«COVID endothelioteca» in testing the hypothesis of induction of genome instability by the SARS-CoV-2 virus in the endothelium of patients who have recovered from COVID-19 DOI Open Access
Natalia Lubinets, A. V. Yusupov, Viacheslav Kravtsov

и другие.

Nauchno-prakticheskii zhurnal «Patogenez», Год журнала: 2023, Номер 21(4), С. 61 - 67

Опубликована: Дек. 26, 2023

Актуальность. Поскольку вирусы способны дестабилизировать геномы соматических клеток в инфицированных ими клеточных популяциях, нами была выдвинута гипотеза о возможной индукции нестабильности генома эндотелии у переболевших COVID-19 и его прогностическом значении. Целью исследования стала проверка гипотезы том, что вирус SARS-CoV-2 проникает эндотелиоциты может индуцировать них нестабильность генома, которая сохраняется COVID-19. Материалы методы. Для проверки выдвинутой было проведено исследование CROSS-SECTION нескольких клиниках Санкт-Петербурга период с 2021 по 2023 гг. За этот был собран сохранён банк биоптатов цитологических препаратов эндотелиоцитами от 51 пациента, перенёсших новую коронавирусную инфекцию (COVID+), 43 пациентов, не (COVID–). Зафиксированный сохранённый информационным сопровождением материал за указанный пандемии мы назвали «ковидной эндотелиотекой», которую используем для гипотез патогенеза новой коронавирусной инфекции, проводя ретроспективно лабораторные (цитопатологические) исследования. В качестве показателя выбрали микроядра (МЯ) межъядерные хромосомные мосты (ХМ) интерфазных эндотелиоцитах препаратах, полученных из удалённых геморроидальных узлов во время геморроидэктомии Результаты. Свыше 70% цитограммах были представлены CD31+ эндотелиоцитами. Исследование более 45 000 эндотелиоцитов, проведенное группе «COVID+» инфекцию, «COVID–», болевших COVID-19, выявило ни одного случая обнаружения или межъядерного хромосомного моста. Таким образом, все 94 пациента имели показатели «МЯ–» «ХМ–». Критерий χ-квадрат, рассчитанный связи показателями «МЯ+» «ХМ+», оказался равным 0,68 (df = 1, p 0,409). Заключение. Выдвинутая об вирусом подтвердилась. По-видимому, ожидаемое влияние SARS-Cov-2 на системную эндотелиопатию (вне лёгких сердца) при обратимо, типовые патофизиологические реакции, обусловливающие «долгий ковид», переоцениваются. Background. Since viruses are capable of destabilizing the genomes somatic cells in cell populations infected by them, we put forward a hypothesis about possible induction genome instability endothelium patients who have recovered from and its prognostic significance. The aim study was to test that virus penetrates endothelial can induce genomic which persists those Materials methods. To hypothesis, conducted several clinics St. Petersburg period 2021-2023. During this period, collected stored bank biopsy specimens cytological preparations with had new coronavirus infection (COVID+) not We called material recorded information support during specified pandemic “covid endotheliosis,” use hypotheses pathogenesis infection, conducting retrospective laboratory (cytopathological) studies. As an indicator endothelium, selected micronuclei (MN) internuclear chromosomal bridges (CB) interphase endotheliocytes obtained removed hemorrhoids hemorrhoidectomy pandemic. Results. Over cytograms were represented cells. A more than 45,000 “COVID+” group suffered “COVID-” did reveal single case detection micronucleus or chromosome bridge. Thus, all indicators “MY–” “HM–”. χ-square criterion, calculated relationship between “MY+” “HM+” indicators, equal 0.68 ((df 0.409). Conclusion. confirmed. Apparently, expected effect on systemic endotheliopathy (outside lungs heart) is reversible typical pathophysiological reactions cause “long Covid” overestimated.

