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Immune Responses in Coronavirus Disease
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Immune Responses in Coronavirus Disease

A special issue of COVID (ISSN 2673-8112).

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 13178

Special Issue Editor

Prof. Dr. Martin H. Bluth

E-Mail Website
Guest Editor
1. Blood Transfusion and Donor Services, Maimonides Medical Center, Brooklyn, NY, USA
2. Department of Pathology, Wayne State University School of Medicine, Detroit, MI, USA
Interests: biomarker discovery; inflammation; immunotherapeutics; IgE/IgG antibody regulation; ADCC
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

COVID-19 has both devastated and revolutionized the way we address pandemic-based health and disease. We have matured from nucleic-acid-based testing, social distancing, personal protective equipment, and stay-at-home mandates to immunization, treatment modalities with side-effect profiling, rapid antigen testing, variation/mutation in COVID-19 infection as well as severity of symptom presentation. While it appears that the worst of the COVID-19 pandemic may be behind us, the question of the state of our functional immune status post-natural infection and/or vaccination remains an area of importance. Initial assessment of anti-COVID-19 immunity status gave rise to various treatment modalities, including COVID-19 Convelescent Plasma, hyper-COVID-19 immunoglobulin preparations, select cellular therapies, and immunization regiments to name a few. What about going forward? How do we know if we have a modicum of functional immunity to combat the current or potential new versions of COVID-19? This includes general anti-COVID-19 immunoglobulin presence, neutralizing antibodies, cellular-based responses and the like. This Special Issue on "Immune Responses in Coronavirus Disease" seeks to explore this important question in greater detail. The relationships of immunoglobulin isotypes and subclasses, dendridic cell activation, and everything in between that can induce functional protective immunity by way of opsonization, neutralization, eradication, as well as minimization of previous, current, and potentially future COVID-19 insults remains the subject matter of this Special Issue. COVID is likely here to stay. Understanding how we immunologically relate to the vestiges of this pandemic will help us navigate how we will interact with it in the days to come.

Prof. Dr. Martin H. Bluth
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. COVID is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • COVID-19
  • Coronavirus
  • immune response
  • neutralizing antibody
  • convelescent plasma

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Published Papers (5 papers)

