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Journal articles on the topic 'Mechanisms of persistence'

Author: Grafiati

Published: 4 June 2025

Last updated: 14 July 2025

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1

Gittins, Zane, and Michael Soltys. "Malware Persistence Mechanisms." Procedia Computer Science 176 (2020): 88–97. http://dx.doi.org/10.1016/j.procs.2020.08.010.

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2

Boris, G. Andryukov, та Lyapun Irina. "Molecular Mechanisms оf Persistence in Bacteria". EC Microbiology 18, № 6 (2022): 33–44. https://doi.org/10.5281/zenodo.6857102.

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A significant mortality rate from infectious diseases is largely mediated by the widespread and uncontrolled use of antibiotics, which has led to the emergence of drug-resistant strains of bacteria. The rapid evolution of 272 bacterial resistance to antimicrobials is a serious challenge for modern health care, mediates the need to create new antibiotic agents, as well as to intensify the study of molecular mechanisms underlying the formation of microorganism resistance. One of these mechanisms is bacterial persistence, manifested by the formation of persistent cells in the culture, which are a

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3

Kulakov, Yu K. "MOLECULAR MECHANISMS OF BRUCELLA PERSISTENCE." Journal of microbiology epidemiology immunobiology, no. 4 (August 28, 2018): 68–76. http://dx.doi.org/10.36233/0372-9311-2018-4-68-76.

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Brucellosis is an infectious, especially dangerous zoonotic disease of agricultural and wild animals, from which it is transmitted to humans and characterized by a chronic course with disability of working-age patients. Bacteria of the genus Brucella are facultative intracellular pathogens capable of multiplying and persisting in the host’s immune cells with the development of chronic infection. The host-specific evolutionary mechanisms allow Brucella to hide and manipulate the systems of innate and acquired cellular immunity to achieve intracellular persistence. The review describes the molec

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4

Oldstone, Michael B. "Viral persistence: mechanisms and consequences." Current Opinion in Microbiology 1, no. 4 (1998): 436–41. http://dx.doi.org/10.1016/s1369-5274(98)80062-3.

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5

Britton, Warwick J., Paul W. Roche, and Nathalie Winter. "Mechanisms of persistence of mycobacteria." Trends in Microbiology 2, no. 8 (1994): 284–88. http://dx.doi.org/10.1016/0966-842x(94)90005-1.

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6

Meuer, Stefan C., and Ulrich Moebius. "Immune mechanisms underlying HBV persistence." Seminars in Virology 5, no. 4 (1994): 289–95. http://dx.doi.org/10.1006/smvy.1994.1032.

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7

Verdikt, Roxane, Olivier Hernalsteens, and Carine Van Lint. "Epigenetic Mechanisms of HIV-1 Persistence." Vaccines 9, no. 5 (2021): 514. http://dx.doi.org/10.3390/vaccines9050514.

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Eradicating HIV-1 in infected individuals will not be possible without addressing the persistence of the virus in its multiple reservoirs. In this context, the molecular characterization of HIV-1 persistence is key for the development of rationalized therapeutic interventions. HIV-1 gene expression relies on the redundant and cooperative recruitment of cellular epigenetic machineries to cis-regulatory proviral regions. Furthermore, the complex repertoire of HIV-1 repression mechanisms varies depending on the nature of the viral reservoir, although, so far, few studies have addressed the specif

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8

Andryukov, Boris G., та Irina N. Lyapun. "Molecular Mechanisms оf Persistence оf Bacteria". Journal of microbiology, epidemiology and immunobiology 97, № 3 (2020): 271–79. http://dx.doi.org/10.36233/0372-9311-2020-97-3-10.

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A significant mortality rate from infectious diseases is largely mediated by the widespread and uncontrolled use of antibiotics, which has led to the emergence of drug-resistant strains of bacteria. The rapid evolution of bacterial resistance to antimicrobials is a serious challenge for modern health care, mediates the need to create new antibiotic agents, as well as to intensify the study of molecular mechanisms underlying the formation of microorganism resistance. One of these mechanisms is bacterial persistence, manifested by the formation of persistent cells in the culture, which are a phe

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9

Borrow, P. "Mechanisms of viral clearance and persistence." Journal of Viral Hepatitis 4, s2 (1997): 16–24. http://dx.doi.org/10.1111/j.1365-2893.1997.tb00176.x.

