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  1. Article ; Online: How can the latent cytomegalovirus cause an increase in all-cause mortality? An answer based on the microcompetition model.

    Polansky, Hanan

    Antiviral therapy

    2021  Volume 25, Issue 7, Page(s) 349–351

    Abstract: Many studies showed the existence of a positive association between cytomegalovirus (CMV) seropositivity and all-cause mortality. In this paper, we use the microcompetition model to explain how the latent CMV sequesters the limiting GABP∙p300/CBP ... ...

    Abstract Many studies showed the existence of a positive association between cytomegalovirus (CMV) seropositivity and all-cause mortality. In this paper, we use the microcompetition model to explain how the latent CMV sequesters the limiting GABP∙p300/CBP transcription complex, which causes abnormal cellular gene expression, a chronic disease and mortality. Since most people harbour the latent CMV, we urge further research on this topic.
    MeSH term(s) Cytomegalovirus/genetics ; Cytomegalovirus Infections ; Humans
    Language English
    Publishing date 2021-02-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 1339842-8
    ISSN 2040-2058 ; 1359-6535
    ISSN (online) 2040-2058
    ISSN 1359-6535
    DOI 10.3851/IMP3384
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4877: Show issues Location:
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    Zs.MO 174: Show issues

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  2. Article ; Online: How microcompetition with latent viruses can cause α synuclein aggregation, mitochondrial dysfunction, and eventually Parkinson's disease.

    Polansky, Hanan / Lori, Gillad

    Journal of neurovirology

    2021  Volume 27, Issue 1, Page(s) 52–57

    Abstract: The cause of most Parkinson's disease cases is unknown. However, it is well documented that mitochondrial dysfunction and misfolded α synuclein aggregation are important cellular abnormalities associated with the disease. In this paper, we use the ... ...

    Abstract The cause of most Parkinson's disease cases is unknown. However, it is well documented that mitochondrial dysfunction and misfolded α synuclein aggregation are important cellular abnormalities associated with the disease. In this paper, we use the microcompetition model to show how latent viruses, which infect the central and peripheral nervous systems, can cause the observed mitochondrial dysfunction and excess α synuclein aggregation, and eventually, Parkinson's disease.
    MeSH term(s) Animals ; Humans ; Latent Infection/metabolism ; Mitochondria/pathology ; Parkinson Disease/pathology ; Protein Aggregation, Pathological/metabolism ; Protein Aggregation, Pathological/pathology ; Virus Latency/physiology ; Viruses/metabolism ; alpha-Synuclein/metabolism
    Chemical Substances alpha-Synuclein
    Language English
    Publishing date 2021-01-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1283265-0
    ISSN 1538-2443 ; 1355-0284
    ISSN (online) 1538-2443
    ISSN 1355-0284
    DOI 10.1007/s13365-020-00929-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4426: Show issues Location:
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  3. Article ; Online: How an increase in the copy number of HSV-1 during latency can cause Alzheimer's disease: the viral and cellular dynamics according to the microcompetition model.

    Polansky, Hanan / Goral, Benjamin

    Journal of neurovirology

    2021  Volume 27, Issue 6, Page(s) 895–916

    Abstract: Numerous studies observed a link between the herpes smplex virus-1 (HSV-1) and Alzheimer's disease. However, the exact viral and cellular dynamics that lead from an HSV-1 infection to Alzheimer's disease are unknown. In this paper, we use the ... ...

    Abstract Numerous studies observed a link between the herpes smplex virus-1 (HSV-1) and Alzheimer's disease. However, the exact viral and cellular dynamics that lead from an HSV-1 infection to Alzheimer's disease are unknown. In this paper, we use the microcompetition model to formulate these dynamics by connecting seemingly unconnected observations reported in the literature. We concentrate on four pathologies characteristic of Alzheimer's disease. First, we explain how an increase in the copy number of HSV-1 during latency can decrease the expression of BECN1/Beclin1, the degradative trafficking protein, which, in turn, can cause a dysregulation of autophagy and Alzheimer's disease. Second, we show how an increase in the copy number of the latent HSV-1 can decrease the expression of many genes important for mitochondrial genome metabolism, respiratory chain, and homeostasis, which can lead to oxidative stress and neuronal damage, resulting in Alzheimer's disease. Third, we describe how an increase in this copy number can reduce the concentration of the NMDA receptor subunits NR1 and NR2b (Grin1 and Grin2b genes), and brain derived neurotrophic factor (BDNF), which can cause an impaired synaptic plasticity, Aβ accumulation and eventually Alzheimer's disease. Finally, we show how an increase in the copy number of HSV-1 in neural stem/progenitor cells in the hippocampus during the latent phase can lead to an abnormal quantity and quality of neurogenesis, and the clinical presentation of Alzheimer's disease. Since the current understanding of the dynamics and homeostasis of the HSV-1 reservoir during latency is limited, the proposed model represents only a first step towards a complete understanding of the relationship between the copy number of HSV-1 during latency and Alzheimer's disease.
    MeSH term(s) Alzheimer Disease/genetics ; DNA Copy Number Variations/genetics ; Herpes Simplex/genetics ; Herpesvirus 1, Human/genetics ; Humans ; Neurons
    Language English
    Publishing date 2021-10-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1283265-0
    ISSN 1538-2443 ; 1355-0284
    ISSN (online) 1538-2443
    ISSN 1355-0284
    DOI 10.1007/s13365-021-01012-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4426: Show issues Location:
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  4. Article ; Online: Coronavirus disease 2019 (COVID-19): first indication of efficacy of Gene-Eden-VIR/Novirin in SARS-CoV-2 infection.

