupus might facilitate viral entry, viremia, and an excessive immune response to SARS-CoV-2. Further, maintaining disease remission in lupus patients is critical to prevent a vicious cycle of demethylation and increased oxidative stress, which will exacerbate susceptibility to SARS-CoV-2 infection during the current pandemic. Epigenetic control of the ACE2 gene might be a target for prevention and therapy in COVID-19.


Subject(s)
Coronavirus Infections/genetics , Epigenesis, Genetic , Genetic Predisposition to Disease , Lupus Erythematosus, Systemic/genetics , Pandemics , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/genetics , Viremia/genetics , Angiotensin-Converting Enzyme 2 , Betacoronavirus/immunology , Betacoronavirus/pathogenicity , CD11a Antigen/genetics , CD11a Antigen/immunology , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Cytokines/genetics , Cytokines/immunology , DNA Methylation , Disease Progression , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , Humans , Interferon Regulatory Factors/genetics , Interferon Regulatory Factors/immunology , Lupus Erythematosus, Systemic/complications , Lupus Erythematosus, Systemic/epidemiology , Lupus Erythematosus, Systemic/immunology , NF-kappa B/genetics , NF-kappa B/immunology , Oxidative Stress/genetics , Oxidative Stress/immunology , Peptidyl-Dipeptidase A/immunology , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , Protein Binding , Receptors, KIR/genetics , Receptors, KIR/immunology , SARS-CoV-2 , Signal Transduction , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/immunology , Viremia/complications , Viremia/epidemiology , Viremia/immunology
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