The ATP/P2X7 axis in human immunodeficiency virus infection of macrophages

Francesca Graziano, Elisa Vicenzi, Guido Poli

Research output: Contribution to journalReview articlepeer-review


HIV-1 infects CD4+ T lymphocytes with a ‘helper’ function and myeloid cells, mostly tissue-resident macrophages. While infection of CD4 T lymphocytes in the absence of combination antiretroviral therapy (cART) leads to their depletion and to a profound immunodeficiency, macrophages are resistant to virus-induced cytopathicity and are a source of infectious virus, particularly in the central nervous system (CNS). Infected macrophages are characterized by accumulating newly formed viral particles (virions) in subcellular vacuoles defined as ‘virus-containing compartments (VCC)’, derived from invaginations of the plasma membrane, that are poorly accessible to antiretroviral agents and anti-HIV antibodies. Several factors favor the accumulation of HIV-1 virions in VCC in vitro, whereas extracellular ATP, via binding to its receptor P2X7, is the only agent described thus far as capable of triggering the rapid release of VCC-sequestered virions without simultaneously causing the death of infected macrophages. Thus, the eATP/P2X7 axis could be exploited to achieve a pharmacological control of VCC-associated viral reservoir in individuals under effective cART.

Original languageEnglish
Pages (from-to)46-52
Number of pages7
JournalCurrent Opinion in Pharmacology
Publication statusPublished - Aug 2019

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery


Dive into the research topics of 'The ATP/P2X7 axis in human immunodeficiency virus infection of macrophages'. Together they form a unique fingerprint.

Cite this