Background and study aim: This study proposed to assess the relation between absolute telomere lengths (TLs) in gastric mucosa and Helicobacter pylori (H. pylori) infection and study the impact of (H. pylori) eradication therapy on TLs. Patients and Methods: This study was conducted on (42) subjects divided into two groups, group I: included (17) H. pylori negative cases served as control group, group II: included (25) H. pylori positive patients. Absolute TLs was measured in base pairs (bp) in gastric mucosa and analyzed by real time polymerase chain reaction (RT-PCR) in all groups and reevaluated in H. pylori positive patients 4 weeks after eradication therapy. Results: Prior to eradication therapy, there was highly significant shortening (P<0.001) in TLs (bp) in gastric mucosa of H. pylori positive patients compared to H. pylori negative controls. While there was highly significant elongation was observed after H. pylori eradication therapy in H. pylori positive patients (P < 0.001). There was significant negative correlation between TLs and ages of patients (P<0.001) while there was no significant relation between TLs and sex (P= 0.5) before and after eradication therapy. Conclusion: H. pylori positive patients had significantly shorter TLs than H. pylori negative controls. TLs were increased after H. pylori eradication therapy in H. pylori positive cases. This finding may indicate the importance of H. pylori eradication to avoid the development of gastric cancer by its effect on TLs.

This work was carried out in collaboration between all authors. Authors AAA and RRAEG are equally contributed in planning and designing the study, collecting the samples, performing the practical laboratory activities, analyzing the results, drafting and revising the manuscript. Author MZO participated in planning and designing the study, clinical evaluation of patients and controls and participated in the interpretation of the results. The three authors read and approved the final manuscript.

Human herpes virus 8 (HHV-8) was first described in 1994. It was also called Kaposi sarcoma-associated herpes virus (KSHV) as it was identified as the underlying infectious cause of Kaposi sarcoma (KS) 1. In 2010, HHV-8 was declared a Group 1 carcinogenic agent by the International Agency for Research on Cancer, highlighting its public health significance 2. The HHV-8 viral genome comprises about a 140-kb long unique region flanked by multiple terminal repeat sequences. The virus is difficult to cultivate, therefore, diagnosis of infection rests on demonstration of antibodies to the virus or detecting viral nucleic acid in clinical specimens 3. HHV-8 prevalence varies between different geographic regions and sub-populations. Worldwide seroprevalence of HHV-8 varies: generally low to moderate for populations in Western countries and Asia 4. Adult HHV-8 seropositivity is very high in eastern and central Africa (70%-90%), where KS is endemic, and lower in southern and northern Africa (10%-40%), including Egypt, where KS is more rare 5 .