Modulation of immunocompetence by cyclosporin A, cyclophosphamide or protein malnutrition potentiates murine cytomegalovirus pneumonitis.

Following intranasal infection with murine cytomegalovirus (MCMV), the levels of viral replication in the lungs of susceptible BALB/c mice were enhanced by treatment with cyclophosphamide (CY), or to a greater extent cyclosporin A (CsA) or the Nu/Nu genotype. Focal inflammation was seen 2-4 days after infection in all groups. This was followed by diffuse interstitial pneumonitis which cleared 12-20 days later in the absence of immunosuppression. Although the initial foci of inflammation were less prominent in infected mice treated with CY or CsA, the most severe interstitial pneumonitis was seen 7 days p.i. in mice given CY, whilst CsA-treatment produced focal and disseminated pneumonitis 7-14 days p.i. and Nu/Nu mice exhibited only the focal response. MCMV-infected mice maintained from weaning on a low protein (4% casein) diet also retained higher titres of virus in their lungs than did normally-fed controls, and displayed more prominent focal pneumonitis.