    Polansky, Hanan / Lori, Gillad

    International journal of antimicrobial agents

    2020  Volume 55, Issue 6, Page(s) 105971

    MeSH term(s) Antiviral Agents/pharmacology ; Betacoronavirus/drug effects ; Coronavirus Infections/drug therapy ; Drug Combinations ; Humans ; Pandemics ; Plant Extracts/pharmacology ; Pneumonia, Viral/drug therapy ; Quercetin/pharmacology ; Selenium/pharmacology
    Chemical Substances Antiviral Agents ; Drug Combinations ; Gene-Eden-VIR ; Plant Extracts ; Quercetin (9IKM0I5T1E) ; Selenium (H6241UJ22B)
    Keywords covid19
    Language English
    Publishing date 2020-04-10
    Publishing country Netherlands
    Document type Letter
    ZDB-ID 1093977-5
    ISSN 1872-7913 ; 0924-8579
    ISSN (online) 1872-7913
    ISSN 0924-8579
    DOI 10.1016/j.ijantimicag.2020.105971
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3368: Show issues Location:
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    Zs.MO 500: Show issues

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  5. Article ; Online: Dynamics of sequestering the limiting p300/CBP, viral cis-regulatory elements, and disease.

    Polansky, Hanan / Schwab, Hava

    Journal of biosciences

    2020  Volume 45

    Abstract: Many studies showed that the p300/CBP coactivator is limiting. Here we review three studies that showed how transcription complexes formed on viral cis-regulator elements compete with cellular transcription complexes by sequestrating the p300/CBP ... ...

    Abstract Many studies showed that the p300/CBP coactivator is limiting. Here we review three studies that showed how transcription complexes formed on viral cis-regulator elements compete with cellular transcription complexes by sequestrating the p300/CBP coactivator. According to the microcompetition model, this sequestering can cause disease. We use the microcompetition model to explain how a specific type of sequestering, caused by a latent virus that has an active cis-regulatory element in its promoter/enhancer that binds the transcription complex p300/CBP ·GABP can cause diseases such as cancer, atherosclerosis, diabetes, and certain autoimmune diseases.
    MeSH term(s) Gene Expression Regulation/immunology ; Gene Expression Regulation/physiology ; Human papillomavirus 18/physiology ; Humans ; Promoter Regions, Genetic ; Regulatory Sequences, Nucleic Acid/physiology ; p300-CBP Transcription Factors/genetics ; p300-CBP Transcription Factors/metabolism
    Chemical Substances p300-CBP Transcription Factors (EC 2.3.1.48)
    Language English
    Publishing date 2020-06-08
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1907: Show issues Location:
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  6. Article ; Online: Effects of Gene-Eden-VIR and Novirin on SARS-CoV: Implications for COVID-19.

    Polansky, Hanan / Lori, Gillad

    Journal of evidence-based integrative medicine

    2020  Volume 25, Page(s) 2515690X20932523

    Abstract: The coronavirus (SARS-CoV-2), which causes COVID-19, is a betacoronavirus closely related to the human severe acute respiratory syndrome (SARS)-coronavirus (SARS-CoV). The recent COVID-19 outbreak created an urgent need for treatment. To expedite the ... ...

    Abstract The coronavirus (SARS-CoV-2), which causes COVID-19, is a betacoronavirus closely related to the human severe acute respiratory syndrome (SARS)-coronavirus (SARS-CoV). The recent COVID-19 outbreak created an urgent need for treatment. To expedite the development of such treatment, pharmaceutical companies and government agencies are currently testing several existing drugs for their effect on the virus. Gene-Eden-VIR and Novirin are natural, broad-spectrum, antiviral treatments proven to be safe and effective in several clinical studies. In this article, we present evidence indicating that the 5 Gene-Eden-VIR/Novirin ingredients have anti-betacoronavirus, and specifically, anti-SARS-CoV effects. We consider this evidence as a first indication of the anti-coronavirus effects of Gene-Eden-VIR/Novirin. Next, we are planning to conduct a clinical study with users of the treatments to test the effects of Gene-Eden-VIR/Novirin on individuals at risk and those infected with the virus.
    MeSH term(s) Antiviral Agents/therapeutic use ; Betacoronavirus ; COVID-19 ; Coronavirus/drug effects ; Coronavirus Infections/drug therapy ; Coronavirus Infections/epidemiology ; Drug Combinations ; Humans ; Pandemics ; Plant Extracts/therapeutic use ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/epidemiology ; Quercetin/therapeutic use ; SARS-CoV-2 ; Selenium/therapeutic use
    Chemical Substances Antiviral Agents ; Drug Combinations ; Gene-Eden-VIR ; Plant Extracts ; Quercetin (9IKM0I5T1E) ; Selenium (H6241UJ22B)
    Keywords covid19
    Language English
    Publishing date 2020-06-18
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2515-690X
    ISSN (online) 2515-690X
    DOI 10.1177/2515690X20932523
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Copy number of latent viruses, oncogenicity, and the microcompetition model.

