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COVID-19: Molecular Research and Novel Therapy
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COVID-19: Molecular Research and Novel Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 April 2026 | Viewed by 3868

Special Issue Editor

Dr. Mihaela Chivu-Economescu

E-Mail Website
Guest Editor
Stefan S. Nicolau Institute of Virology, 030304 Bucharest, Romania
Interests: immunology and immune response during viral infections; oncology; immunotherapy; intracellular signalling; targeted therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since the COVID-19 pandemic, significant progress has been made in understanding the virus's pathogenic mechanisms, host–pathogen interactions, and the immunological responses that impact the disease’s outcome. These discoveries have boosted the development of antiviral drugs, vaccines, and diagnostic tools, offering improved possibilities in the fight against this global pandemic.

This Special Issue focuses on "COVID-19: Molecular Research and Novel Therapy", and welcomes original research articles, reviews, and short communications on the molecular mechanisms of SARS-CoV-2 infection, host immune responses, including innate and adaptive immunity, inflammation and immune evasion, development of antiviral agents, immunotherapies, and vaccines.

We look forward to receiving valuable contributions from the researchers all around the world, hoping to reveal cutting-edge knowledge that will contribute to the global effort to understand the pathogenesis of SARS-CoV-2, to reveal advancements in therapeutic interventions, and, at the same time, help the efforts to prevent and respond to other pandemics.

Dr. Mihaela Chivu-Economescu
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 250 words) can be sent to the Editorial Office for assessment.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • SARS-CoV-2
  • virus-host interaction
  • immune response
  • antiviral agents
  • vaccines

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Published Papers (4 papers)

