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Viruses
Special Issues
Aging and Comorbidities of COVID-19
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Aging and Comorbidities of COVID-19

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "SARS-CoV-2 and COVID-19".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 7455

Special Issue Editor

Dr. François Trottein

E-Mail Website
Guest Editor
Institut Pasteur de Lille, Center for Infection and Immunity of Lille, F-59019 Lille, France
Interests: SARS-CoV-2; comorbidities; aging; microbiota; COVID-19; sequelae
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging and preexisting comorbid conditions ranging from hypertension, malignancies, chronic infections, chronic metabolic (obesity, diabetes), pulmonary, kidney, and cardiovascular diseases exacerbate the severity of COVID-19. Scientists and clinicians are trying to understand how SARS-CoV-2 exacerbates the acute and the long-term phases of the disease in advanced aged and comorbid populations. Relevant preclinical models can be studied to decipher early and late outcomes of infection in these high-risk populations at the level of single cells, organoids, tissues, and whole organisms. For all these studies, the combination of different technical approaches ranging from multi-omics to imaging is a very useful tool. Research in the field is expected to provide important information, including knowledge to identify targets for better controlling early and late COVID-19 outcomes in comorbid and aged individuals.

This Special Issue of Viruses will be devoted to analyzing recent advances in the field and will propose future directions to improve our understanding of SARS-CoV-2–host interactions in the context of aging and comorbidities. Scientists worldwide are welcome to contribute with articles, brief reports, technical notes, and reviews to show how they consider aging and comorbidities in preclinical models of COVID-19. In particular, we aim to discuss how aging and comorbid conditions exacerbate disease in COVID-19 patients and how the information emanating from animal models is amenable to better prognosis methods, preventive measures, and therapies in patients.

Prof. Dr. François Trottein
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. Viruses 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 2600 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

  • SARS-CoV-2
  • aging
  • comorbidity
  • preclinical models
  • prognosis
  • therapies

Published Papers (3 papers)

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Research

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12 pages, 1060 KiB  
Article
Liver Involvement during SARS-CoV-2 Infection Is Associated with a Worse Respiratory Outcome in COVID-19 Patients
by Ciro Romano, Domenico Cozzolino, Riccardo Nevola, Marianna Abitabile, Caterina Carusone, Francesca Cinone, Giovanna Cuomo, Francesco Nappo, Ausilia Sellitto, Giuseppina Rosaria Umano, Luigi Elio Adinolfi, Aldo Marrone and Luca Rinaldi
Viruses 2023, 15(9), 1904; https://doi.org/10.3390/v15091904 - 10 Sep 2023
Cited by 2 | Viewed by 1730
Abstract
Coronavirus disease of 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may be complicated by life-threatening interstitial pneumonia. SARS-CoV-2 infection may also damage several tissues and/or organs beyond the lungs, including the liver. However, controversy still exists as to whether [...] Read more.
Coronavirus disease of 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may be complicated by life-threatening interstitial pneumonia. SARS-CoV-2 infection may also damage several tissues and/or organs beyond the lungs, including the liver. However, controversy still exists as to whether SARS-CoV-2-induced liver alterations can have an impact on the outcome of COVID-19. The aim of this study was therefore to assess whether SARS-CoV-2-infected patients with liver abnormalities at the time of hospital referral had a worse outcome with respect to patients with no liver biochemistry alterations. To this end, the medical records of 123 patients admitted to our COVID center between the end of 2020 and spring 2021 were retrospectively reviewed. Patients were divided into two groups: those with normal liver biochemistries (group 1, 77 patients) and those with altered liver function tests (group 2, 46 patients). Serum levels of aminotransferases (AST and ALT) and bile duct cell injury markers (γ-GT and ALP) were used to dichotomize patients. A higher percentage of patients with liver enzyme alterations were found to develop COVID-19 pneumonia with respect to group 1 patients (74% vs. 65%); moreover, they needed more days of respiratory support and, more importantly, more intensive administration of supplemental oxygen. A statistically significant correlation was also found between aminotransferase levels and duration of respiratory support. The mortality rate was not superior in group 2 vs. group 1 patients. In conclusion, liver abnormalities on admission predisposed COVID-19 patients to development of more severe interstitial pneumonia, because of a longer requirement for supplemental oxygen and a more intensive respiratory support, indicative of a worse disease evolution in these patients. Full article
(This article belongs to the Special Issue Aging and Comorbidities of COVID-19)
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20 pages, 4923 KiB  
Article
Diet-Induced Obesity and NASH Impair Disease Recovery in SARS-CoV-2-Infected Golden Hamsters
by François Briand, Valentin Sencio, Cyril Robil, Séverine Heumel, Lucie Deruyter, Arnaud Machelart, Johanna Barthelemy, Gemma Bogard, Eik Hoffmann, Fabrice Infanti, Oliver Domenig, Audrey Chabrat, Virgile Richard, Vincent Prévot, Ruben Nogueiras, Isabelle Wolowczuk, Florence Pinet, Thierry Sulpice and François Trottein
Viruses 2022, 14(9), 2067; https://doi.org/10.3390/v14092067 - 17 Sep 2022
Cited by 4 | Viewed by 2693
Abstract
Obese patients with non-alcoholic steatohepatitis (NASH) are prone to severe forms of COVID-19. There is an urgent need for new treatments that lower the severity of COVID-19 in this vulnerable population. To better replicate the human context, we set up a diet-induced model [...] Read more.
Obese patients with non-alcoholic steatohepatitis (NASH) are prone to severe forms of COVID-19. There is an urgent need for new treatments that lower the severity of COVID-19 in this vulnerable population. To better replicate the human context, we set up a diet-induced model of obesity associated with dyslipidemia and NASH in the golden hamster (known to be a relevant preclinical model of COVID-19). A 20-week, free-choice diet induces obesity, dyslipidemia, and NASH (liver inflammation and fibrosis) in golden hamsters. Obese NASH hamsters have higher blood and pulmonary levels of inflammatory cytokines. In the early stages of a SARS-CoV-2 infection, the lung viral load and inflammation levels were similar in lean hamsters and obese NASH hamsters. However, obese NASH hamsters showed worse recovery (i.e., less resolution of lung inflammation 10 days post-infection (dpi) and lower body weight recovery on dpi 25). Obese NASH hamsters also exhibited higher levels of pulmonary fibrosis on dpi 25. Unlike lean animals, obese NASH hamsters infected with SARS-CoV-2 presented long-lasting dyslipidemia and systemic inflammation. Relative to lean controls, obese NASH hamsters had lower serum levels of angiotensin-converting enzyme 2 activity and higher serum levels of angiotensin II—a component known to favor inflammation and fibrosis. Even though the SARS-CoV-2 infection resulted in early weight loss and incomplete body weight recovery, obese NASH hamsters showed sustained liver steatosis, inflammation, hepatocyte ballooning, and marked liver fibrosis on dpi 25. We conclude that diet-induced obesity and NASH impair disease recovery in SARS-CoV-2-infected hamsters. This model might be of value for characterizing the pathophysiologic mechanisms of COVID-19 and evaluating the efficacy of treatments for the severe forms of COVID-19 observed in obese patients with NASH. Full article
(This article belongs to the Special Issue Aging and Comorbidities of COVID-19)
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Review

