Role of macrophages in bypassing the inhibitory activity of Newcastle disease virus on the T-suppressor-cell circuit which regulates contact sensitivity to picryl chloride.

The interaction between the paramyxovirus of Newcastle disease virus (NDV) and the T-suppressor-cell circuit which regulates the expression phase of contact sensitivity reaction to picryl chloride was investigated. NDV infection impairs the T-acceptor-cell (Tacc) activity, as demonstrated by the failure of Tacc from mice infected with NDV both on Day 0 and on Day 3 to release the nonspecific inhibitor of the passive transfer of contact sensitivity. Tacc from NDV-infected mice fail to bind appreciable amounts of exogenous T suppressor factor, so indicating that the virus eliminates this T-cell population. However, macrophages from mice infected with NDV are able to release a nonspecific inhibitor of the passive transfer of contact sensitivity, indicating that the inhibition of Tacc activity in mice infected with NDV is bypassed by macrophages, so that the T-suppressor circuit is functionally active in NDV-infected mice. The mechanism of the selective inhibition of the Tacc activity by NDV is discussed.