Role of Connexin and Pannexin containing channels in HIV infection and NeuroAIDS

Shaily Malik, Eliseo Eugenin

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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

Original languageEnglish (US)
JournalNeuroscience Letters
DOIs
StateAccepted/In press - Jan 1 2017
Externally publishedYes

Fingerprint

Connexins
Gap Junctions
Virus Diseases
HIV-1
Neuroglia
Neurons
Poisons
Brain
Recycling
Communicable Diseases
Neurotransmitter Agents
Cell Differentiation
Growth
Therapeutics

Keywords

  • AIDS
  • Gap junction
  • Hemichannel
  • HIV
  • Reservoirs

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Role of Connexin and Pannexin containing channels in HIV infection and NeuroAIDS. / Malik, Shaily; Eugenin, Eliseo.

In: Neuroscience Letters, 01.01.2017.

Research output: Contribution to journalArticle

@article{b072efc6df184bc99247fdd87abcc1f1,
title = "Role of Connexin and Pannexin containing channels in HIV infection and NeuroAIDS",
abstract = "Neuron-Glia crosstalk is essential for efficient synaptic communication, cell growth and differentiation, neuronal activity, neurotransmitter recycling, and brain immune response. The master regulators of this neuron-glia communication are connexin containing Gap Junctions (GJs) and Hemichannels (HCs) as well as pannexin HCs. However, the role of these channels under pathological conditions, especially in infectious diseases is still in exploratory stages. Human Immunodeficiency Virus-1 (HIV) is one such infectious agent that takes advantage of the host intercellular communication systems, GJs and HCs, to exacerbate viral pathogenesis in the brain in spite of the antiretroviral therapy effectively controlling viral replication in the periphery. Although most infectious agents lead to total {"}shutdown{"} of gap junctional communication in parenchymal cells, HIV infection maintains and {"}hijacks{"} GJs and HCs to enable few infected cells to spread toxic intracellular agents to neighboring uninfected cells aggravating viral neuropathology even in the absence of viral replication. In this mini-review, we present a comprehensive overview of the role of GJs and HCs in augmenting HIV neuropathogenesis.",
keywords = "AIDS, Gap junction, Hemichannel, HIV, Reservoirs",
author = "Shaily Malik and Eliseo Eugenin",
year = "2017",
month = "1",
day = "1",
doi = "10.1016/j.neulet.2017.09.005",
language = "English (US)",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",

}

TY - JOUR

T1 - Role of Connexin and Pannexin containing channels in HIV infection and NeuroAIDS

AU - Malik, Shaily

AU - Eugenin, Eliseo

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Neuron-Glia crosstalk is essential for efficient synaptic communication, cell growth and differentiation, neuronal activity, neurotransmitter recycling, and brain immune response. The master regulators of this neuron-glia communication are connexin containing Gap Junctions (GJs) and Hemichannels (HCs) as well as pannexin HCs. However, the role of these channels under pathological conditions, especially in infectious diseases is still in exploratory stages. Human Immunodeficiency Virus-1 (HIV) is one such infectious agent that takes advantage of the host intercellular communication systems, GJs and HCs, to exacerbate viral pathogenesis in the brain in spite of the antiretroviral therapy effectively controlling viral replication in the periphery. Although most infectious agents lead to total "shutdown" of gap junctional communication in parenchymal cells, HIV infection maintains and "hijacks" GJs and HCs to enable few infected cells to spread toxic intracellular agents to neighboring uninfected cells aggravating viral neuropathology even in the absence of viral replication. In this mini-review, we present a comprehensive overview of the role of GJs and HCs in augmenting HIV neuropathogenesis.

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

KW - AIDS

KW - Gap junction

KW - Hemichannel

KW - HIV

KW - Reservoirs

UR - http://www.scopus.com/inward/record.url?scp=85028996351&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85028996351&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2017.09.005

DO - 10.1016/j.neulet.2017.09.005

M3 - Article

C2 - 28886986

AN - SCOPUS:85028996351

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

ER -