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10

Olszewski, Michal A., Yanmei Zhang, and Gary B. Huffnagle. "Mechanisms of cryptococcal virulence and persistence." Future Microbiology 5, no. 8 (2010): 1269–88. http://dx.doi.org/10.2217/fmb.10.93.

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11

Rima, Bertus K., and W. Paul Duprex. "Molecular mechanisms of measles virus persistence." Virus Research 111, no. 2 (2005): 132–47. http://dx.doi.org/10.1016/j.virusres.2005.04.005.

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12

Tsai, Kuen-Nan, Cheng-Fu Kuo, and Jing-Hsiung James Ou. "Mechanisms of Hepatitis B Virus Persistence." Trends in Microbiology 26, no. 1 (2018): 33–42. http://dx.doi.org/10.1016/j.tim.2017.07.006.

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13

Kusner, David J. "Mechanisms of mycobacterial persistence in tuberculosis." Clinical Immunology 114, no. 3 (2005): 239–47. http://dx.doi.org/10.1016/j.clim.2004.07.016.

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14

Hofer, Ursula. "The search for persistence mechanisms continues." Nature Reviews Microbiology 17, no. 10 (2019): 589. http://dx.doi.org/10.1038/s41579-019-0257-7.

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15

Pan, Xiaozhou, Wenxin Liu, Qingqing Du, Hong Zhang, and Dingding Han. "Recent Advances in Bacterial Persistence Mechanisms." International Journal of Molecular Sciences 24, no. 18 (2023): 14311. http://dx.doi.org/10.3390/ijms241814311.

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The recurrence of bacterial infectious diseases is closely associated with bacterial persisters. This subpopulation of bacteria can escape antibiotic treatment by entering a metabolic status of low activity through various mechanisms, for example, biofilm, toxin–antitoxin modules, the stringent response, and the SOS response. Correspondingly, multiple new treatments are being developed. However, due to their spontaneous low abundance in populations and the lack of research on in vivo interactions between persisters and the host’s immune system, microfluidics, high-throughput sequencing, and mi

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16

Aliyeva, Saxavat. "Mechanisms ensuring persistence of gender stereotypes." Scientific Works 18, no. 1 (2024): 172–80. http://dx.doi.org/10.62706/bqiz.2024.v18i1.123.

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The persistence of gender stereotypes is sustained by a complex interplay of cultural traditions, social conditioning, cognitive biases, media influences, and institutional structures. Cultural traditions lay the foundation by transmitting societal norms across generations, shaping expectations around gender roles. Social conditioning reinforces these norms as individuals internalize societal expectations from an early age. Cognitive biases contribute to stereotypical thinking, solidifying traditional gender norms.

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17

Skrzypacz, Andrzej, and Juuso Toikka. "Mechanisms for Repeated Trade." American Economic Journal: Microeconomics 7, no. 4 (2015): 252–93. http://dx.doi.org/10.1257/mic.20140173.

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How does feasibility of efficient repeated trade depend on the features of the environment such as persistence of values, private information about their evolution, or trading frequency? We derive a necessary and sufficient condition for efficient, unsubsidized, and voluntary trade, which implies that efficient contracting requires sufficient congruence of expectations. This translates to bounds on persistence of values and on private information about their evolution, and distinguishes increasing patience from more frequent interaction; the latter need not facilitate efficiency even when the

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18

Tarannum, Asfiha, Cristian Camilo Rodríguez-Almonacid, Jorge Salazar-Bravo, and Zemfira N. Karamysheva. "Molecular Mechanisms of Persistence in Protozoan Parasites." Microorganisms 11, no. 9 (2023): 2248. http://dx.doi.org/10.3390/microorganisms11092248.

