The latent cytomegalovirus decreases telomere
length by microcompetition

• Authors: Hanan Polansky , Adrian Javaherian
• Languages of publication: EN

Abstracts

EN

Reduced telomere length has been associated
with aging and age-related diseases. Latent infection with
the Cytomegalovirus (CMV) induces telomere shortening
in the infected cells. Latent CMV infection may cause
reduced telomere length via GABP transcription factor
deficiency, according to the Microcompetition Theory.
Microcompetition and viral-induced transcription factor
deficiency is important since most people harbor a latent
viral infection.

Keywords

EN

Latent virus; microcompetition; transcriptionfactor; telomere

• Publisher: De Gruyter Open
• Journal: Open Medicine
• Year: 2014
• Volume: 10
• Issue: 1

Dates

received

26 - 4 - 2015

online

27 - 5 - 2015

accepted

30 - 4 - 2015

Contributors

author

Hanan Polansky

• The Center for the Biology of Chronic Disease
  (CBCD), Valley Cottage, NY 10989, USA

author

Adrian Javaherian

• The Center for the Biology of Chronic Disease
  (CBCD), Valley Cottage, NY 10989, USA

References

• [1] Drury S.S., Theall K., Gleason M.M., Smyke A.T., De Vivo I.,Wong J.Y.Y. et al., Telomere length and early severe socialdeprivation: linking early adversity and cellular aging, Mol.Psychiatry, 2012, 17(7), 719-727[Crossref]
• [2] van de Berg P.J., Griffiths S.J., Yong S.L., Macaulay R.,Bemelman F.J., Jackson S. et al., Cytomegalovirus InfectionReduces Telomere Length of the Circulating T Cell Pool, J.Immunol. 2010, 184, 3417-3423[WoS]
• [3] Polansky H., Microcompetition with Foreign DNA and the Originof Chronic Disease., The Center for the Biology of ChronicDisease, New York, 2003
• [4] Liu B.H., Wang X., Ma Y.X., Wang S., CMV Enhancer/HumanPDGF-Beta Promoter for Neuron-Specific Transgene Expression,Gene Ther., 2004, 11(1), 52-60[Crossref]
• [5] Slobedman B., Mocarski E.S., Quantitative Analysis of LatentHuman Cytomegalovirus, J. Virol., 1999, 73(6), 4806-4812
• [6] Adam G.I., Miller S.J., Ulleras E., Franklin G.C., Cell-Type-Specific Modulation of PDGF-B Regulatory Elements via ViralEnhancer Competition: A Caveat for the Use of ReferencePlasmids in Transient Transfection Assays, Gene, 1996, 178(1),25-29
• [7] Yu S., Cui K., Jothi R., Zhao D.M., Jing X., Zhao K. et al., GABPcontrols a critical transcription regulatory module that isessential for maintenance and differentiation of hematopoieticstem/progenitor cells, Blood, 2011, 117(7), 2166-2178[WoS]
• [8] Sarek G., Vannier J.B., Panier S., Petrini J.H.J., Boulton S.J.,TRF2 Recruits RTEL1 to Telomeres in S Phase to Promote T-LoopUnwinding, Molecular Cell, 2015, 57(4), 622-635[Crossref]
• [9] Spyridopoulos I., Hoffmann J., Aicher A., Brummendorf T.H.,Doerr H.W., Zeiher A.M. et al., Accelerated Telomere Shorteningin Leukocyte Subpopulations of Patients With Coronary HeartDisease, Circulation, 2009, 120, 1364-1372[WoS]
• [10] Nan W.Q., Ling Z., Bing C., The influence of the telomeretelomerasesystem on diabetes mellitus and its vascularcomplications, Expert Opin. Ther. Targets., 2015, 19(6)
• [11] Ji Y.N., An L., Zhan P., Chen X.H., Cytomegalovirus infection andcoronary heart disease risk: a meta-analysis, Molecular BiologyReports, 2012, 39(6), 6537-6546[WoS][Crossref]
• [12] Mendy A., Gasana J., Vieira E.R., Diallo H., Prospective studyof cytomegalovirus seropositivity and risk of mortality fromdiabetes, Acta Diabetol., 2014, 51, 723-729[WoS]
• [13] Green M., Michaels M.G., Epstein-Barr Virus Infectionand Posttransplant Lymphoproliferative Disorder, Am. J.Transplant., 2013, 13(s3), 41-54[Crossref][WoS]
• [14] Reddehase M.J., Cytomegaloviruses: From MolecularPathogenesis to Intervention. Volume 2, Horizon ScientificPress, United Kingdom, 2013
• [15] Bernstein D.I., Bellamy A.R., Hook III E.W., Levin M.J., WaldA., Ewell M.G. et al., Epidemiology, Clinical Presentation, andAntibody Response to Primary Infection With Herpes SimplexVirus Type 1 and Type 2 in Young Women, Clin. Infect. Dis.,2013, 56(3), 344-351[Crossref]

Identifiers

DOI

10.1515/med-2015-0042