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Research

21 pages, 2450 KB  
Article
A Unique Patient Stratification Method Combined with a Machine Learning Approach Identifies Novel Genetic Susceptibility and Protective Factors for Severe COVID-19 in a Hungarian Population
by Alexandra Neller, Mátyás Bukva, Bence Gálik, József Kun, Nikoletta Nagy, Ferenc Somogyvári, Valéria Endrész, Margit Pál, Barbara Anna Bokor, Zsófia Blazovich, Ádám Visnyovszky, Balázs Bende, Péter Urbán, Szilvia Kovácsné Levang, Zoltán Péterfi, Gábor L. Kovács, Katalin Gombos, Attila Gyenesei and Márta Széll
Int. J. Mol. Sci. 2026, 27(5), 2358; https://doi.org/10.3390/ijms27052358 - 3 Mar 2026
Viewed by 10
Abstract
Intensive research has shown that severe COVID-19 outcomes are influenced by antiviral pathways and immune responses, both shaped by genetic predisposition. In this study, we aimed to identify genetic variants associated with disease severity in a cohort of Hungarian patients. We applied a [...] Read more.
Intensive research has shown that severe COVID-19 outcomes are influenced by antiviral pathways and immune responses, both shaped by genetic predisposition. In this study, we aimed to identify genetic variants associated with disease severity in a cohort of Hungarian patients. We applied a novel stratification method based on age, disease severity, and clinical background to classify patients by susceptibility to severe COVID-19. Whole-exome sequencing (WES) was performed on 168 individuals, and gene mutation loads were assessed. Using a Random Forest machine learning approach, we identified variants of 877 genes that distinguished between severe and non-severe cases. We further categorized these genes as either susceptibility or protective factors. Gene-set enrichment analysis highlighted the most affected biological pathways. Our findings support the development of personalized diagnostic tools to assess the risk of severe COVID-19 and guide targeted treatment strategies. Our findings further extend the results of previous studies, providing novel insights into the genetic determinants of COVID-19 severity. Full article
(This article belongs to the Special Issue COVID-19: Molecular Research and Novel Therapy)
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10 pages, 1558 KB  
Communication
The Impact of IgG Glycosylation in SARS-CoV-2 Infection vs. Vaccination: A Statistical Analysis
by Adriána Kutás, Attila Garami and Csaba Váradi
Int. J. Mol. Sci. 2026, 27(2), 946; https://doi.org/10.3390/ijms27020946 - 18 Jan 2026
Viewed by 247
Abstract
This study investigates the glycosylation patterns of serum IgG antibodies in relation to COVID-19 infection and vaccination, highlighting the potential of specific glycan profiles as biomarkers for immune responses. Using Spearman correlation analysis, distinct associations among glycan levels and various clinical laboratory parameters [...] Read more.
This study investigates the glycosylation patterns of serum IgG antibodies in relation to COVID-19 infection and vaccination, highlighting the potential of specific glycan profiles as biomarkers for immune responses. Using Spearman correlation analysis, distinct associations among glycan levels and various clinical laboratory parameters were identified, revealing complex, non-linear interactions that influence immune dynamics. Significant differences were observed in sialylated glycan profiles across patient groups, indicating that vaccination and natural infection elicit unique immune mechanisms and suggesting that vaccination induces favorable glycosylation changes. Notably, high-mannose glycans were found to correlate with other glycan types, underscoring their critical role in the immune response and suggesting their potential as biomarkers to differentiate between infection- and vaccination-induced immunity. The findings suggest that understanding these glycosylation dynamics may enhance diagnostic and therapeutic strategies, providing valuable tools for differentiating between immune responses elicited by infection and vaccination. Overall, this study contributes to the understanding of glycosylation’s impact on immune function in the context of COVID-19, emphasizing the importance of specific glycan markers, such as sialylated and high-mannose structures, in clinical applications. Full article
(This article belongs to the Special Issue COVID-19: Molecular Research and Novel Therapy)
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20 pages, 3581 KB  
Article
Long-Term Durability and Variant-Specific Modulation of SARS-CoV-2 Humoral and Cellular Immunity over Two Years
by Lilia Matei, Mihaela Chivu-Economescu, Laura Denisa Dragu, Camelia Grancea, Coralia Bleotu, Raluca Hrișcă, Corneliu Petru Popescu, Carmen C. Diaconu and Simona Maria Ruţă
Int. J. Mol. Sci. 2025, 26(16), 8106; https://doi.org/10.3390/ijms26168106 - 21 Aug 2025
Cited by 1 | Viewed by 1524
Abstract
There is an increasing need to understand the long-term dynamics and quality of SARS-CoV-2 immune memory—both humoral and cellular—particularly with emerging variants. This study aimed to evaluate immune durability and variant-specific modulation through a longitudinal analysis of individuals with diverse SARS-CoV-2 exposure histories, [...] Read more.
There is an increasing need to understand the long-term dynamics and quality of SARS-CoV-2 immune memory—both humoral and cellular—particularly with emerging variants. This study aimed to evaluate immune durability and variant-specific modulation through a longitudinal analysis of individuals with diverse SARS-CoV-2 exposure histories, over two years after infection and/or vaccination. The study involved assessing anti-spike IgG and IgA levels over time and analyzing their relationship with neutralizing activity against both ancestral and Omicron SARS-CoV-2 variants. Persistence of T cell responses was evaluated using intracellular cytokine staining (ICS) and activation-induced marker (AIM) assays. Anti-S IgG levels remained stable over time and increased after each immune stimulation, suggesting cumulative immune memory. Neutralizing capacity correlated strongly with IgG levels, showing long-term stability for pre-Omicron variants, but a moderate decline for Omicron. CD4+ and CD8+ T cell responses persisted across all groups, largely unaffected by Omicron mutations. However, cytokine profiles revealed subtle, variant-dependent changes. These findings underscore the durability of cellular immunity and the comparatively reduced robustness of Omicron-specific humoral responses. Such insights are crucial for understanding long-term protection against evolving SARS-CoV-2 variants and guiding public health strategies. Full article
(This article belongs to the Special Issue COVID-19: Molecular Research and Novel Therapy)
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18 pages, 3425 KB  
Article
SARS-CoV-2 ORF7a Protein Impedes Type I Interferon-Activated JAK/STAT Signaling by Interacting with HNRNPA2B1
by Yujie Wen, Chaochao Li, Tian Tang, Chao Luo, Shan Lu, Na Lyu, Yongxi Li and Rong Wang
Int. J. Mol. Sci. 2025, 26(12), 5536; https://doi.org/10.3390/ijms26125536 - 10 Jun 2025
Cited by 1 | Viewed by 1376
Abstract
The pandemic of Coronavirus Disease 2019 has triggered a worldwide public health emergency. Its pathogen, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has developed multiple strategies for effectively evading the host immune defenses, including inhibition of interferon (IFN) signaling. Several viral proteins of [...] Read more.
The pandemic of Coronavirus Disease 2019 has triggered a worldwide public health emergency. Its pathogen, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has developed multiple strategies for effectively evading the host immune defenses, including inhibition of interferon (IFN) signaling. Several viral proteins of SARS-CoV-2 are believed to interfere with IFN signaling. In this study, we found that the SARS-CoV-2 accessory protein ORF7a considerably impaired IFN-activated Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling via suppression of the nuclear translocation of IFN-stimulated gene factor 3 (ISGF3) and the activation of STAT2. ORF7a dampened STAT2 activation without altering the expression and phosphorylation of Janus kinases (JAKs). A co-immunoprecipitation (co-IP) assay was performed to gather ORF7a protein, but it failed to precipitate STAT2. Interestingly, mass spectrometry and immunoblotting analyses of the ORF7a co-IP product revealed that ORF7a interacted with an RNA-binding protein, heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1), and HNRNPA2B1 was related to the inhibitory effect of ORF7a on STAT2 phosphorylation. Moreover, examination of ORF7a deletion constructs revealed that the C-terminal region of ORF7a (amino acids 96 to 122) is crucial for suppressing IFN-induced JAK/STAT signaling activation. In conclusion, we discovered that SARS-CoV-2 ORF7a antagonizes type I IFN-activated JAK/STAT signaling by interacting with HNRNPA2B1, and the C-terminal region of ORF7a is responsible for its inhibitory effect. Full article
(This article belongs to the Special Issue COVID-19: Molecular Research and Novel Therapy)
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