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Protozoan parasites are known for their remarkable capacity to persist within the bodies of vertebrate hosts, which frequently results in prolonged infections and the recurrence of diseases. Understanding the molecular mechanisms that underlie the event of persistence is of paramount significance to develop innovative therapeutic approaches, given that these pathways still need to be thoroughly elucidated. The present article provides a comprehensive overview of the latest developments in the investigation of protozoan persistence in vertebrate hosts. The focus is primarily on the function of

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19

Shanker, V., D. Haranath, and G. Swati. "Persistence Mechanisms and Applications of Long Afterglow Phosphors." Defect and Diffusion Forum 361 (January 2015): 69–94. http://dx.doi.org/10.4028/www.scientific.net/ddf.361.69.

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This article presents a broad review of long persistence (LP) materials that are a special kind of photon energy storage and conversion materials. They are also known as long afterglow phosphors or long decay phosphors (LDP). These phosphors can be readily excited by any ordinary household lamp, sunlight and/or ambient room lights and glow continuously in the dark for hours together without involving any radioactive elements. It is the modifications that are made to crystalline host lattice that exhibit these unusual properties related to persistence due to effective doping of some transition

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20

De Groote, Valerie N., Maarten Fauvart, Cyrielle I. Kint, et al. "Pseudomonas aeruginosa fosfomycin resistance mechanisms affect non-inherited fluoroquinolone tolerance." Journal of Medical Microbiology 60, no. 3 (2011): 329–36. http://dx.doi.org/10.1099/jmm.0.019703-0.

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Pseudomonas aeruginosa is an opportunistic pathogen that poses a threat in clinical settings due to its intrinsic and acquired resistance to a wide spectrum of antibiotics. Additionally, the presence of a subpopulation of cells surviving high concentrations of antibiotics, called persisters, makes it virtually impossible to eradicate a chronic infection. The mechanism underlying persistence is still unclear, partly due to the fact that it is a non-inherited phenotype. Based on our findings from a previously performed screening effort for P. aeruginosa persistence genes, we hypothesize that cro

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21

Jarvis, Michael, A. "Mechanisms of human cytomegalovirus persistence and latency." Frontiers in Bioscience 7, no. 1-3 (2002): d1575. http://dx.doi.org/10.2741/jarvis.

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22

Middleton, D. A. J., and R. M. Nisbet. "POPULATION PERSISTENCE TIME: ESTIMATES, MODELS, AND MECHANISMS." Ecological Applications 7, no. 1 (1997): 107–17. http://dx.doi.org/10.1890/1051-0761(1997)007[0107:pptema]2.0.co;2.

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23

Frisk, Gun. "Mechanisms of chronic enteroviral persistence in tissue." Current Opinion in Infectious Diseases 14, no. 3 (2001): 251–56. http://dx.doi.org/10.1097/00001432-200106000-00002.

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24

Oldstone, Michael B. A. "Viral persistence: Parameters, mechanisms and future predictions." Virology 344, no. 1 (2006): 111–18. http://dx.doi.org/10.1016/j.virol.2005.09.028.

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25

Miller, Craig S. "Pleiotropic mechanisms of virus survival and persistence." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 100, no. 2 (2005): S27—S36. http://dx.doi.org/10.1016/j.tripleo.2005.03.017.

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26

LANZER, M., U. GROSS, and H. MOLL. "Mechanisms of parasite persistence and immune evasion." Parasitology Today 13, no. 1 (1997): 1–3. http://dx.doi.org/10.1016/s0169-4758(96)30033-1.

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27

Rapp, Fred, and Joan M. Cory. "Mechanisms of persistence in human virus infections." Microbial Pathogenesis 4, no. 2 (1988): 85–92. http://dx.doi.org/10.1016/0882-4010(88)90050-2.

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28

Boxus, M., and L. Willems. "Mechanisms of HTLV-1 persistence and transformation." British Journal of Cancer 101, no. 9 (2009): 1497–501. http://dx.doi.org/10.1038/sj.bjc.6605345.

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29

Cohn, Lauren, Jack A. Elias, and Geoffrey L. Chupp. "Asthma: Mechanisms of Disease Persistence and Progression." Annual Review of Immunology 22, no. 1 (2004): 789–815. http://dx.doi.org/10.1146/annurev.immunol.22.012703.104716.

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30

Nelson, Jay A. "Mechanisms of human cytomegalovirus persistence and latency." Frontiers in Bioscience 7, no. 4 (2002): d1575–1582. http://dx.doi.org/10.2741/a862.