    Polansky, Hanan / Schwab, Hava

    Oncotarget

    2018  Volume 9, Issue 60, Page(s) 31568–31569

    Language English
    Publishing date 2018-08-03
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.25804
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Dynamics of sequestering the limiting p300/CBP, viral cis-regulatory elements, and disease

    Polansky, Hanan / Schwab, Hava

    Journal of biosciences. 2020 Dec., v. 45, no. 1

    2020  

    Abstract: Many studies showed that the p300/CBP coactivator is limiting. Here we review three studies that showed how transcription complexes formed on viral cis-regulator elements compete with cellular transcription complexes by sequestrating the p300/CBP ... ...

    Abstract Many studies showed that the p300/CBP coactivator is limiting. Here we review three studies that showed how transcription complexes formed on viral cis-regulator elements compete with cellular transcription complexes by sequestrating the p300/CBP coactivator. According to the microcompetition model, this sequestering can cause disease. We use the microcompetition model to explain how a specific type of sequestering, caused by a latent virus that has an active cis-regulatory element in its promoter/enhancer that binds the transcription complex p300/CBP·GABP can cause diseases such as cancer, atherosclerosis, diabetes, and certain autoimmune diseases.
    Keywords atherosclerosis ; autoimmune diseases ; diabetes ; enhancer elements ; latent period ; neoplasms ; promoter regions ; transactivators
    Language English
    Dates of publication 2020-12
    Size p. 79.
    Publishing place Springer India
    Document type Article
    Note golden set ; Review
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    DOI 10.1007/s12038-020-00051-4
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 5290: Show issues

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  9. Article: How a disruption of the competition between HIF-1 and p53 for limiting p300/CBP by latent viruses can cause disease.

    Polansky, Hanan / Schwab, Hava

    Genes & cancer

    2018  Volume 9, Issue 5-6, Page(s) 153–154

    Language English
    Publishing date 2018-12-24
    Publishing country United States
    Document type Editorial
    ZDB-ID 2538519-7
    ISSN 1947-6027 ; 1947-6019
    ISSN (online) 1947-6027
    ISSN 1947-6019
    DOI 10.18632/genesandcancer.178
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: How latent viruses cause breast cancer: An explanation based on the microcompetition model.

    Polansky, Hanan / Schwab, Hava

    Bosnian journal of basic medical sciences

    2019  Volume 19, Issue 3, Page(s) 221–226

    Abstract: Most breast cancer cases show a decrease in the concentration of the breast cancer type 1 susceptibility protein (BRCA1). However, only a small portion of these cases have a mutated BRCA1 gene. Although many attempts have been made to identify the reason ...

    Abstract Most breast cancer cases show a decrease in the concentration of the breast cancer type 1 susceptibility protein (BRCA1). However, only a small portion of these cases have a mutated BRCA1 gene. Although many attempts have been made to identify the reason for the decrease in BRCA1 concentration in sporadic, non-heritable breast cancer cases, the cause is still unknown. In this review, we use the Microcompetition Model to explain how certain latent viruses, which are frequently detected in breast cancer tumors, can decrease the expression of the BRCA1 gene and cause the development of breast tumors.
    MeSH term(s) BRCA1 Protein/genetics ; BRCA1 Protein/metabolism ; Breast Neoplasms/etiology ; Breast Neoplasms/genetics ; Breast Neoplasms/virology ; Down-Regulation ; Female ; GA-Binding Protein Transcription Factor/metabolism ; Genes, BRCA1 ; Humans ; Models, Biological ; Retroviridae/isolation & purification ; Retroviridae/pathogenicity ; Virus Latency/physiology
    Chemical Substances BRCA1 Protein ; BRCA1 protein, human ; GA-Binding Protein Transcription Factor ; GABPA protein, human
    Language English
    Publishing date 2019-08-20
    Publishing country Bosnia and Herzegovina
    Document type Journal Article ; Review
    ZDB-ID 2240029-1
    ISSN 1840-4812 ; 1512-8601
    ISSN (online) 1840-4812
    ISSN 1512-8601
    DOI 10.17305/bjbms.2018.3950
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6314: Show issues Location:
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