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Telomeres and Telomerase

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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.

Telomeres and Telomerase

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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.

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Updated: Jun 28, 2026

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis

Published on: April 17, 2017

Telomere length in Hepatitis C.

Y Kitay-Cohen¹, L Goldberg-Bittman, R Hadary

¹Liver Institute, Meir Hospital, Kfar-Saba, Israel; Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.

Cancer Genetics and Cytogenetics

|November 11, 2008

Summary

Patients with chronic hepatitis C virus (HCV) infection exhibit shorter telomeres in leukocytes compared to those in remission or healthy controls. This telomere shortening in active HCV infection is linked to overall lower telomere levels, not increased cell turnover.

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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

Area of Science:

Genetics
Immunology
Hepatology

Background:

Telomeres protect chromosome ends; their shortening is linked to cellular senescence and diseases like cancer.
Hepatitis C virus (HCV) infection can cause liver fibrosis, cellular senescence, and is associated with B-cell lymphoma and hepatocellular carcinoma.
HCV infection may accelerate telomere shortening through hepatocyte cell-cycle turnover.

Purpose of the Study:

To assess and compare relative telomere length in leukocytes of patients with chronic HCV, those in HCV remission, and healthy controls.
To validate a novel manual evaluation method for telomere length assessment against spectral imaging.
To investigate the relationship between telomere length and cell-cycle turnover in HCV infection.

Main Methods:

Fluorescence in situ hybridization (FISH) protocol (DAKO) used to determine telomere fluorescence intensity and number in leukocytes.
Manual evaluation of telomere length, validated using Applied Spectral Imaging (ASI) software.
Analysis of leukocytes from 22 patients with chronic HCV, age- and sex-matched patients in remission, and healthy controls.

Main Results:

Leukocytes from patients with chronic HCV infection displayed significantly shorter telomeres than those from patients in remission and healthy controls.
A correlation was observed between telomere signal intensity and telomere length: low intensity indicated shorter telomeres, high intensity indicated longer telomeres.
Findings were confirmed by ASI telomere software, validating the manual evaluation method.

Conclusions:

Telomere shortening in leukocytes of patients with active HCV infection is likely due to a lower overall telomere level, rather than increased cell cycle turnover.
The novel manual evaluation method is accurate and valid for assessing relative telomere length in HCV patients.
Telomere length assessment may offer insights into the pathogenesis of HCV-related complications.