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Susceptibility to Cytomegalovirus Infection May Be Dependent on the Cytokine Response to the Virus
  1. Lois J. Geist,
  2. Sara L. Hinde
  1. 1From the Department of Internal Medicine (L.J.G.), University of Iowa College of Medicine, Iowa City
  2. 2Department of Veterans Affairs (S.L.H.), University of Iowa College of MedicineIowa City.
  1. Address correspondence to: Lois J. Geist, MD, University of Iowa College of Medicine, C33D GH, Iowa City, IA 52242. E-mail lois-geist{at}
  2. This work was supported by a VA Merit Review (to L.J.G.).


Background Cytomegalovirus (CMV) infection is an important cause of morbidity and mortality in an immunocompromised host. Pulmonary infection with CMV results in an inflammatory response, which includes the local production of cytokines. Cytokine production stimulated by CMV infection serves to activate a series of immunologic responses involved in viral clearance. Previous work has demonstrated that different mouse strains express variable sensitivity to CMV infection.

Methods Using mouse strains that express sensitive (BALB/cj) and resistant (C57BL/6) CMV phenotypes, we asked whether the differences in susceptibility to infection were caused by differences in pulmonary cytokine production after intraperitoneal infection with CMV.

Results C57 mice demonstrated a higher total bronchoalveolar lavage (BAL) and BAL lymphocyte count at 3 and 7 days after intraperitoneal infection compared with BALB mice. There were no differences in BAL cytokine production; however, we were able to demonstrate differences in CMV DNA load in the lungs of BALB mice compared with that of C57 mice. In addition, there appeared to be increased whole-lung production of the TH2 cytokine IL-10 in the BALB mice versus the C57 mice.

Conclusions This observation suggests that the genetic susceptibility to CMV infection may, in part, be regulated by differences in cytokines production within the local environment.

  • interleukin-10
  • viral infection
  • cytomegalovirus
  • genetic susceptibility
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