Previous studies in our laboratory have documented that in utero
chlordane exposure caused a significant enhancement in the survival of the offspring to influenza A virus
infection, and a depressed delayed type
hypersensitivity (DTH) response to
oxazolone. To correlate these 2 effects, we assayed influenza A virus-specific DTH response, and found that it was significantly decreased in
chlordane-treated offspring. Virus-specific T-cell blastogenesis was also assayed in
chlordane-treated animals. No significant differences due to the
chlordane treatment were found in virus-specific T-cell blastogenesis, suggesting that the DTH depression did not result from a paucity of
antigen-reactive T-cells. To determine whether enhanced survival was due, in part, to the effects of
chlordane on virus replication, rather than on immunological alteration alone, the kinetics of influenza virus replication in the lungs of
chlordane- and vehicle-treated animals were determined. In utero
chlordane treatment caused no significant differences in in vivo virus replication. These data suggest that increased survival was due to a decrease in virus-specific DTH and its associated pathology.