Язык: Русский

Cells that survive acute SARS-CoV-2 infection contribute to inflammation and lung regeneration in mice DOI Creative Commons
Ruangang Pan, David K. Meyerholz, Stanley Perlman

и другие.

mBio, Год журнала: 2025, Номер unknown

Опубликована: Янв. 29, 2025

ABSTRACT Post-acute sequelae of COVID-19 involves several organs, but its basis remains poorly understood. Some infected cells in mice survive the acute infection and persist for extended periods respiratory tract not other tissues. Here, we describe two experimental models severe syndrome coronavirus-2 (SARS-CoV-2) to assess effect viral virulence on previously cells. Both approaches use lineage tracking In with a highly pathogenic mouse-adapted SARS-CoV-2, alveolar type 2 (AT2) 1 (AT1) survived infection. These became activated, differentiated into an AT2-to-AT1 transitional cell state (KRT8 + pre-alveolar state). Additionally, nearby uninfected AT2 upregulated marker KRT8, thereby contributing lung regeneration. sensitized by transduction Ad5-hACE2, is nonlethal, AT1 Consequently, recovery these was more rapid. Taken together, results provide explanation how SARS-CoV-2 contributes poor outcomes affects clinical We also identified new mechanism which impacts recovery, even at times when infectious virus cannot be detected. IMPORTANCE A major consequence pandemic that many survivors have long-term sequelae, are well involve being common site effects. Many can found (SARS-CoV-2). this study, focused lungs, particular interest fate role were some surviving both contribute immune response lungs involved recovery. findings illustrate unexplored aspects from induced pneumonia may relevant understanding post-acute COVID-19.

Язык: Английский

Процитировано

0
Genetic and Epigenetic Intersections in COVID-19-Associated Cardiovascular Disease: Emerging Insights and Future Directions DOI Creative Commons
Hussein Sabit, Borros Arneth, Afaf Altrawy

и другие.

Biomedicines, Год журнала: 2025, Номер 13(2), С. 485 - 485

Опубликована: Фев. 16, 2025

The intersection of COVID-19 and cardiovascular disease (CVD) has emerged as a significant area research, particularly in understanding the impact antiplatelet therapies like ticagrelor clopidogrel. been associated with acute complications, including myocardial infarction, thrombosis, heart failure, exacerbated by virus's ability to trigger widespread inflammation endothelial dysfunction. MicroRNAs (miRNAs) play critical role regulating these processes modulating gene expressions involved platelet function, inflammation, vascular homeostasis. This study explores potential miRNAs such miR-223 miR-126 biomarkers for predicting resistance or responsiveness patients disease. Identifying miRNA signatures linked drug efficacy could optimize treatment strategies at high risk thrombotic events during infection. Moreover, miRNA-mediated pathways offers new insights into how SARS-CoV-2 exacerbates CVD, through mechanisms cytokine storms damage. findings this research lead personalized therapeutic approaches, improving patient outcomes reducing mortality COVID-19-associated events. With global implications, addresses urgent need effective management CVD context COVID-19, focusing on integration molecular enhance precision therapy.

Язык: Английский

Процитировано

0
Identification and mechanism analysis of biomarkers related to butyrate metabolism in COVID-19 patients DOI Creative Commons
Wenchao Zhou, Hui Li, Juan Zhang

и другие.

Annals of Medicine, Год журнала: 2025, Номер 57(1)

Опубликована: Март 12, 2025

Background Butyrate may inhibit SARS-CoV-2 replication and affect the development of COVID-19. However, there have been no systematic comprehensive analyses role butyrate metabolism-related genes (BMRGs) in

Язык: Английский

Процитировано

0
P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication DOI Creative Commons
Clara Husser, Hyesoo Kwon, Klara Andersson

и другие.

Microorganisms, Год журнала: 2024, Номер 12(3), С. 443 - 443

Опубликована: Фев. 22, 2024

While having already killed more than 7 million of people worldwide in 4 years, SARS-CoV-2, the etiological agent COVID-19, is still circulating and evolving. Understanding pathogenesis virus capital importance. It was shown that vitro vivo infection with SARS-CoV-2 can lead to cell cycle arrest but effect on associated mechanisms are unclear. By stopping cells G1 phase as well targeting several pathways involved using inhibitors small interfering RNAs, we were able determine late beneficial for replication. This independent p53 dependent CDC25A-CDK2/cyclin E pathway. These data give a new understanding highlight some possible targets development novel therapeutic approaches.

