Bleomycin treatment causes enhancement of virus replication in the lungs of SHIV-infected macaques

Dhillon, Navneet K.; Pinson, David M.; Dhillon, Sukhbir; Tawfik, Ossama; Danley, Marsha; Davis, Marilyn; Nemon, Olga; Mayo, Matthew S.; Kumar, Anil; Tsai, Yi Jou; Kumar, Amit; Buch, Shilpa

doi:10.1152/ajplung.00293.2006

Cited by 5 publications

(4 citation statements)

References 38 publications

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“…The most likely site of viral replication is the alveolar macrophage [31]. These findings are similar to the enhanced localized viral replication elicited by bleomycin in SIV-infected macaques [32]. These findings suggest that HIV+ alcoholic subjects have greater activation of viral replication, or alternatively, decreased capacity to control viral reactivation during opportunistic infections.…”

Section: Alcohol-mediated Immunomodulation and Its Impact On Hiv Diseasementioning

confidence: 71%

Biomedical Consequences of Alcohol Use Disorders in the HIV-Infected Host

Molina¹,

Bagby²,

Nelson

2014

CHR

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Alcohol abuse is the most common and costly form of drug abuse in the United States. It is well known that alcohol abuse contributes to risky behaviors associated with greater incidence of human immunodeficiency virus (HIV) infections. As HIV has become a more chronic disease since the introduction of antiretroviral therapy, it is expected that alcohol use disorders will have an adverse effect on the health of HIV-infected patients. The biomedical consequences of acute and chronic alcohol abuse are multisystemic. Based on what is currently known of the comorbid and pathophysiological conditions resulting from HIV infection in people with alcohol use disorders, chronic alcohol abuse appears to alter the virus infectivity, the immune response of the host, and the progression of disease and tissue injury, with specific impact on disease progression. The combined insult of alcohol abuse and HIV affects organ systems, including the central nervous system, the immune system, the liver, heart, and lungs, and the musculoskeletal system. Here we outline the major pathological consequences of alcohol abuse in the HIV-infected individual, emphasizing its impact on immunomodulation, erosion of lean body mass associated with AIDS wasting, and lipodystrophy. We conclude that interventions focused on reducing or avoiding alcohol abuse are likely to be important in decreasing morbidity and improving outcomes in people living with HIV/AIDS.

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Section: Alcohol-mediated Immunomodulation and Its Impact On Hiv Diseasementioning

confidence: 71%

Biomedical Consequences of Alcohol Use Disorders in the HIV-Infected Host

Molina¹,

Bagby²,

Nelson

2014

CHR

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“…Quantitative analysis of CXCL10 mRNA was done by quantitative Real-Time PCR using the SYBR Green detection method. RT2 PCR primer pair set for CXCL10 was obtained from SuperArray Bioscience and amplification of CXCL10 from first strand cDNA was performed as described earlier [35] using ABI Prism 7700 sequence detector. Data were normalized using Ct values for the house-keeping gene hypoxanthine-guanine phosphoribosyl transferase (HPRT) in each sample.…”

Section: Methodsmentioning

confidence: 99%

HIV-1 Tat Co-Operates with IFN-γ and TNF-α to Increase CXCL10 in Human Astrocytes

et al. 2009

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HIV-associated neurological disorders (HAND) are estimated to affect 60% of the HIV infected population. HIV-encephalitis (HIVE), the pathological correlate of the most severe form of HAND is often characterized by glial activation, cytokine/chemokine dysregulation, and neuronal damage and loss. However, the severity of HIVE correlates better with glial activation rather than viral load. One of the characteristic features of HIVE is the increased amount of the neurotoxic chemokine, CXCL10. This chemokine can be released from astroglia activated with the pro-inflammatory cytokines IFN-γ and TNF-α, in conjunction with HIV-1 Tat, all of which are elevated in HIVE. In an effort to understand the pathogenesis of HAND, this study was aimed at exploring the regulation of CXCL10 by cellular and viral factors during astrocyte activation. Specifically, the data herein demonstrate that the combined actions of HIV-1 Tat and the pro-inflammatory cytokines, IFN-γ and TNF-α, result in the induction of CXCL10 at both the RNA and protein level. Furthermore, CXCL10 induction was found to be regulated transcriptionally by the activation of the p38, Jnk, and Akt signaling pathways and their downstream transcription factors, NF-κB and STAT-1α. Since CXCL10 levels are linked to disease severity, understanding its regulation could aid in the development of therapeutic intervention strategies for HAND.

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“…Quantitative analysis of CXCL10 mRNA was done by quantitative real-time PCR using the SYBR Green detection method. RT2 PCR primer pair set for CXCL10 was obtained from SuperArray Bioscience and amplification of CXCL10 from first strand cDNA was performed as described earlier (Dhillon et al, 2007b).…”

Section: Cxcl10 Mrna Analysismentioning

confidence: 99%

Proinflammatory cytokines and HIV‐1 synergistically enhance CXCL10 expression in human astrocytes

Williams

Dhillon

Hegde

et al. 2008

Glia

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HIV encephalitis (HIVE), the pathologic correlate of HIV-associated dementia (HAD) is characterized by astrogliosis, cytokine/chemokine dysregulation and neuronal degeneration. Increasing evidence suggests that inflammation is actively involved in the pathogenesis of HAD. In fact, the severity of HAD/HIVE correlates more closely with the presence of activated glial cells than with the presence and amount of HIV-infected cells in the brain. Astrocytes, the most numerous cell type within the brain, provide an important reservoir for the generation of inflammatory mediators, including interferon-γ inducible peptide-10 (CXCL10), a neurotoxin and a chemoattractant, implicated in the pathophysiology of HAD. Additionally, the pro-inflammatory cytokines, IFN-γ and TNF-α, are also markedly increased in CNS tissues during HIV-1 infection. In the present study we hypothesized that the interplay of host cytokines and HIV-1 could lead to enhanced expression of the toxic chemokine, CXCL10. Our findings demonstrate a synergistic induction of CXCL10 mRNA and protein in human astrocytes exposed to HIV-1 and the proinflammatory cytokines. Signaling molecules, including JAK, STATs, MAPK (via activation of Erk1/2, AKT, and p38), and NF-κB were identified as instrumental in the synergistic induction of CXCL10. Understanding the mechanisms involved in HIV-1 and cytokine mediated up-regulation of CXCL10 could aid in the development of therapeutic modalities for HAD.

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Bleomycin treatment causes enhancement of virus replication in the lungs of SHIV-infected macaques

Cited by 5 publications

References 38 publications

Biomedical Consequences of Alcohol Use Disorders in the HIV-Infected Host

Biomedical Consequences of Alcohol Use Disorders in the HIV-Infected Host

HIV-1 Tat Co-Operates with IFN-γ and TNF-α to Increase CXCL10 in Human Astrocytes

Proinflammatory cytokines and HIV‐1 synergistically enhance CXCL10 expression in human astrocytes

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