scholarly journals The Examination of Viral Characteristics of HIV-1 CRF07_BC and Its Potential Interaction with Extracellular Galectin-3

Pathogens ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 425
Author(s):  
Chih-Yen Lin ◽  
Wen-Hung Wang ◽  
Szu-Wei Huang ◽  
Chun-Sheng Yeh ◽  
Ruei-Yu Yuan ◽  
...  
Keyword(s):  
Drug Users ◽  
Potential Interaction ◽  
Enzyme Linked Immunosorbent Assay ◽  
Virus Infectivity ◽  
Promoting Effect ◽  
Galectin 3 ◽  
Emerging Virus ◽  
Hiv 1 ◽  
Envelope Gp120

HIV-1 CRF07_BC is a B’ and C subtype recombinant emerging virus and many of its viral characteristics remain unclear. Galectin-3 (Gal3) is a β-galactose binding lectin that has been reported as a pattern recognition receptor (PRR) and is known to mediate adhesion between cells and microbes. This study aims to examine the viral characteristics of HIV-1 CRF07_BC virus and the role of extracellular galectin-3 in HIV-1 CRF07_BC infection. A total of 28 HIV-1+ injecting drug users (IDUs) were recruited and 24 (85.7%) were identified as HIV-1 CRF07_BC. Results indicate that significant higher serum galectin-3 was measured in CRF07_BC infected patients and CRF07_BC infection triggered significant galectin-3 expression (p < 0.01). Viral characteristics demonstrate that CRF07_BC virions display a higher level of envelope gp120 spikes. The virus infectivity assay demonstrated that co-treatment with galectin-3 significantly promoted CRF07_BC attachment and internalization (p < 0.01). A co-immunoprecipitation assay showed that pulldown galectin-3 co-precipitated both CD4 and gp120 proteins. Results from an enzyme-linked immunosorbent assay (ELISA) indicate that the galectin-3 promoting effect occurs through enhancement of the interaction between gp120 and CD4. This study suggests that CRF07_BC was predominant in HIV-1+ IDUs and CRF07_BC utilized extracellular galectin-3 to enhance its infectivity via stabilization of the gp120-CD4 interaction.

scholarly journals Amino Acid Deletions in p6Gag Domain of HIV-1 CRF07_BC Ameliorate Galectin-3 Mediated Enhancement in Viral Budding

2020 ◽  
Vol 21 (8) ◽  
pp. 2910 ◽  
Author(s):  
Wen-Hung Wang ◽  
Chun-Sheng Yeh ◽  
Chih-Yen Lin ◽  
Ruei-Yu Yuan ◽  
Aspiro Nayim Urbina ◽  
...  
Keyword(s):  
Amino Acid ◽  
Drug Users ◽  
Potential Effect ◽  
Promoting Effect ◽  
Viral Budding ◽  
Subtype B ◽  
Infectious Clones ◽  
Galectin 3 ◽  
Hiv 1

HIV-1 CRF07_BC is a recombinant virus with amino acid (a.a.) deletions in p6Gag, which are overlapped with the Alix-binding domain. Galectin-3 (Gal3), a β-galactose binding lectin, has been reported to interact with Alix and regulate HIV-1 subtype B budding. This study aims to evaluate the role of Gal3 in HIV-1 CRF07_BC infection and the potential effect of a.a. deletions on Gal3-mediated regulation. A total of 38 HIV-1+ injecting drug users (IDUs) were enrolled in the study. Viral characterization and correlation of Gal3 were validated. CRF07_BC containing 7 a.a. deletions and wild-type in the p6Gag (CRF07_BC-7d and -wt) were isolated and infectious clones were generated. Viral growth kinetic and budding assays using Jurkat-CCR5/Jurkat-CCR5-Gal3 cells infected with CRF07_BC were performed. Results indicate that 69.4% (25/38) of the recruited patients were identified as CRF07_BC, and CRF07_BC-7d was predominant. Slow disease progression and significantly higher plasma Gal3 were noted in CRF07_BC patients (p < 0.01). Results revealed that CRF07_BC infection resulted in Gal3 expression, which was induced by Tat. Growth dynamic and budding assays indicated that Gal3 expression in Jurkat-CCR5 cells significantly enhanced CRF07_BC-wt replication and budding (p < 0.05), while the promoting effect was ameliorated in CRF07_BC-7d. Co-immunoprecipitation found that deletions in the p6Gag reduced Gal-3-mediated enhancement of the Alix–Gag interaction.

