TH2 cytokines have been presented as the factors responsible for the lack of Thl responses as well as the preferred phenotype of virus-expressing T cells. If there is such substantial evidence against the beneficial effects of Th2 cytokines, what purpose could its virostatic inhibition in macrophages serve the host? Or is it benefitting the virus? We believe Th2 cytokines may help both virus and host for different reasons. From the point of view of the host, although Th2 cytokines inhibit effective Th l responses, they are also potent regulators which dampen a chronical ly act ivated immune system and reduce the potentially enhancing effects of TNF, ILl and IL6 in virus expression and immune dysfunction. We could postulate that this accounts for the elevated levels of Th2 cytokines seen in HIV-infected patients by Emilie et al. and others irrespective of disease progression. Macrophage-derived I L l 0 has been shown not to be directly related to Th2type responses, serving as an immune deactivating stimulus. Therefore, Th2 cytokines might actually be a factor in reducing viral load if one accepts the corre la t ion between TNFtx-IL I IL6 /NF-Kb/HIV (see Virelizier and Kaplan, et al.). However, from the point of view of the virus, this effect may be part of a general mechanisms of persis tence in vivo, since, in addition to reducing Th l responses, the preferential viral production by Th2 T ceils would also inhibit virus in macrophages. This inhibition would subsequently protect newly infected macrophages from any effec t ive immune clearance of infected Th2 cytokine-producing T cells by CTL. The result would be a renewed expression of virus from newly infected macrophages recovering from the Th2 actions in a TNF, ILl and IL6-rich environment.