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31

Mzingwane, Mayibongwe L., and Caroline T. Tiemessen. "Mechanisms of HIV persistence in HIV reservoirs." Reviews in Medical Virology 27, no. 2 (2017): e1924. http://dx.doi.org/10.1002/rmv.1924.

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32

Lee, Steve P. "Control mechanisms of Epstein-Barr virus persistence." Seminars in Virology 5, no. 4 (1994): 281–88. http://dx.doi.org/10.1006/smvy.1994.1031.

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33

Wynn, Michelle L., Paul M. Kulesa, and Santiago Schnell. "Computational modelling of cell chain migration reveals mechanisms that sustain follow-the-leader behaviour." Journal of The Royal Society Interface 9, no. 72 (2012): 1576–88. http://dx.doi.org/10.1098/rsif.2011.0726.

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Follow-the-leader chain migration is a striking cell migratory behaviour observed during vertebrate development, adult neurogenesis and cancer metastasis. Although cell–cell contact and extracellular matrix (ECM) cues have been proposed to promote this phenomenon, mechanisms that underlie chain migration persistence remain unclear. Here, we developed a quantitative agent-based modelling framework to test mechanistic hypotheses of chain migration persistence. We defined chain migration and its persistence based on evidence from the highly migratory neural crest model system, where cells within

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34

Lukic, Ruzica, Bojana Lukovic, Nevena Gajovic, Slava Prljic, and Slobodanka Djukic. "Mechanisms of Intracellular Chlamydiae Survival." Serbian Journal of Experimental and Clinical Research 17, no. 2 (2016): 145–52. http://dx.doi.org/10.1515/sjecr-2016-0010.

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AbstractChlamydiae are Gram-negative, non-motile, obligate intracellular, and spherically shaped bacteria with a diameter of 0.2-1.5 μm. Chlamydiae are present in several different morphological forms: the elementary body, the reticular body, and in the last several years, there has been the observation of a third form known as the persistent or atypical form. The intracellular localization of Chlamydia provides a unique replication cycle that occurs inside a membrane-surrounded vacuole in the host cell cytoplasm and is significantly different from the method of multiplication of other microor

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35

Easterbrook, Judith D., and Sabra L. Klein. "Immunological Mechanisms Mediating Hantavirus Persistence in Rodent Reservoirs." PLoS Pathogens 4, no. 11 (2008): e1000172. http://dx.doi.org/10.1371/journal.ppat.1000172.

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36

Duwyn, Alisha, and Andrew S. MacDougall. "When anthropogenic-related disturbances overwhelm demographic persistence mechanisms." Journal of Ecology 103, no. 3 (2015): 761–68. http://dx.doi.org/10.1111/1365-2745.12382.

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37

Merlo, Emiliano, Pedro Bekinschtein, Sietse Jonkman, and Jorge H. Medina. "Molecular Mechanisms of Memory Consolidation, Reconsolidation, and Persistence." Neural Plasticity 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/687175.

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38

Christaki, Eirini, Markella Marcou, and Andreas Tofarides. "Antimicrobial Resistance in Bacteria: Mechanisms, Evolution, and Persistence." Journal of Molecular Evolution 88, no. 1 (2019): 26–40. http://dx.doi.org/10.1007/s00239-019-09914-3.

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39

Brady, R. A., J. G. Leid, J. W. Costerton, and M. E. Shirtliff. "Osteomyelitis: Clinical overview and mechanisms of infection persistence." Clinical Microbiology Newsletter 28, no. 9 (2006): 65–72. http://dx.doi.org/10.1016/j.clinmicnews.2006.04.001.

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40

Randall, Richard E., and Diane E. Griffin. "Within host RNA virus persistence: mechanisms and consequences." Current Opinion in Virology 23 (April 2017): 35–42. http://dx.doi.org/10.1016/j.coviro.2017.03.001.

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41

Krump, Nathan A., Wei Liu, and Jianxin You. "Mechanisms of persistence by small DNA tumor viruses." Current Opinion in Virology 32 (October 2018): 71–79. http://dx.doi.org/10.1016/j.coviro.2018.09.002.

