Inhibition of Morphine-Potentiated HIV-1 Replication in Peripheral Blood Mononuclear Cells With the Nuclease-Resistant 2-5A Agonist Analog, 2-5AN6B

Homan, Joseph W.; Steele, Amber D.; Martinand‐Mari, Camille; Rogers, Thomas J.; Henderson, Earl E.; Charubala, Ramamurthy; Pfleiderer, Wolfgang; Reichenbach, Nancy L.; Suhadolnik, Robert J.

doi:10.1097/00042560-200205010-00002

Cited by 23 publications

(28 citation statements)

References 52 publications

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“…Morphine suppressed IFN-␣ expression in PBMCs and lymphocytes. 2,45 Morphine suppresses Sendai virus-induced IFN-␣ production by PBMCs. 2 Morphine also inhibits the release of IFN-␣ by Sindbis virus-infected monocytes.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Anti-HIV MicroRNA Expression

Wang

Zhou

et al. 2011

The American Journal of Pathology

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Several micro RNAs (miRNAs) have the ability to inhibit HIV replication in target cells. Thus, we investigated the impact of opioids (morphine and heroin), widely abused drugs among people infected with HIV, on the expression of cellular anti-HIV miRNAs in monocytes. We found that morphine-treated monocytes expressed lower levels of cellular anti-HIV miRNAs than untreated cells. In addition, morphine treatment of monocytes compromised type I interferon (IFN)-induced anti-HIV miRNA expression. These findings paralleled the observation that morphine treatment of monocytes enhanced HIV replication. These morphine-mediated actions on the anti-HIV miRNAs and HIV could be antagonized by the opioid receptor antagonists (naltrexone or Cys2, Tyr3, Arg5, Pen7-amide). Furthermore, the in vitro impact of morphine on miRNA expression was confirmed by the in vivo observation that heroin-dependent subjects had significantly lower levels of anti-HIV miRNAs (miRNA-28, 125b, 150, and 382) in peripheral blood mononuclear cells than the healthy subjects. These in vitro and in vivo findings indicate that opioid use impairs intracellular innate anti-HIV mechanism(s) in monocytes, contributing to cell susceptibility to HIV infection. (Am J

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Section: Discussionmentioning

confidence: 99%

Inhibition of Anti-HIV MicroRNA Expression

Wang

Zhou

et al. 2011

The American Journal of Pathology

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“…PBMCs treated with DAMGO ([Dala 2 , N-Me-Phe 4 , Gly-ol 5 ] enkephalin), a ligand of MOR, produce CCL2, CCL5, and CXCL10 proinflammatory chemokines (Wetzel et al 2000). When treated with 2-5A N6B , an inhibitor of morphine-potentiated HIV replication, PBMCs showed elevated expression of CCL2 and CCL5 (Homan et al 2002). (For a more comprehensive review on opioid receptors and inflammation, see Rogers and Peterson 2003).…”

Section: Morphinementioning

confidence: 99%

Neuroimmunity and the Blood–Brain Barrier: Molecular Regulation of Leukocyte Transmigration and Viral Entry into the Nervous System with a Focus on NeuroAIDS

Buckner

Luers

Calderon

et al. 2006

Jrnl NeuroImmune Pharm

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HIV infection of the central nervous system (CNS) can result in neurologic dysfunction with devastating consequences in a significant number of individuals with AIDS. Two main CNS complications in individuals with HIV are encephalitis and dementia, which are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, bloodbrain barrier (BBB) disruption, and eventual damage and/or loss of neurons. One of the major mediators of NeuroAIDS is the transmigration of HIV-infected leukocytes across the BBB into the CNS. This review summarizes new key findings that support a critical role of the BBB in regulating leukocyte transmigration. In addition, we discuss studies on communication among cells of the immune system, BBB, and the CNS parenchyma, and suggest how these interactions contribute to the pathogenesis of Neuro-AIDS. We also describe some of the animal models that have been used to study and characterize important mechanisms that have been proposed to be involved in HIV-induced CNS dysfunction. Finally, we review the pharmacologic interventions

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“…Induction of IFN expression in response to viral infection regulates post-translational modification of transcription factors, including IFN regulatory factor (IRF)-3 and IRF-7 [173][174][175], which play a key role in initiating the cellular antiviral response. In addition, IRF-5 has a key role in IRF-3-and IRF-7-mediated IFN activation pathway [172].…”

Section: Intrahepatic Ifns and Hcvmentioning

confidence: 99%

Drug abuse, innate immunity and hepatitis C virus

Zhang

2006

Reviews in Medical Virology

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Since its discovery in 1989, hepatitis C virus (HCV) has become a major public health problem. HCV chronically infects an estimated 170 million people worldwide. The seroprevalence of anti-HCV antibody in the United States has been estimated at 1.8%, which corresponds to approximately 4 million people. HCV is the most common chronic blood borne infection in the United States, and the leading cause of liver transplantation in developed countries. Injection drug use is the dominant mode of HCV transmission and accounts for up to 90% of current infections. Opiates and other drug abuse, such as alcohol, have been implicated as cofactors in the pathogenesis of HCV disease. Injection drug use has been the most common risk factor identified in alcoholics with HCV infection. Both opiates and alcohol contribute significantly to morbidity and mortality from HCV disease. These drugs most likely act synergistically to promote the development and progression of HCV disease. However, there is limited information available concerning the interaction of the drug abuse with the host cell innate immunity against HCV infection, which is a major barrier to fundamental understanding of the immunopathogenesis of HCV disease. Therefore, defining the role of the drug abuse in the development of chronic HCV infection is of crucial importance and should provide practical guidance toward the reduction of risk factors that interfere with therapeutic approaches for HCV infection and disease. This review paper focuses on the interplay between drug abuse (opiates and alcohol), innate immunity and HCV in the context of the development of HCV disease.

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Inhibition of Morphine-Potentiated HIV-1 Replication in Peripheral Blood Mononuclear Cells With the Nuclease-Resistant 2-5A Agonist Analog, 2-5AN6B

Cited by 23 publications

References 52 publications

Inhibition of Anti-HIV MicroRNA Expression

Inhibition of Anti-HIV MicroRNA Expression

Neuroimmunity and the Blood–Brain Barrier: Molecular Regulation of Leukocyte Transmigration and Viral Entry into the Nervous System with a Focus on NeuroAIDS

Drug abuse, innate immunity and hepatitis C virus

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