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Research

14 pages, 1760 KiB  
Article
Does COVID-19 Really Exacerbate Urticaria? A Survey of 166 Patients in China
by Qian Yang, Zihao Zou, Wei Cao, Yunzhou Shi, Xianjun Xiao, Sijue Chen and Ying Li
COVID 2023, 3(12), 1707-1720; https://doi.org/10.3390/covid3120118 - 21 Nov 2023
Viewed by 2510
Abstract
The COVID-19 pandemic significantly disrupted global healthcare systems. The impacts of SARS-CoV-2 infection on urticaria and its management are unknown. This study aimed to collect information about patients with urticaria infected with SARS-CoV-2 and to investigate the impact of SARS-CoV-2 infection on urticaria [...] Read more.
The COVID-19 pandemic significantly disrupted global healthcare systems. The impacts of SARS-CoV-2 infection on urticaria and its management are unknown. This study aimed to collect information about patients with urticaria infected with SARS-CoV-2 and to investigate the impact of SARS-CoV-2 infection on urticaria severity, course, and treatment to better support recovery. This was a questionnaire-based study of patients with urticaria infected with SARS-CoV-2. Changes in urticaria severity (measured with the urticaria activity score (UAS)), course, and treatment were assessed before, during, and after SARS-CoV-2 infection. The mean (±SD) UAS scores were 5.17 ± 1.67, 4.23 ± 1.98, and 4.37 ± 1.93 before, during, and after SARS-CoV-2 infection, respectively (F = 8.839, p < 0.01). The median (IQR) wheal score was 0.464 (0.464, 0.763), 0.464 (0.138, 0.763), and 0.464 (0.138, 0.763) before, during, and after infection, respectively (Kruskal–Wallis H-test, H = 12.230, p = 0.02). The median (IQR) pruritus score was 0.695 (0.395, 0.695), 0.394 (0.123, 0.695), and 0.394 (0.123, 0.695) before, during, and after infection, respectively (Kruskal–Wallis H-test, H = 21.001, p < 0.01). Within the limitations of a questionnaire study, urticaria appears to improve during SARS-CoV-2 infection and worsens slightly after recovery, and the frequency of Western medicine use increases. Full article
(This article belongs to the Special Issue Immune Responses in Coronavirus Disease)
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17 pages, 1976 KiB  
Article
The rs2228145 Variant of the Interleukin-6 Receptor (IL-6R) Gene Impacts on In Vitro Cellular Responses to SARS-CoV-2 VOC B1.1.7 Recombinant Spike Protein
by Saira Sarwar, Rebecca Aicheler, Lee Butcher, Katie Rees, Stephen Potter, Richard Rowlands and Richard Webb
COVID 2023, 3(10), 1554-1570; https://doi.org/10.3390/covid3100106 - 3 Oct 2023
Viewed by 2279
Abstract
Given the variability in inflammatory responses to SARS-CoV-2 infection observed within human populations, we aimed to develop an in vitro model system (based on monocyte-macrophages, a key relevant cell type) that could yield insights regarding the impact of rs2228145, a clinically relevant polymorphism [...] Read more.
Given the variability in inflammatory responses to SARS-CoV-2 infection observed within human populations, we aimed to develop an in vitro model system (based on monocyte-macrophages, a key relevant cell type) that could yield insights regarding the impact of rs2228145, a clinically relevant polymorphism within the coding region of a key inflammatory gene in the body’s response to SARS-CoV-2 infection: the interleukin-6 receptor (IL-6R) gene. Three monocyte-macrophage cell-lines (U937, THP-1, MM6) were shown to exhibit AA, AC and CC rs2228145 genotypes, respectively, and to exhibit an MM6 > THP-1 > U937 pattern regarding basal levels of soluble IL-6R (sIL-6R) release. Similar MM6 > THP-1 > U937 patterns were seen regarding the extents to which (i) circulating levels of the IL-6/sIL-6R ‘active complex’ increased and (ii) phosphorylation of the downstream transcription-factor STAT3 occurred, following treatment with SARS-CoV-2 spike protein (SP). Moreover, a blocking antibody for the ACE-2 entry receptor for SARS-CoV-2 suppressed effects (i) and (ii), suggesting that interaction between SP and ACE-2 is the initial event that triggers IL-6/IL-6R signalling in our system. Production of IL-8 occurred to greater extents in A549 lung epithelial cells treated with tissue-culture supernatants from SP-treated MM6 cultures than SP-treated THP-1 or U937 cultures. Our data indicate that the rs2228145 genotype significantly impacts upon SP-associated IL-6/sIL-6R signalling in vitro, suggesting that it may influence in vivo risk of developing severe COVID-19 and/or long-COVID symptoms following infection by SARS-CoV-2. Thus, the rs2228145 genotype may have potential as a biomarker that differentiates between patients at risk of developing severe and/or prolonged symptoms following infection by SARS-CoV-2 and those who are at less risk. Full article
(This article belongs to the Special Issue Immune Responses in Coronavirus Disease)
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12 pages, 1810 KiB  
Article
Detection of Neutralizing Antibodies in COVID-19 Patients from Steve Biko Academic Hospital Complex: A Pilot Study
by Mankgopo Kgatle, Joseph Musonda Chalwe, Donald van der Westhuizen, Shuting Xu, Botle Precious Damane, Precious Mathebela, Veronica Ueckermann, Simnikiwe Mayaphi, Hosana Gomes Rodrigues, Pedro Moura-Alves, Honest Ndlovu, Yonwaba Mzizi, Lusanda Zongo, Henry Hairwadzi, Mariza Vorster, Jan Rijn Zeevaart and Mike Sathekge
COVID 2023, 3(7), 999-1010; https://doi.org/10.3390/covid3070072 - 3 Jul 2023
Viewed by 2766
Abstract
A correlation between neutralization activity after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination and protection against coronavirus disease 2019 (COVID-19) has been demonstrated by several studies. Here, we detect SARS-CoV-2 neutralizing antibody (NAB) production in COVID-19 patients from the Steve Biko Academic [...] Read more.
