Abstract

Tumor necrosis factor-α (TNF-α) appears to play an important role in HIV encephalitis (HIVE). TNF2, a polymorphism of TNF-α, associates with higher levels of TNF-α and severe manifestations of some infections. We studied 44 acquired immunodeficiency syndrome (AIDS) patients with autopsy-proven HIVE and/or HIV leukoencephalopathy (HIVLE) (HIVE/LE) and 30 AIDS patients without HIVE/LE. TNF2 did not associate with presence of HIVE/LE ( p>0.5). Moreover, the TNF-α regulatory element TTATTTAT within the 3′-untranslated region was intact in HIVE/LE brains, and HLA-DR3 did not associate with HIVE/LE. Other host factors or, more likely, viral factors may be responsible for the development of HIVE/LE.

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