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22 pages, 1603 KiB  
Review
Endoplasmic Reticulum Stress in Elderly Patients with COVID-19: Potential of Melatonin Treatment
by Giou-Teng Yiang, Chia-Chao Wu, Chien-Lin Lu, Wan-Chung Hu, Yi-Ju Tsai, Yiao-Mien Huang, Wen-Lin Su and Kuo-Cheng Lu
Viruses 2023, 15(1), 156; https://doi.org/10.3390/v15010156 - 04 Jan 2023
Cited by 5 | Viewed by 2380
Abstract
Aging processes, including immunosenescence, inflammation, inflammasome formation, genomic instability, telomeric attrition, and altered autophagy, are involved in viral infections and they may contribute to increased pathophysiological responses to the SARS-CoV-2 infection in the elderly; this poses additional risks of accelerated aging, which could [...] Read more.
Aging processes, including immunosenescence, inflammation, inflammasome formation, genomic instability, telomeric attrition, and altered autophagy, are involved in viral infections and they may contribute to increased pathophysiological responses to the SARS-CoV-2 infection in the elderly; this poses additional risks of accelerated aging, which could be found even after recovery. Aging is associated with oxidative damage. Moreover, SARS-CoV-2 infections may increase the production of reactive oxygen species and such infections will disturb the Ca++ balance via an endoplasmic reticulum (ER) stress-mediated unfolded protein response. Although vaccine development and anti-inflammation therapy lower the severity of COVID-19, the prevalence and mortality rates are still alarming in some countries worldwide. In this review, we describe the involvement of viral proteins in activating ER stress transducers and their downstream signals and in inducing inflammation and inflammasome formation. Furthermore, we propose the potential of melatonin as an ER stress modulator, owing to its antioxidant, anti-inflammatory, and immunoregulatory effects in viral infections. Considering its strong safety profile, we suggest that additive melatonin supplementation in the elderly could be beneficial in treating COVID-19. Full article
(This article belongs to the Special Issue Aging and Comorbidities of COVID-19)
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