作者: Shaily Malik , Eliseo A. Eugenin
DOI: 10.1016/J.NEULET.2017.09.005
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摘要: Abstract Neuron-Glia crosstalk is essential for efficient synaptic communication, cell growth and differentiation, neuronal activity, neurotransmitter recycling, brain immune response. The master regulators of this neuron-glia communication are connexin containing Gap Junctions (GJs) Hemichannels (HCs) as well pannexin HCs. However, the role these channels under pathological conditions, especially in infectious diseases still exploratory stages. Human Immunodeficiency Virus-1 (HIV) one such agent that takes advantage host intercellular systems, GJs HCs, to exacerbate viral pathogenesis spite antiretroviral therapy effectively controlling replication periphery. Although most agents lead total “shutdown” gap junctional parenchymal cells, HIV infection maintains “hijacks” HCs enable few infected cells spread toxic intracellular neighboring uninfected aggravating neuropathology even absence replication. In mini-review, we present a comprehensive overview augmenting neuropathogenesis.