Role of Cations in the Interaction of Pradimicins with HIV-1 Envelope gp120

2013 ◽  
Vol 13 (16) ◽  
pp. 1907-1915 ◽  
Author(s):  
Bart Hoorelbeke ◽  
Youngju Kim ◽  
Toshikazu Oki ◽  
Yasuhiro Igarashi ◽  
Jan Balzarini
Keyword(s):  
Hiv 1 ◽  
Envelope Gp120

scholarly journals Role of Interferon-Gamma (Ifn-γ) in Immune Response Regulation in Hiv-1 and Hiv-1 + Mycobacterium Tuberculosis (Tb) Infected Patients / Interferona-gamma (Ifn-γ) Loma Imūnās Atbildes Regulēšanā Pacientiem Ar HIV-1 un HIV-1 + mycobacterium Tuberculosis

2016 ◽  
Vol 70 (4) ◽  
pp. 211-214
Author(s):  
Inga Januškevica ◽  
Baiba Rozentāle ◽  
Elvīra Hagina ◽  
Jeīena Eglīte ◽  
Tatjana Kolupajeva ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Viral Load ◽  
University Hospital ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Counts ◽  
Cd4 Cell Counts ◽  
Ifn Γ ◽  
Cd4 Cell ◽  
Hiv 1

Abstract The aim of this research was to investigate the role of IFN-γ in interaction between IL-10, IL-18, IL-1b, CD4 cell counts and HIV-1 RNA viral load in the development of HIV-1 in patients co-infected with Mycobacterium tuberculosis (TB). The study was conducted by Rīga East Clinical University Hospital with data from the HIV-1 register, in collaboration with the RSU Joint Laboratory of Clinical Immunology and Immunogenetics. 200 HIV-1 infected patients and 184 HIV-1 with TB co-infection patients divided in four groups were included in the study. IFN-γ, IL-10, IL-18, IL-1b levels were measured in serum with commercially enzyme-linked immunosorbent assay (ELISA Vector-Best Corporation, Novosibirsk, Russia). CD4 cell counts were measured by flow Partec IVD cytometry (USA). HIV-1 RNA quantification was performed using the COBAS AmpliPrep/COBAS Taqman HIV-1 Test (Germany). All groups were compared with each another. IFN-γ production was significantly lower, and IL-10 and CD4 cell counts were significantly higher, in HIV-1 patients without TB compared with the other groups. The group with HIV-1 and TB had significantly elevated IL-18 production. HIV patients with primary TB had significantly elevated IFN-γ production and HIV-1 RNA viral load and significantly lower IL-10 production.

scholarly journals The possible mediatory role of adipokines in the association between low carbohydrate diet and depressive symptoms among overweight and obese women

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257275
Author(s):  
Leila Setayesh ◽  
Reyhane Ebrahimi ◽  
Sara Pooyan ◽  
Habib Yarizadeh ◽  
Elaheh Rashidbeygi ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Transforming Growth Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
Significant Difference ◽  
Low Carbohydrate ◽  
Galectin 3 ◽  
Pai 1