A correlation between neutralization activity after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination and protection against coronavirus disease 2019 (COVID-19) has been demonstrated by several studies. Here, we detect SARS-CoV-2 neutralizing antibody (NAB) production in COVID-19 patients from the Steve Biko Academic Hospital complex (SBAH), South Africa (SA). Samples from COVID-19 patients (mild to severe) were collected. SARS-CoV-2 rapid assays, genotyping (Delta and Omicron variants) and enzyme-linked immunosorbent assays (ELISA) were performed. IBM® Statistical Package for the Social Sciences (SPSS®) version 28 was used for inferential statistical analysis, and the data were presented using the Prism9 software (version 9.4.1). A total of 137 laboratory-confirmed COVID-19 patients, 12 vaccine recipients and 8 unvaccinated participants were evaluated. The production of SARS-CoV-2 NABs was observed in some of the COVID-19 cases, mainly in severe cases, although this should be noted with caution due to the small sample size of this pilot study. NABs were also observed in asymptomatic participants, with the most being found in recipients (n = 6) of the BNT162b2 (Pfizer-BioNTech) COVID-19 vaccine. We found a strong presence of NABs in COVID-19 patients, specifically in mild and severe cases. Severe infection was associated with higher NAB production (82%). Full article
(This article belongs to the Special Issue Immune Responses in Coronavirus Disease)
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15 pages, 1199 KiB  
Article
Assessment of Serum Electrolytes, Biochemical, and Inflammatory Markers in Predicting COVID-19 Severity in COPD Patients
by Farzana Mim, Md. Selim Reza, Md. Ibrahim Khalil, Nurul Karim, Hussain Md. Shahjalal, Md. Ibrahim Hossain and Md. Sabir Hossain
COVID 2023, 3(6), 792-806; https://doi.org/10.3390/covid3060059 - 24 May 2023
Viewed by 1818
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is the most prevalent long-term respiratory condition. Patients with COPD experience detrimental effects of COVID-19 infection. Objective: To figure out whether COPD is a risk factor influencing the progression of COVID-19 and to explore the clinical value [...] Read more.
Background: Chronic obstructive pulmonary disease (COPD) is the most prevalent long-term respiratory condition. Patients with COPD experience detrimental effects of COVID-19 infection. Objective: To figure out whether COPD is a risk factor influencing the progression of COVID-19 and to explore the clinical value of laboratory biomarkers to assess the severity of COVID-19 in patients with COPD comorbidity. Methods: In total, 1572 participants aged 35 to 70 years were enrolled to a tertiary hospital in Bangladesh between March 2022 and October 2022. Participants were categorized into four groups: (1) control, (2) COPD, (3) COVID-19, and (4) COVID-19 with COPD, and blood levels of clinical laboratory markers were assessed to analyze how these markers differ among the study groups. Results: COVID-19 patients with COPD had a significantly lower level of sodium (131.81 ± 2.8 mmol/L) and calcium (1.91 ± 0.28 mmol/L), and a significantly higher level of NT-proBNP (568.45 ± 207.40 pg/mL), bilirubin (1.34 ± 0.54 mg/dL), fibrinogen (577.27 ± 145.24 mg/dL), D-dimer (2.97 ± 2.25 μg/mL), C-reactive protein (71.08 ± 62.42 mg/L), interleukin-6 (166.47 ± 174.39 pg/mL), and procalcitonin (0.25 ± 0.30 ng/mL) compared to other study groups patients (p < 0.0001). In addition, the GOLD 4 group demonstrated significantly altered clinical parameters among COVID-19 patients with COPD. Furthermore, NT-proBNP, interleukin 6, D-dimer, C-reactive protein, and fibrinogen demonstrated excellent diagnostic performance in predicting disease severity among the COVID-19 patients with COPD, with a cut-off value of 511.2 pg/mL, 51.375 pg/mL, 1.645 μg/mL, 40.2 mg/L, and 510 mg/dL, respectively. Our results also indicate that inflammatory markers had significant positive correlations with the biochemical and coagulation markers in the COVID-19 patients suffering with COPD (p < 0.0001). Conclusions: NT-proBNP, interleukin 6, D-dimer, C-reactive protein, and fibrinogen are the most potential parameters for differentiating severe cases of COVID-19. Full article
(This article belongs to the Special Issue Immune Responses in Coronavirus Disease)
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25 pages, 6853 KiB  
Article
Macrophage-Induced Exacerbation of Nasopharyngeal Inflammatory Lymphocytes in COVID-19 Disease
by Mohamad Ammar Ayass, Trivendra Tripathi, Natalya Griko, Ramya Ramankutty Nair, Jin Zhang, Kevin Zhu, Wanying Cao, Victor Pashkov, Tutku Okyay, Sharda Kalla Singh and Lina Abi-Mosleh
COVID 2023, 3(4), 567-591; https://doi.org/10.3390/covid3040041 - 13 Apr 2023
Cited by 1 | Viewed by 2912
Abstract
The nasal microenvironment plays a crucial role in the transmission, modulation, and clinical progression of COVID-19; however, the immune responses at the site of viral entry remain poorly understood. We deciphered the link between nasopharyngeal (NP) immune and inflammatory response that triggers cytokine/chemokine [...] Read more.
The nasal microenvironment plays a crucial role in the transmission, modulation, and clinical progression of COVID-19; however, the immune responses at the site of viral entry remain poorly understood. We deciphered the link between nasopharyngeal (NP) immune and inflammatory response that triggers cytokine/chemokine storms in the nasal route of COVID-19-positive patients. We used RT-PCR, multiplex ELISA, flow cytometry, and LC-MS/MS to decipher nasopharyngeal immune perturbations associated with severe COVID-19. In addition, we performed in vitro assays using cultured human monocytes-derived macrophages trained both in the presence and absence of SARS-CoV-2 trimeric spike protein(s) and co-cultured with and without autologous human peripheral blood mononuclear cells (hPBMCs)/total T-cells/CD8 T-cells. In vitro immune perturbations were examined by flow cytometry and LC-MS/MS assays. Our findings confirm that macrophages orchestrate NP immune inflammatory responses and highlight the cytokine/chemokine storms associated with the increased CD8+T-cells along with Tregs, Th1, and Th17.1 T-helper cells. We observed a correlation between in vitro and nasal findings that trained macrophages, profoundly M2c, differentially promote the inflammatory surfactome on CD8 T-cells, including ITGAM, LGALS3, CD38, TKT, LRPAP1, and SSBP1. The findings of this study conclude that inflammatory lymphocyte perturbations within the nasopharynx of COVID-19 patients may enforce immune homeostasis during SARS-CoV-2-infection and contribute to COVID-19 pathology. This study explored the therapeutic target proteins that could facilitate the development of new medications, which could allow for immediate treatment of possible emerging viral infections. Full article
(This article belongs to the Special Issue Immune Responses in Coronavirus Disease)
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