Язык: Английский

Процитировано

1
DNA Damage in Moderate and Severe COVID-19 Cases: Relation to Demographic, Clinical, and Laboratory Parameters DOI Open Access
Tigran Harutyunyan, Anzhela Sargsyan,

Lily Kalashyan

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(19), С. 10293 - 10293

Опубликована: Сен. 24, 2024

The ability of the SARS-CoV-2 virus to cause DNA damage in infected humans requires its study as a potential indicator COVID-19 progression. was studied leukocytes 65 patients stratified by sex, age, and disease severity relation demographic, clinical, laboratory parameters. In combined group patients, shown be elevated compared controls (12.44% vs. 5.09%,

Язык: Английский

Процитировано

1
Exploring the Relationship between Telomere Length and Cognitive Changes in Post-COVID-19 Subjects DOI Creative Commons

Guillermo Efrén Villar-Juárez,

Alma Delia Genis‐Mendoza,

J. Nicolas I. Martínez-López

и другие.

Biomedicines, Год журнала: 2024, Номер 12(10), С. 2296 - 2296

Опубликована: Окт. 10, 2024

Background/Objectives: Emerging evidence suggests that patients suffering from COVID-19 may experience neurocognitive symptoms. Furthermore, other studies indicate a probable association between leukocyte telomere length (LTL) and changes in subjects with post-COVID-19 condition. Our study was designed to determine the correlation cognitive subjects. Methods: This included 256 subjects, categorized based on SARS-CoV-2 infection 2020 2023. In addition, psychiatric diagnosis were considered. Moreover, MoCA MMSE scales applied. Telomere determined using polymerase chain reaction, statistical analysis employed ANOVA X2 tests. Results: We identified decrease LTL individuals conditions compared those without (p ≤ 0.05). However, no found impairment post-COVID-19. Conclusions: The findings suggest is affected by infection. Nonetheless, this important finding requires further research monitoring neurological post-COVID

Язык: Английский

Процитировано

0
SARS-CoV-2 predation of Golgi-bound PI4P primes the massive activation of the DNA Damage Response kinase ATM in the cytoplasm DOI Open Access
Antoine Rebendenne,

Caroline Soulet,

Ana Luiza Chaves Valadão

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Дек. 6, 2024

Abstract Like all viruses, SARS-CoV-2, the causative agent of COVID-19, relies on host cell resources to replicate. Our study reveals that, among these resources, SARS-CoV-2 hijacks oxysterol-binding protein 1 (OSBP1) transporter exploit Golgi-bound phosphatidylinositol-4-phosphate (PI4P) pool. This leads a depletion Golgi-resident PI4P, triggering activation ATM DNA Damage Response (DDR) kinase in cytoplasm. As such, ATM, typically anchored PI4P at Golgi an inactive state, undergoes auto-phosphorylation and cytoplasmic release upon SARS-CoV-2-induced depletion. Conversely, pharmacological inhibition auto-phosphorylation, which stabilizes its interaction with significantly impairs replication. The requirement for impact might be conserved across coronaviruses, as similar effects were observed HCoV-229E. Finally, SARS-CoV-2-induced, pre-activation primes cells accelerated response damage, contribute severe outcomes COVID-19 cancer patients undergoing chemo- or radiotherapy. Therefore, this uncovers damage-independent mode highlights potential inhibitors therapeutic agents against COVID-19.

Язык: Английский

Процитировано

0
Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link DOI Creative Commons
Abdelbasset Amara, Saoussen Trabelsi, Abdul Hai

и другие.

Pathogens, Год журнала: 2024, Номер 13(12), С. 1070 - 1070

Опубликована: Дек. 6, 2024

The COVID-19 infection caused by SARS-CoV-2 in late 2019 posed unprecedented global health challenges of massive proportions. persistent effects have become a subject significant concern amongst the medical and scientific community. This article aims to explore probability link between risk lung cancer development. First, this reports that induces severe inflammatory response cellular stress, potentially leading tumorigenesis through common pathways cancer. These include JAK/STAT3 pathway which is activated after initiation cytokine storm following infection. involved proliferation, differentiation, immune homeostasis. also hyperactivated serves as thereof. It predisposes patients myriad molecular mechanisms such DNA damage, genomic instability, cell cycle dysregulation. Another probable based on possibility an oncogenic nature hijacking p53 protein, oxidative stress interfering with repair mechanisms. Finally, highlights overexpression SLC22A18 gene can be overexpressed ZEB1 transcription factor, was found highly expressed during

Язык: Английский

Процитировано

0
«COVID endothelioteca» in testing the hypothesis of induction of genome instability by the SARS-CoV-2 virus in the endothelium of patients who have recovered from COVID-19 DOI Open Access
Natalia Lubinets, A. V. Yusupov, Viacheslav Kravtsov

и другие.

