Reciprocal transactivation between HIV-1 and other human viruses

Virology. 2006 Aug 15;352(1):1-13. doi: 10.1016/j.virol.2006.04.006. Epub 2006 May 24.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Gene Expression Regulation, Viral
  • Gene Products, tat / metabolism*
  • HIV-1 / metabolism
  • HIV-1 / pathogenicity*
  • Humans
  • Trans-Activators / metabolism
  • Transcriptional Activation*
  • Viral Proteins / genetics
  • Viral Proteins / metabolism
  • Virus Diseases / physiopathology
  • Virus Diseases / virology
  • Viruses / metabolism
  • Viruses / pathogenicity*
  • tat Gene Products, Human Immunodeficiency Virus


  • Gene Products, tat
  • Trans-Activators
  • Viral Proteins
  • tat Gene Products, Human Immunodeficiency Virus