To better understand the pathogenesis of interstitial pneumonitis after marrow transplantation, we have studied the interactions of CMV and GVH in a murine model. In the nonirradiated F1 hybrid model of GVH, which is directed toward the major histocompatibility antigens, simultaneous murine CMV (MCMV) infection and GVH act synergistically. The manifestations of GVH, including splenic enlargement and loss of cell-mediated lympholysis responses, are dramatically increased. Significantly, mice with both MCMV and GVH develop severe, diffuse interstitial pneumonitis not seen with either MCMV or GVH alone. This pneumonitis is characterized by a marked increase in lung weight, inflammatory changes involving both the interstitial and perivascular structures, and an increase in lung T lymphocytes of donor origin. To further examine the role of virus in the genesis of pneumonitis during concurrent MCMV infection and GVH, we have evaluated the effects of antiviral treatment on the course of MCMV infection and the occurrence and severity of pneumonitis in this model. Our findings indicate that administering ganciclovir during MCMV infection and GVH suppresses replication of virus but does not alter the frequency and only moderately alters the severity of interstitial pneumonitis. Thus, factors other than direct damage by the virus to the lungs are responsible for pneumonitis.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Infectious Diseases|
|State||Published - 1988|
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health