Reciprocal transactivation between HIV-1 and other human viruses.

A variety of rare clinical syndromes are seen with strikingly increased prevalence in HIV-1-infected individuals, many with underlying viral etiologies. The emergence of these diseases in AIDS reflects a reduction in the ability of the immune system to mount an adequate defense against viruses in general due to the damage inflicted to the immune system by HIV-1 infection. However, in many cases, it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses. This can occur either directly by HIV-1 proteins such as Tat enhancing the activity of heterologous viral promoters, and/or indirectly by HIV-1 inducing the expression of cytokines and activation of their downstream signaling that eventually promotes the multiplication of the other virus. In a reciprocal manner, the effects of other viruses can enhance the pathogenicity of HIV-1 infection in individuals with AIDS through stimulation of the HIV-1 promoter activity and genome expression. The purpose of this review is to examine the cross-interactions between these viruses and HIV-1.