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Updated: Jul 14, 2026

Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
08:26

Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins

Published on: August 31, 2017

Ganciclovir inhibits lymphocyte proliferation by impairing DNA synthesis

Minoo Battiwalla1, Yiyuan Wu, Rajinder P S Bajwa

  • 1Department of Medicine, Roswell Park Cancer Institute, Buffalo, New York 14202, USA. minoo.battiwalla@roswellpark.org <minoo.battiwalla@roswellpark.org>

Biology of Blood and Marrow Transplantation : Journal of the American Society for Blood and Marrow Transplantation
|June 21, 2007
PubMed

Insights

Ganciclovir effectively prevents cytomegalovirus (CMV) disease after stem cell transplants but may harm immune recovery. This antiviral drug suppresses T-lymphocyte proliferation, potentially impacting long-term transplant outcomes.

Area of Science:

  • Immunology
  • Hematology
  • Virology

Background:

  • Cytomegalovirus (CMV) disease mortality in allogeneic hematopoietic stem cell transplant (HSCT) recipients has decreased due to ganciclovir. However, ganciclovir has not improved overall survival and recurrent CMV antigenemia predicts malignancy relapse.
  • Prolonged ganciclovir exposure is linked to increased relapse rates in HSCT patients, suggesting potential negative impacts beyond CMV control.

Purpose of the Study:

  • To investigate the hypothesis that ganciclovir negatively affects immune reconstitution post-HSCT.
  • To determine the in vitro effect of ganciclovir on normal human T-lymphocyte activation and proliferation.

Main Methods:

  • Assessed T-lymphocyte activation and proliferation using PHA-induced (3)H-thymidine uptake.
  • Measured the impact of ganciclovir and foscarnet at therapeutic concentrations on lymphocyte responses.
  • Evaluated ganciclovir's effect on bromodeoxyuridine incorporation, lymphocyte survival, and apoptosis.

Main Results:

  • Therapeutic concentrations of ganciclovir significantly reduced T-lymphocyte activation and proliferation.
  • Ganciclovir impaired DNA synthesis in proliferating lymphocytes, as indicated by reduced bromodeoxyuridine incorporation.
  • Foscarnet did not exhibit the same suppressive effect on T-lymphocyte proliferation at tested concentrations. Ganciclovir did not induce lymphocyte apoptosis or impair survival.

Conclusions:

  • Ganciclovir suppresses T-lymphocyte proliferation in vitro by inhibiting DNA synthesis.
  • These findings suggest ganciclovir may have detrimental implications for T-lymphocyte function and immune reconstitution following allogeneic bone marrow transplantation (BMT).
  • Further research is warranted to explore strategies to mitigate ganciclovir's impact on immune recovery in HSCT recipients.

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