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42

Nagajyothi, Fnu, Fabiana S. Machado, Barbara A. Burleigh, et al. "Mechanisms of Trypanosoma cruzi persistence in Chagas disease." Cellular Microbiology 14, no. 5 (2012): 634–43. http://dx.doi.org/10.1111/j.1462-5822.2012.01764.x.

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43

Kirk, David S., and Andrew V. Papachristos. "Cultural Mechanisms and the Persistence of Neighborhood Violence." American Journal of Sociology 116, no. 4 (2011): 1190–233. http://dx.doi.org/10.1086/655754.

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44

Balaban, NQ. "Persistence: mechanisms for triggering and enhancing phenotypic variability." Current Opinion in Genetics & Development 21, no. 6 (2011): 768–75. http://dx.doi.org/10.1016/j.gde.2011.10.001.

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45

Bhakdi, Sucharit. "Mechanisms of invasion and persistence of infectious agents." Medical Microbiology and Immunology 201, no. 4 (2012): 407. http://dx.doi.org/10.1007/s00430-012-0275-9.

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46

Michiels, Joran Elie, Bram Van den Bergh, Natalie Verstraeten, and Jan Michiels. "Molecular mechanisms and clinical implications of bacterial persistence." Drug Resistance Updates 29 (November 2016): 76–89. http://dx.doi.org/10.1016/j.drup.2016.10.002.

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47

Bozzi, G., F. R. Simonetti, S. A. Watters, et al. "No evidence of ongoing HIV replication or compartmentalization in tissues during combination antiretroviral therapy: Implications for HIV eradication." Science Advances 5, no. 9 (2019): eaav2045. http://dx.doi.org/10.1126/sciadv.aav2045.

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HIV persistence during combination antiretroviral therapy (cART) is the principal obstacle to cure. Mechanisms responsible for persistence remain uncertain; infections may be maintained by persistence and clonal expansion of infected cells or by ongoing replication in anatomic locations with poor antiretroviral penetration. These mechanisms require different strategies for eradication, and determining their contributions to HIV persistence is essential. We used phylogenetic approaches to investigate, at the DNA level, HIV populations in blood, lymphoid, and other infected tissues obtained at c

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48

Barbato, Christian, Carla Petrella, and Antonio Minni. "Insights into Molecular and Cellular Mechanisms of NeuroCOVID." Cells 13, no. 21 (2024): 1790. http://dx.doi.org/10.3390/cells13211790.

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49

Boichenko, M. N., E. V. Budanova, E. O. Kravtsova, E. V. Volchkova, and O. F. Belaya. "Some molecular mechanisms of development typhoid fever persistence infection." Infekcionnye bolezni 18, no. 2 (2020): 84–87. http://dx.doi.org/10.20953/1729-9225-2020-2-84-87.

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The overview presents data on the development of typhoid fever persistence infection associated with the expression of genes specific for S. Typhi pathogenicity island 7 (OSP7). Development of is linked with expression of Salmonella pathogenicity island 7 (SPI7), which is specific for S. Typhi. Expression of the gene tviA from SPI7 promotes S. Typhi to escape recognition by immune system. Other 4 genes of SPI7 are linked with synthesis and secretion of typhoid genotoxin, which by inducing demage of immune cells DNA, is putative cause development of persistence infection. Key words: S. Typhi, S

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50

Bailey, Drew H., Greg J. Duncan, Flávio Cunha, Barbara R. Foorman, and David S. Yeager. "Persistence and Fade-Out of Educational-Intervention Effects: Mechanisms and Potential Solutions." Psychological Science in the Public Interest 21, no. 2 (2020): 55–97. http://dx.doi.org/10.1177/1529100620915848.

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Some environmental influences, including intentional interventions, have shown persistent effects on psychological characteristics and other socially important outcomes years and even decades later. At the same time, it is common to find that the effects of life events or interventions diminish and even disappear completely, a phenomenon known as fade-out. We review the evidence for persistence and fade-out, drawing primarily on evidence from educational interventions. We conclude that (a) fade-out is widespread and often coexists with persistence; (b) fade-out is a substantive phenomenon, not

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