Background Previous studies showed the possible association between obesity, dietary pattern, and depressive symptoms. Due to the lack of enough data to confirm the association of obesity and depression in the Middle East, here, we aimed to explore the possible mediatory role of adipokines Galectin-3, transforming growth factor-beta (TGF-β), and endothelial plasminogen activator inhibitor (PAI-1) in the association between low carbohydrate diet (LCD) and depressive symptoms. Methods A total of 256 women aged 17–56 years old were grouped based on their LCD score. Depression anxiety stress scales-21 (DASS-21) self-administered questionnaire was used to evaluate the three negative emotional states of stress, depressive symptoms, and anxiety. Body composition and dietary intake were assessed. Enzyme-linked immunosorbent assay (ELISA) was used to measure the serum levels of Galectin-3, TGF-β, and PAI-1. Results No significant difference was observed regarding Galectin-3, TGF-β, and PAI-1 levels between the groups with dissimilar adherence to LCD or the groups with different levels of depressive symptoms (P>0.05). However, there was a negative association between LCD score as a covariant and depressive symptoms as an independent variable (P = 0.02) and remarkably, a regression model linear analysis using Galectin-3, TGF-β, and PAI-1 as confounding variables indicated the mediatory role of these adipokines in this association (P>0.05). In other words, adipokines eliminated the significance of the relationship between adherence to LCD and depressive symptoms. Conclusion It seems that higher adherence to LCD is probably associated with a lower prevalence of depressive symptoms in obese adults through the mediatory role of adipokines.

scholarly journals Production of Interferons and β-Chemokines by Placental Trophoblasts of HIV-1-Infected Women

2001 ◽  
Vol 9 (2) ◽  
pp. 95-104 ◽  
Author(s):  
Bang-Ning Lee ◽  
Hunter Hammill ◽  
Edwina J. Popek ◽  
Stanley Cron ◽  
Claudia Kozinetz ◽  
...  
Keyword(s):  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Trophoblastic Cells ◽  
Inflammatory Protein ◽  
Β Protein ◽  
Immunodeficiency Virus ◽  
Vertical Transmission Of Hiv ◽  
And Control ◽  
Hiv 1

Objective:The mechanism whereby the placental cells of a human immunodeficiency virus (HIV)-1-infected mother protect the fetus from HIV-1 infection is unclear. Interferons (IFNs) inhibit the replication of viruses by acting at various stages of the life cycle and may play a role in protecting against vertical transmission of HIV-1. In addition the β-chemokines RANTES (regulated on activation T cell expressed and secreted), macrophage inflammatory protein-1-α (MIP-1α), and MIP-1β can block HIV-1 entry into cells by preventing the binding of the macrophage-trophic HIV-1 strains to the coreceptorCCR5. In this study the production of IFNs and β-chemokines by placental trophoblasts of HIV-1-infected women who were HIV-1 non-transmitters was examined.Methods:Placental trophoblastic cells were isolated from 29 HIV-1-infected and 10 control subjects. Supernatants of trophoblast cultures were tested for the production of IFNs and β-chemokines by enzyme linked immunosorbent assay (ELISA). Additionally, HIV-1-gag and IFN-β transcripts were determined by a semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) assay.Results:All placental trophoblasts of HIV-1-infected women contained HIV-1-gag transcripts. There were no statistical differences in the median constitutive levels of IFN-α and IFN-γ produced by trophoblasts of HIV-1- infected and control subjects. In contrast, trophoblasts of HIV-1-infected women constitutively produced significantly higher levels of IFN-β protein than trophoblasts of control subjects. Furthermore, the median levels of β-chemokines produced by trophoblasts of HIV-infected and control women were similar.Conclusions:Since there was no correlation between the placental HIV load and the production of interferons or β-chemokines, the role of trophoblast-derived IFNs and β-chemokines in protecting the fetus from infection with HIV-1 is not clear.

scholarly journals Myocardial Ischemia Reperfusion Injury: Apoptotic, Inflammatory and Oxidative Stress Role of Galectin-3

2018 ◽  
Vol 50 (3) ◽  
pp. 1123-1139 ◽  
Author(s):  
Suhail Al-Salam ◽  
Satwat Hashmi
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Wild Type ◽  
Galectin 3 ◽  
And Oxidative Stress

