COVID-19 and Global Chronic Disease 2025: New Challenges

A special issue of Diseases (ISSN 2079-9721).

Deadline for manuscript submissions: 31 December 2025 | Viewed by 1316

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Thoracic Surgery, A. Gemelli University Hospital Foundation IRCCS, I-00168 Rome, Italy
Interests: imaging in lung cancer; imaging in pleural and mediastinal tumors; PET CT scan in thoracic neoplasms
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Special Issue Information

Dear Colleagues,

Coronavirus disease 2019 (COVID-19) is the condition caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since the COVID-19 pandemic in 2020, our perspectives on healthcare systems and research have changed. This crisis emphasized the connection between clinical practice, health policies and research. On 5 May 2023, the head of the World Health Organization declared “with great hope” an end to COVID-19 as a public health emergency. However, the end of the pandemic will not be the end of COVID-19. New SARS-CoV-2 variants are still being detected, and it is necessary to continue protecting the most vulnerable people against the disease and its complications. In this way, many pivotal points are open and need to be clarified by the scientific community, from bench to bedside.

Aim and Scope:

This Special Issue, titled “COVID-19 and Global Chronic Disease 2025: New Challenges”, aims at reporting the state of the art and the new challenges resulting from COVID-19. In particular, we would like to discuss and analyze diagnostic aspects, new therapies, public health policies and social aspects related to this condition and its complications. We invite worldwide eminent scholars and emerging researchers to submit high-scientific-level articles on the topics indicated by the keywords below.

Prof. Dr. Ludovico Abenavoli
Dr. Filippo Lococo
Guest Editors

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Keywords

  • COVID-19
  • long COVID
  • virus
  • therapy
  • disease
  • patients
  • healthcare
  • research
  • epidemiology
  • artificial intelligence

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Research

23 pages, 11168 KiB  
Article
Persistent Inflammation, Maladaptive Remodeling, and Fibrosis in the Kidney Following Long COVID-like MHV-1 Mouse Model
by Rajalakshmi Ramamoorthy, Anna Rosa Speciale, Emily M. West, Hussain Hussain, Nila Elumalai, Klaus Erich Schmitz Abe, Madesh Chinnathevar Ramesh, Pankaj B. Agrawal, Arumugam R. Jayakumar and Michael J. Paidas
Diseases 2025, 13(8), 246; https://doi.org/10.3390/diseases13080246 - 5 Aug 2025
Viewed by 511
Abstract
Background: Accumulating evidence indicates that SARS-CoV-2 infection results in long-term multiorgan complications, with the kidney being a primary target. This study aimed to characterize the long-term transcriptomic changes in the kidney following coronavirus infection using a murine model of MHV-1-induced SARS-like illness and [...] Read more.
Background: Accumulating evidence indicates that SARS-CoV-2 infection results in long-term multiorgan complications, with the kidney being a primary target. This study aimed to characterize the long-term transcriptomic changes in the kidney following coronavirus infection using a murine model of MHV-1-induced SARS-like illness and to evaluate the therapeutic efficacy of SPIKENET (SPK). Methods: A/J mice were infected with MHV-1. Renal tissues were collected and subjected to immunofluorescence analysis and Next Generation RNA Sequencing to identify differentially expressed genes associated with acute and chronic infection. Bioinformatic analyses, including PCA, volcano plots, and GO/KEGG pathway enrichment, were performed. A separate cohort received SPK treatment, and comparative transcriptomic profiling was conducted. Gene expression profile was further confirmed using real-time PCR. Results: Acute infection showed the upregulation of genes involved in inflammation and fibrosis. Long-term MHV-1 infection led to the sustained upregulation of genes involved in muscle regeneration, cytoskeletal remodeling, and fibrotic responses. Notably, both expression and variability of SLC22 and SLC22A8, key proximal tubule transporters, were reduced, suggesting a loss of segment-specific identity. Further, SLC12A1, a critical regulator of sodium reabsorption and blood pressure, was downregulated and is associated with the onset of polyuria and hydronephrosis. SLC transporters exhibited expression patterns consistent with tubular dysfunction and inflammation. These findings suggest aberrant activation of myogenic pathways and structural proteins in renal tissues, consistent with a pro-fibrotic phenotype. In contrast, SPK treatment reversed the expression of most genes, thereby restoring the gene profiles to those observed in control mice. Conclusions: MHV-1-induced long COVID is associated with persistent transcriptional reprogramming in the kidney, indicative of chronic inflammation, cytoskeletal dysregulation, and fibrogenesis. SPK demonstrates robust therapeutic potential by normalizing these molecular signatures and preventing long-term renal damage. These findings underscore the relevance of the MHV-1 model and support further investigation of SPK as a candidate therapy for COVID-19-associated renal sequelae. Full article
(This article belongs to the Special Issue COVID-19 and Global Chronic Disease 2025: New Challenges)
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