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Review
. 2023 Dec:73:102404.
doi: 10.1016/j.coph.2023.102404. Epub 2023 Sep 19.

The role of Pannexin-1 channels, ATP, and purinergic receptors in the pathogenesis of HIV and SARS-CoV-2

Cristian A Hernandez  1 , Eliseo A Eugenin  2
Affiliations
Review

The role of Pannexin-1 channels, ATP, and purinergic receptors in the pathogenesis of HIV and SARS-CoV-2

Cristian A Hernandez et al. Curr Opin Pharmacol. 2023 Dec.

Abstract

Infectious agents such as human immune deficiency virus-1 (HIV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) use host proteins to infect, replicate, and induce inflammation within the host. A critical component of these diseases is the axis between pannexin-1 channels, extracellular ATP, and purinergic receptors. Here, we describe the potential therapeutic role of Pannexin-1/purinergic approaches to prevent or reduce the devastating consequences of these pathogens.

Keywords: ATP; COVID-19; Connexin; Gap junctions; Hemichannels; NeuroHIV.

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Figure 1
Figure 1
Pannexin-1 functions during SARS-CoV-2 and HIV infection, releasing ATP and activating purinergic receptors. a. In healthy or non-pathological conditions, Pannexin-1 is in a closed state, and ATP and other inflammatory molecules are not released. b. During acute HIV infection, HIV binding to host cell receptors CD4 and CCR5/CXCR4 or HIV replication induces Pannexin-1 opening. c. During acute SARS-CoV-2 entry using host cell receptor ACE2 and replication, Pannexin-1 opens and releases ATP. d. During chronic HIV infection, Pannexin-1 is constitutively open, despite undetectable viral replication due to effective antiretroviral therapy.
See this image and copyright information in PMC

References

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      ** This paper studied the interaction between SARS-CoV-2 and Pannexin-1, which showed that SARS-CoV-2 infection or S protein induces Pannexin-1 opening within primary airway epithelial cells. Further, this opening of Pannexin-1 was important for replication because the inhibition of Pannexin-1 decreased SARS-CoV-2 replication, determined by FISH.

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