Background/Aims: Myocardial reperfusion has the potential to salvage the ischemic myocardium after a period of coronary occlusion. Reperfusion, however, can cause a wide spectrum of deleterious effects. Galectin-3 (GAL-3), a beta galactoside binding lectin, is closely associated with myocardial infarction (MI), myocardial fibrosis and heart failure. In our study, we investigated its role in ischemia-reperfusion injuries (IR) as this phenomenon is extremely relevant to the early intervention after acute MI. Methods: C57B6/J wild type (WT) mice and GAL-3 knockout (KO) mice were used for murine model of IR injury in the heart where a period of 30 minutes ischemia was followed by 24 hours of reperfusion. Heart samples were processed for immunohistochemical and immunofluorescent labeling, morphometric analysis, western blot and enzyme-linked immunosorbent assay to identify the apoptotic, inflammatory and oxidative stress role of GAL-3. Results: Our results show that there was a significant increase in GAL-3 levels in the heart which shows GAL-3 is playing a role in the ischemia reperfusion injury. Troponin I was also significantly higher in GAL-3-KO group than wild type. Our study shows that GAL-3 is associated with an increase in the antioxidant activity in the IR injured myocardium. Antioxidant enzymes superoxide dismutase, glutathione and catalase were found to be significantly raised in the GAL-3 wild type IR as compared to the GAL-3 KO IR group. A significant increase in apoptotic activity is seen in GAL-3 KO IR group as compared with GAL-3 wild IR group. Conclusion: Our study shows that GAL-3 can affect the redox pathways, controlling cell survival and death, and plays a protective role on the myocardium following IR injury.

scholarly journals Interactive Effects of Morphine on HIV Infection: Role in HIV-Associated Neurocognitive Disorder

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Pichili Vijaya Bhaskar Reddy ◽  
Sudheesh Pilakka-Kanthikeel ◽  
Shailendra K. Saxena ◽  
Zainulabedin Saiyed ◽  
Madhavan P. N. Nair
Keyword(s):  
Drug Abuse ◽  
Hiv Infection ◽  
Injection Drug Users ◽  
Drug Users ◽  
Public Health Problem ◽  
Mapk Signaling ◽  
Interactive Effects ◽  
Hiv 1 ◽  
Neural Dysfunction

HIV epidemic continues to be a severe public health problem and concern within USA and across the globe with about 33 million people infected with HIV. The frequency of drug abuse among HIV infected patients is rapidly increasing and is another major issue since injection drug users are at a greater risk of developing HIV associated neurocognitive dysfunctions compared to non-drug users infected with HIV. Brain is a major target for many of the recreational drugs and HIV. Evidences suggest that opiate drug abuse is a risk factor in HIV infection, neural dysfunction and progression to AIDS. The information available on the role of morphine as a cofactor in the neuropathogenesis of HIV is scanty. This review summarizes the results that help in understanding the role of morphine use in HIV infection and neural dysfunction. Studies show that morphine enhances HIV-1 infection by suppressing IL-8, downregulating chemokines with reciprocal upregulation of HIV coreceptors. Morphine also activates MAPK signaling and downregulates cAMP response element-binding protein (CREB). Better understanding on the role of morphine in HIV infection and mechanisms through which morphine mediates its effects may help in devising novel therapeutic strategies against HIV-1 infection in opiate using HIV-infected population.

scholarly journals HIV-1 outbreak among injecting drug users in Greece, 2011: a preliminary report

2011 ◽  
Vol 16 (36) ◽  
Author(s):  
D Paraskevis ◽  
G Nikolopoulos ◽  
C Tsiara ◽  
D Paraskeva ◽  
A Antoniadou ◽  
...  
Keyword(s):  
Molecular Epidemiology ◽  
Preliminary Report ◽  
Drug Users ◽  
Potential Role ◽  
Injecting Drug Users ◽  
Newly Diagnosed ◽  
Hiv 1

A significant increase (more than 10-fold) in the number of newly diagnosed HIV-1 infections among injecting drug users (IDUs) was observed in Greece during the first seven months of 2011. Molecular epidemiology results revealed that a large proportion (96%) of HIV-1 sequences from IDUs sampled in 2011 fall within phylogenetic clusters suggesting high levels of transmission networking. Cases originated from diverse places outside Greece supporting the potential role of immigrant IDUs in the initiation of this outbreak.

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