@article{3d59b9a965814027878ea98d3e5d116e,
title = "The role of Pannexin-1 channels and extracellular ATP in the pathogenesis of the human immunodeficiency virus",
abstract = "Only recently, the role of large ionic channels such as Pannexin-1 channels and Connexin hemichannels has been implicated in several physiological and pathological conditions, including HIV infection and associated comorbidities. These channels are in a closed stage in healthy conditions, but in pathological conditions including HIV, Pannexin-1 channels and Connexin hemichannels become open. Our data demonstrate that acute and chronic HIV infection induces channel opening (Pannexin and Connexin channels), ATP release into the extracellular space, and subsequent activation of purinergic receptors in immune and non-immune cells. We demonstrated that Pannexin and Connexin channels contribute to HIV infection and replication, the long-term survival of viral reservoirs, and comorbidities such as NeuroHIV. Here, we discuss the available data to support the participation of these channels in the HIV life cycle and the potential therapeutic approach to prevent HIV-associated comorbidities.",
keywords = "Anti-retroviral, Cure, HIV-1, Latency, Reactivation, Reservoirs",
author = "Daniela D{\textquoteright}Amico and Silvana Valdebenito and Eugenin, {Eliseo A.}",
note = "Funding Information: We want to thank the National NeuroAIDS Tissue Consortium (NNTC) for providing all human samples. Also, we want to thank the NeuroBioBank for providing tissues of uninfected individuals and the Gulf Coast Regional Blood Center (Houston, TX). We thank NINDS and NIMH for allocating significant resources to explore whether Panx-1 channels could be a potential blocker of HIV-CNS disease. We are also grateful for the outstanding professionalism and expertise of Dr. Janice Clements{\textquoteright}s group at John Hopkins. We also want to thanks Heather Lander for her assistance in proofing and editing the manuscript. Figures were created with biorender.com. Funding Information: This work was funded by the National Institute of Mental Health grant, MH096625 and MH128082, the National Institute of Neurological Disorders and Stroke, NS105584, and the UTMB internal funding (to E.A.E.). The NNTC is made possible through funding from the NIMH and NINDS by the following grants: Manhattan HIV Brain Bank (MHBB): U24MH100931; Texas NeuroAIDS Research Center (TNRC): U24MH100930; National Neurological AIDS Bank (NNAB): U24MH100929; California NeuroAIDS Tissue Network (CNTN): U24MH100928; and Data Coordinating Center (DCC): U24MH100925. Publisher Copyright: {\textcopyright} 2021, The Author(s), under exclusive licence to Springer Nature B.V.",
year = "2021",
month = dec,
doi = "10.1007/s11302-021-09817-3",
language = "English (US)",
volume = "17",
pages = "563--576",
journal = "Purinergic Signalling",
issn = "1573-9538",
publisher = "Springer Netherlands",
number = "4",
}