Enhancement of human immunodeficiency virus type 1 infection by cationic liposomes: the role of CD4, serum and liposome-cell interactions

Konopka, Krystyna; Stamatatos, Leonidas; Larsen, Charles E.; Davis, Brian R.; Düzgüneş, Nejat

doi:10.1099/0022-1317-72-11-2685

Cited by 22 publications

(12 citation statements)

References 61 publications

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“…To this end, virus strains requiring addition of DEAE-dextran for cell-free but not for cell-to-cell infection were used in nonlymphoid (HeLa TZM-bl) cells. DEAE-dextran is a nonspecific polycation commonly used to enhance the association of viruses, including HIV, with target cells via relatively nonspecific charge interactions (2,23) and may severely affect gp120 interactions with the cell surface such as to interfere with the inhibitory effect of gp120-targeting neutralizing antibodies. The results in reference 1 are in contrast to previous observations that virus attachment inhibitors, including CD4-IgG2 (7) and others (24) effectively block cell-to-cell transmission with equal potency to cell-free transmission.…”

Section: Discussionmentioning

confidence: 99%

Antiretroviral Agents Effectively Block HIV Replication after Cell-to-Cell Transfer

Permanyer

Ballana

Ruiz

et al. 2012

J Virol

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Cell-to-cell transmission of HIV has been proposed as a mechanism contributing to virus escape to the action of antiretrovirals and a mode of HIV persistence during antiretroviral therapy. Here, cocultures of infected HIV-1 cells with primary CD4+T cells or lymphoid cells were used to evaluate virus transmission and the effect of known antiretrovirals. Transfer of HIV antigen from infected to uninfected cells was resistant to the reverse transcriptase inhibitors (RTIs) zidovudine (AZT) and tenofovir, but was blocked by the attachment inhibitor IgGb12. However, quantitative measurement of viral DNA production demonstrated that all anti-HIV agents blocked virus replication with similar potency to cell-free virus infections. Cell-free and cell-associated infections were equally sensitive to inhibition of viral replication when HIV-1 long terminal repeat (LTR)-driven green fluorescent protein (GFP) expression in target cells was measured. However, detection of GFP by flow cytometry may incorrectly estimate the efficacy of antiretrovirals in cell-associated virus transmission, due to replication-independent Tat-mediated LTR transactivation as a consequence of cell-to-cell events that did not occur in short-term (48-h) cell-free virus infections. In conclusion, common markers of virus replication may not accurately correlate and measure infectivity or drug efficacy in cell-to-cell virus transmission. When accurately quantified, active drugs blocked proviral DNA and virus replication in cell-to-cell transmission, recapitulating the efficacy of antiretrovirals in cell-free virus infections andin vivo.

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Section: Discussionmentioning

confidence: 99%

Antiretroviral Agents Effectively Block HIV Replication after Cell-to-Cell Transfer

Permanyer

Ballana

Ruiz

et al. 2012

J Virol

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“…After 12 h, 50 l of serially diluted viral stocks (a serial 4-fold dilution) was added to appropriate wells in complete DMEM supplemented with 25 g/ml of DEAE-dextran (catalog no. D9885; Sigma, St. Louis, MO) (27). Six hours postinfection, medium in the wells was replaced with 100 l of complete DMEM.…”

Section: Methodsmentioning

confidence: 99%

Functional Incompatibility between the Generic NF-κB Motif and a Subtype-Specific Sp1III Element Drives the Formation of the HIV-1 Subtype C Viral Promoter

