Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Jan 11:9:4.
doi: 10.1186/1742-4690-9-4.

Interactions between prostaglandins, leukotrienes and HIV-1: possible implications for the central nervous system

Jonathan Bertin  1 , Corinne Barat, Sylvie Méthot, Michel J Tremblay
Affiliations
Review

Interactions between prostaglandins, leukotrienes and HIV-1: possible implications for the central nervous system

Jonathan Bertin et al. Retrovirology. .

Abstract

In HIV-1-infected individuals, there is often discordance between viremia in peripheral blood and viral load found in the central nervous system (CNS). Although the viral burden is often lower in the CNS compartment than in the plasma, neuroinflammation is present in most infected individuals, albeit attenuated by the current combined antiretroviral therapy. The HIV-1-associated neurological complications are thought to result not only from direct viral replication, but also from the subsequent neuroinflammatory processes. The eicosanoids - prostanoids and leukotrienes - are known as potent inflammatory lipid mediators. They are often present in neuroinflammatory diseases, notably HIV-1 infection. Their exact modulatory role in HIV-1 infection is, however, still poorly understood, especially in the CNS compartment. Nonetheless, a handful of studies have provided evidence as to how these lipid mediators can modulate HIV-1 infection. This review summarizes findings indicating how eicosanoids may influence the progression of neuroAIDS.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Metabolic pathway of AA transformation into eicosanoid products. Once a cell is activated by a proinflammatory stimulus that engages a Gαq-coupled seven-transmembrane receptor, AA can be cleaved by cytosolic PLA2 from phospholipids that compose cellular membranes (mostly nuclear, endoplasmic reticulum or Golgi membranes)[173]. Free AA can subsequently be converted into different eicosanoid products by different enzymes (represented in blue), notably the COX and LO pathways. This review will mainly focus on the prostanoids - PGE2, and 15d-PGJ2 prostaglandins - and on 5-LO products, namely LTs. Only eicosanoids and pathways of interest in this paper are depicted.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Davis LE, Hjelle BL, Miller VE, Palmer DL, Llewellyn AL, Merlin TL, Young SA, Mills RG, Wachsman W, Wiley CA. Early viral brain invasion in iatrogenic human immunodeficiency virus infection. Neurology. 1992;42:1736–1739. - PubMed
    1. Kraft-Terry SD, Stothert AR, Buch S, Gendelman HE. HIV-1 neuroimmunity in the era of antiretroviral therapy. Neurobiol Dis. 2010;37:542–548. - PMC - PubMed
    1. Antinori A, Arendt G, Becker JT, Brew BJ, Byrd DA, Cherner M, Clifford DB, Cinque P, Epstein LG, Goodkin K, Gisslen M, Grant I, Heaton RK, Joseph J, Marder K, Marra CM, McArthur JC, Nunn M, Price RW, Pulliam L, Robertson KR, Sacktor N, Valcour V, Wojna VE. Updated research nosology for HIV-associated neurocognitive disorders. Neurology. 2007;69:1789–1799. - PMC - PubMed
    1. Evers S, Rahmann A, Schwaag S, Frese A, Reichelt D, Husstedt IW. Prevention of AIDS dementia by HAART does not depend on cerebrospinal fluid drug penetrance. AIDS Res Hum Retroviruses. 2004;20:483–491. - PubMed
    1. Wright E. Neurocognitive impairment and neuroCART. Curr Opin HIV AIDS. 2011;6:303–308. - PubMed

MeSH terms