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. Author manuscript; available in PMC: 2020 Mar 16.
Published in final edited form as: Neurosci Lett. 2017 Sep 5;695:86–90. doi: 10.1016/j.neulet.2017.09.005

Figure 1. Role of Panx1 uHCs in HIV neuropathogenesis.

Figure 1

(A) Binding of HIV to host CD4 receptor and CCR5/CXCR4 co-receptors in CD4+ T-lymphocytes and monocytes (1) leads to opening of Panx1 uHCs (2). As a result, ATP is released through the Panx1 uHCs (3), which then activates purinergic receptors (4). Downstream signaling through purinergic receptors leads to membrane depolarization and actin rearrangement which facilitates the entry of HIV virions into the cells (5). (B) At later stages, ATP released from HIV infected cells via Panx1 uHCs also leads to inflammation and contributes to BBB disruption. We propose that circulating ATP levels may be considered as a biomarker for cognitive disease in the HIV-infected population. Furthermore, as a consequence of Panx1 uHC opening, there is efflux of ART from the cells leading to a lower intracellular concentration of antiretrovirals which may be ineffective against the virus. Glutamate, which is also released from the Panx1 uHCs is a prime mediator of CNS compromise. Hence, it is imperative to decipher the role of Panx1 uHCs in HIV neuropathogenesis.