Nauchno-prakticheskii zhurnal «Patogenez», Год журнала: 2023, Номер 21(4), С. 61 - 67

Опубликована: Дек. 26, 2023

Актуальность. Поскольку вирусы способны дестабилизировать геномы соматических клеток в инфицированных ими клеточных популяциях, нами была выдвинута гипотеза о возможной индукции нестабильности генома эндотелии у переболевших COVID-19 и его прогностическом значении. Целью исследования стала проверка гипотезы том, что вирус SARS-CoV-2 проникает эндотелиоциты может индуцировать них нестабильность генома, которая сохраняется COVID-19. Материалы методы. Для проверки выдвинутой было проведено исследование CROSS-SECTION нескольких клиниках Санкт-Петербурга период с 2021 по 2023 гг. За этот был собран сохранён банк биоптатов цитологических препаратов эндотелиоцитами от 51 пациента, перенёсших новую коронавирусную инфекцию (COVID+), 43 пациентов, не (COVID–). Зафиксированный сохранённый информационным сопровождением материал за указанный пандемии мы назвали «ковидной эндотелиотекой», которую используем для гипотез патогенеза новой коронавирусной инфекции, проводя ретроспективно лабораторные (цитопатологические) исследования. В качестве показателя выбрали микроядра (МЯ) межъядерные хромосомные мосты (ХМ) интерфазных эндотелиоцитах препаратах, полученных из удалённых геморроидальных узлов во время геморроидэктомии Результаты. Свыше 70% цитограммах были представлены CD31+ эндотелиоцитами. Исследование более 45 000 эндотелиоцитов, проведенное группе «COVID+» инфекцию, «COVID–», болевших COVID-19, выявило ни одного случая обнаружения или межъядерного хромосомного моста. Таким образом, все 94 пациента имели показатели «МЯ–» «ХМ–». Критерий χ-квадрат, рассчитанный связи показателями «МЯ+» «ХМ+», оказался равным 0,68 (df = 1, p 0,409). Заключение. Выдвинутая об вирусом подтвердилась. По-видимому, ожидаемое влияние SARS-Cov-2 на системную эндотелиопатию (вне лёгких сердца) при обратимо, типовые патофизиологические реакции, обусловливающие «долгий ковид», переоцениваются. Background. Since viruses are capable of destabilizing the genomes somatic cells in cell populations infected by them, we put forward a hypothesis about possible induction genome instability endothelium patients who have recovered from and its prognostic significance. The aim study was to test that virus penetrates endothelial can induce genomic which persists those Materials methods. To hypothesis, conducted several clinics St. Petersburg period 2021-2023. During this period, collected stored bank biopsy specimens cytological preparations with had new coronavirus infection (COVID+) not We called material recorded information support during specified pandemic “covid endotheliosis,” use hypotheses pathogenesis infection, conducting retrospective laboratory (cytopathological) studies. As an indicator endothelium, selected micronuclei (MN) internuclear chromosomal bridges (CB) interphase endotheliocytes obtained removed hemorrhoids hemorrhoidectomy pandemic. Results. Over cytograms were represented cells. A more than 45,000 “COVID+” group suffered “COVID-” did reveal single case detection micronucleus or chromosome bridge. Thus, all indicators “MY–” “HM–”. χ-square criterion, calculated relationship between “MY+” “HM+” indicators, equal 0.68 ((df 0.409). Conclusion. confirmed. Apparently, expected effect on systemic endotheliopathy (outside lungs heart) is reversible typical pathophysiological reactions cause “long Covid” overestimated.

Язык: Русский

Процитировано

0