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      Exploratory Study on Micronuclei and Metanuclear Abnormalities in Exfoliated Buccal Cells of COVID-19 Suspected Patients

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          Abstract

          Context:

          SARS-CoV-2 virus causes COVID-19 by infecting nasal and oral cavities primarily by attaching its spike proteins to ACE 2 receptors expressed in epithelial cells.

          Aim:

          This study was done to evaluate the micronucleated cell count, metanuclear abnormalities, and genotoxic factor in exfoliated buccal mucosal cell among the COVID-19 suspected patients.

          Settings and Design:

          This cross-sectional study was conducted at AIIMS, Mangalagiri, between August and October 2022.

          Methods:

          One hundred COVID-19 suspected patients were recruited for this study after obtaining informed and written consent; buccal smear was obtained and stained for papanicolaou test (PAP). The PAP-stained slides were analyzed for micronuclei (MN), pyknotic, karyolytic, and karyorrhexic cell count, respectively. Based on their reverse transcription-polymerase chain reaction (RT-PCR) report, the patients were grouped into COVID-19 positive and negative groups.

          Statistical Analysis:

          The genotoxicity factor was calculated using the micronucleated cell count from both the groups using mean and standard deviation.

          Results:

          The MN, micronucleated cell, pyknotic, karyolitic, and karyorrhexic cell count in COVID-19 positive patients were 24.12, 15.24, 3.08, 2.88 and 4.40, respectively, than COVID-19 negative patients 5.69, 8.17, 1.08, 1.00 and 2.43, respectively. The genotoxicity factor for SARS-CoV-2 was 2.68 which is a positive genotoxic effect on buccal mucosal cells.

          Conclusion:

          SARS-CoV-2 increases the expression of micronucleated cells, pyknotic cells, karyolytic cells, and karyorhexic cells and concludes SARS-CoV-2 is having cytogenotoxic effect on the buccal mucosal cells. This can be used as a reliable marker in identifying the early carcinogenic effects of virus causing COVID-19.

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          Most cited references34

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          A pneumonia outbreak associated with a new coronavirus of probable bat origin

          Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
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            Molecular mechanisms of micronucleus, nucleoplasmic bridge and nuclear bud formation in mammalian and human cells.

            Micronuclei (MN) and other nuclear anomalies such as nucleoplasmic bridges (NPBs) and nuclear buds (NBUDs) are biomarkers of genotoxic events and chromosomal instability. These genome damage events can be measured simultaneously in the cytokinesis-block micronucleus cytome (CBMNcyt) assay. The molecular mechanisms leading to these events have been investigated over the past two decades using molecular probes and genetically engineered cells. In this brief review, we summarise the wealth of knowledge currently available that best explains the formation of these important nuclear anomalies that are commonly seen in cancer and are indicative of genome damage events that could increase the risk of developmental and degenerative diseases. MN can originate during anaphase from lagging acentric chromosome or chromatid fragments caused by misrepair of DNA breaks or unrepaired DNA breaks. Malsegregation of whole chromosomes at anaphase may also lead to MN formation as a result of hypomethylation of repeat sequences in centromeric and pericentromeric DNA, defects in kinetochore proteins or assembly, dysfunctional spindle and defective anaphase checkpoint genes. NPB originate from dicentric chromosomes, which may occur due to misrepair of DNA breaks, telomere end fusions, and could also be observed when defective separation of sister chromatids at anaphase occurs due to failure of decatenation. NBUD represent the process of elimination of amplified DNA, DNA repair complexes and possibly excess chromosomes from aneuploid cells.
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              TNF alpha and the TNF receptor superfamily: structure-function relationship(s).

              Tumour Necrosis Factor alpha (TNF alpha), is an inflammatory cytokine produced by macrophages/monocytes during acute inflammation and is responsible for a diverse range of signalling events within cells, leading to necrosis or apoptosis. The protein is also important for resistance to infection and cancers. TNF alpha exerts many of its effects by binding, as a trimer, to either a 55 kDa cell membrane receptor termed TNFR-1 or a 75 kDa cell membrane receptor termed TNFR-2. Both these receptors belong to the so-called TNF receptor superfamily. The superfamily includes FAS, CD40, CD27, and RANK. The defining trait of these receptors is an extra cellular domain comprised of two to six repeats of cysteine rich motifs. Additionally, a number of structurally related "decoy receptors" exist that act to sequester TNF molecules, thereby rescuing cells from apoptosis. The crystal structures of TNF alpha, TNF beta, the extracellular domain of TNFR-1 (denoted sTNFR-1), and the TNF beta sTNFR-1 complex have been defined by crystallography. This article will review the structure/function relationships of the TNF alpha and the TNF receptor superfamily. It will also discuss insights as to how structural features play a role in the pleiotropic effects of TNF alpha. Copyright 2000 Wiley-Liss, Inc.
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                Author and article information

                Journal
                J Cytol
                J Cytol
                JCytol
                J Cytol
                Journal of Cytology
                Wolters Kluwer - Medknow (India )
                0970-9371
                0974-5165
                Jan-Mar 2024
                28 December 2023
                : 41
                : 1
                : 28-33
                Affiliations
                [1 ]Final MBBS Student, All India Institute of Medical Sciences (AIIMS) Mangalagiri, Andhra Pradesh, India
                [2 ]Department of Anatomy, All India Institute of Medical Sciences (AIIMS) Mangalagiri, Andhra Pradesh, India
                [3 ]Department of Community and Family Medicine, All India Institute of Medical Sciences (AIIMS) Mangalagiri, Andhra Pradesh, India
                [4 ]Department of Anatomy, All India Institute of Medical Sciences (AIIMS) Madurai, Tamil Nadu, India
                [5 ]Department of ENT, All India Institute of Medical Sciences (AIIMS) Mangalagiri, Andhra Pradesh, India
                [6 ]Department of Anatomy, Saveetha Medical College and Hospital, SIMATS, Saveetha University, Chennai, Tamil Nadu, India
                Author notes
                Address for correspondence: Dr. Sankaran Ponnusamy Kasirajan, Department of Anatomy, All India Institute of Medical Sciences (AIIMS) Mangalagiri, Andhra Pradesh, India. E-mail: drpks@ 123456live.com
                Article
                JCytol-41-28
                10.4103/joc.joc_53_23
                10810081
                4b9d334a-a419-48af-b984-ac901429e39a
                Copyright: © 2023 Journal of Cytology

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 25 March 2023
                : 10 July 2023
                : 21 November 2023
                Categories
                Original Article

                Pathology
                buccal mucosal cells,covid 19,micronuclei
                Pathology
                buccal mucosal cells, covid 19, micronuclei

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