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Adenovirus-Induced Liver Pathology Is Mediated Through TNF Receptors I and II but Is Independent of TNF or Lymphotoxin

Hikmat Hayder^*, Robert V. Blanden^*, Heinrich Körner^1,, D. Sean Riminton, Jonathon D. Sedgwick^2, and Arno Müllbacher^3,*

^* Division of Immunology and Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra, Australia; and Centenary Institute of Cancer Medicine and Cell Biology, Royal Prince Alfred Hospital, Sydney, Australia

Mice infected with an adenovirus mutant in which the E3 region is deleted, including TNF-resistance genes, develop fatal liver pathology within 3–4 days after infection. At least 10-fold more wild-type virus was needed to cause comparable pathology. These results indicate that the E3 region is critically involved in modulating the pathogenesis of adenovirus infection and that TNF may play a role in liver damage. To explore the latter possibility, the course of disease was examined in infected mice lacking TNFR-I and/or TNFRII, TNF only, or both TNF and lymphotoxin-. Only mice lacking both TNFRI and TNFRII were protected from the lethal affects of the mutant adenovirus. Mice deficient in TNF or TNF and lymphotoxin- displayed the fatal pathology. This outcome is consistent with the existence of another related ligand that binds TNFRI/II to mediate liver damage during infection with this mutant.

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