https://stm2.bookpi.org/CCLRD/issue/feed 2025-12-27T10:35:01+00:00 Open Journal Systems <p>The COVID-19 pandemic, caused by the SARS-CoV-2 virus, began spreading across India in March 2020. Initially, very little was known about the virus’s pathogenesis or its impact on human tissues. Over time, extensive research revealed its modes of transmission, mechanisms of infection in the lungs and other organs, and led to the development of effective vaccines. Vaccinated individuals were observed to experience milder symptoms and fewer complications compared to unvaccinated patients. Despite global control efforts, the virus continues to circulate, infecting millions—often with less severe manifestations than in the early stages of the pandemic.</p> <p>SARS-CoV-2 remains a challenging pathogen to eliminate, with the potential to cause repeated infections in both symptomatic and asymptomatic individuals. Although much has been understood about its systemic effects, the possibility of nuclear material damage in host cells has not been fully established.</p> <p>This book provides comprehensive insights into nuclear damage associated with COVID-19, including the formation of micronuclei, metanuclear alterations, genotoxicity levels, and the possible underlying mechanisms induced by SARS-CoV-2. It also presents nasal cytological changes observed in infected patients and analyses the inflammatory infiltrate ratios, comparing findings between infected and non-infected groups.</p> <p>In addition, this edition incorporates recent findings on <strong>Laryngopharyngeal Reflux Disease (LPR)</strong>—a condition in which gastric contents reflux into the upper aerodigestive tract, potentially aggravating mucosal inflammation and epithelial changes. As both SARS-CoV-2 infection and LPR can cause cytological alterations and oxidative damage at the cellular level, their combined understanding offers valuable insights into epithelial response, nuclear abnormalities, and mucosal health.</p> <p>The second edition expands on the original content with updated data, refined analyses, and integrated discussion on both COVID-19 and LPR-related cytological and genotoxic changes, aiming to provide readers with a broader and deeper understanding of epithelial cell pathology in these interrelated conditions.</p> https://stm2.bookpi.org/CCLRD/article/view/755 2025-12-27T10:35:01+00:00 Yogita Poojari Ambati Gowtham Sai B Vishnu Pranav Donkada Hemanth Bonamsetty Senthil Murugan P K Sankaran [email protected]

<p><strong>Introduction:</strong> SARS-CoV-2 infection and laryngopharyngeal reflux (LPR) both expose the upper aerodigestive tract to injurious biological agents—viral particles and gastric refluxate, respectively. These exposures can trigger mucosal inflammation, oxidative stress, and genotoxic changes detectable through cytological and immunohistochemical evaluation.</p> <p><strong>Aim:</strong> This study aimed to assess genotoxicity and oxidative DNA damage in exfoliated mucosal cells of individuals with suspected COVID-19 and patients with LPR, and to evaluate epithelial–mesenchymal transition (EMT)–related markers to understand early mucosal remodelling.</p> <p><strong>Settings and Design:</strong> A cross-sectional study conducted at AIIMS, Mangalagiri, between August 2022 and February 2024.</p> <p><strong>Methods:</strong> Exfoliated buccal or pharyngeal mucosal samples were collected from 86 COVID-19-suspected individuals (18–45 years) undergoing RT-PCR testing and from clinically diagnosed LPR patients with healthy controls. Smears were stained using the Papanicolaou technique for cytological analysis, and immunohistochemistry was performed to evaluate oxidative DNA damage (8-OHdG) and EMT markers (E-cadherin, N-cadherin). Micronucleated cells, inflammatory infiltrates, and oxidative marker expression were quantified. Statistical analysis was done using independent t-tests and ANOVA, with significance set at p &lt; 0.05.</p> <p><strong>Results:</strong> COVID-19 RT-PCR–positive subjects showed significantly elevated micronucleated cells, total micronuclei, and inflammatory cell counts compared to RT-PCR–negative individuals, along with intense 8-OHdG expression indicating marked oxidative DNA damage. LPR patients similarly demonstrated increased oxidative stress with strong 8-OHdG staining and higher micronucleated cell frequencies than healthy controls. While E-cadherin expression remained largely preserved, N-cadherin showed moderate upregulation in LPR patients, suggesting an early EMT-related cadherin shift. Both conditions exhibited a reduced epithelial-to-inflammatory cell ratio, reflecting ongoing mucosal injury and remodelling.</p> <p><strong>Conclusion:</strong> Both SARS-CoV-2 infection and chronic laryngopharyngeal reflux exert measurable genotoxic and oxidative effects on mucosal epithelial cells. The increased micronuclei formation, heightened 8-OHdG expression, and early EMT-associated changes indicate genomic instability and mucosal remodelling driven by persistent inflammation and oxidative stress. These findings underscore the importance of early detection and targeted interventions to prevent progression toward long-term mucosal damage and potential malignant transformation.</p>

2025-12-27T00:00:00+00:00 Copyright (c) 2025 Author(s). The licensee is the publisher (BP International).