Verma

Rajagopalan

Lotke

et al. 2016

J Virol

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Of the various genetic subtypes of human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2) and simian immunodeficiency virus (SIV), only in subtype C of HIV-1 is a genetically variant NF-B binding site found at the core of the viral promoter in association with a subtype-specific Sp1III motif. How the subtype-associated variations in the core transcription factor binding sites (TFBS) influence gene expression from the viral promoter has not been examined previously. Using panels of infectious viral molecular clones, we demonstrate that subtype-specific NF-B and Sp1III motifs have evolved for optimal gene expression, and neither of the motifs can be replaced by a corresponding TFBS variant. The variant NF-B motif binds NF-B with an affinity 2-fold higher than that of the generic NF-B site. Importantly, in the context of an infectious virus, the subtype-specific Based on genetic variation, human immunodeficiency virus type 1 (HIV-1) is classified into four distinct groups (M, N, O, and P), and group M is subclassified into nine molecular subtypes (A, B, C, D, F, G, H, J, and K) and numerous circulating recombinant forms, including A/E (1). The global distribution of HIV-1 subtypes is uneven, with C, A, and B being the most widespread subtypes. Subtype C is predominant in southern and eastern African countries, India, and Nepal and in recombinant forms in China, and it is currently emerging in southern Brazil. Subtype C is responsible for approximately half of the global HIV-1 infections and more than 95% of the infections in India (2). The factors that contribute to the widespread expansion of subtype C are not well understood. Diverse viral subtypes differ from one another up to 30 to 35% in certain gene segments, such as the envelope (3). A genetic variation to this large an extent is expected to have a significant impact on the biological properties of the subtypes influencing their relative fitness properties. Subtype-specific genetic variations in elements such as the viral promoter (enhancer and other regulatory elements), regulatory proteins, and structural proteins may underlie the biological differences, although drawing such a correlation between these factors may not always be possible.The individual components of the viral promoter, including the modulator region, the enhancer, and the core promoter, are characterized by several subtype-specific molecular variations. Such differences have been mapped to many transcription factor binding sites (TFBS), including USF, c-Myb, NF-AT, Ap-1, NF-B, and Sp1, and regulatory elements such as the TATA box and

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“…Virus (multiplicity of infection range, 0.009 -0.65) was added in medium containing 40 g/ml DEAE-dextran to give a final volume of 200 l per well. DEAE-dextran enhances the in vitro infectivity of some HIV-1 strains (28), and its use in this system was suggested by Transzyme. After incubating the plates for 48 h at 37°C in room air containing 5% CO 2 , the cells were lysed using the manufacturer's lysis protocol and luciferase activity was measured with the Steady-Glo Luciferase Assay System (Promega, Madison, WI) using a Tecan luminometer running Magellan software (Tecan, Research Triangle Park, NC).…”

Section: Indicator Cellsmentioning

confidence: 99%

Activity of α- and θ-Defensins against Primary Isolates of HIV-1

Wang

Owen

Rudolph

et al. 2004

The Journal of Immunology

181

149

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θ-Defensins are lectin-like, cyclic octadecapeptides found in the leukocytes of nonhuman primates. They are also homologues of the more familiar α-defensins expressed by humans and certain other mammals. This study compares the ability of six θ-defensins (hominid retrocyclins 1–3 and rhesus θ-defensins 1–3) and four human α-defensins (human neutrophil peptides (HNPs) 1–4) to bind gp120 and CD4. In addition, we compared the ability of these θ-defensins and HNP-1 to protect J53-BL cells (an indicator cell line) from primary HIV-1 isolates that varied in subtype and coreceptor usage. The most potent θ-defensin, retrocyclin-2, bound with exceptionally high affinity to gp120 (KD, 9.4 nM) and CD4 (KD, 6.87 nM), and its effectiveness against subtype B isolates (IC50, 1.05 ± 0.28 μg/ml; 520 ± 139 nM) was approximately twice as great as that of HNP-1 on a molar basis. We also show, for the first time, that human α-defensins, HNPs 1–3, are lectins that bind with relatively high affinity to gp120 (KD range, 15.8–52.8 nM) and CD4 (KD range, 8.0–34.9 nM). Proteins found in human and FBS bound exogenous HNP-2 and retrocyclin-1, and competed with their ability to bind gp120. However, even the low concentrations of α-defensins found in normal human serum suffice to bind over half of the gp120 spikes on HIV-1 and a higher percentage of cell surface CD4 molecules. Although this report principally concerns the relationship between carbohydrate-binding and the antiviral properties of α- and θ-defensins, the lectin-like behavior of defensins may contribute to many other activities of these multifunctional peptides.

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Enhancement of human immunodeficiency virus type 1 infection by cationic liposomes: the role of CD4, serum and liposome-cell interactions

Cited by 22 publications

References 61 publications

Antiretroviral Agents Effectively Block HIV Replication after Cell-to-Cell Transfer

Antiretroviral Agents Effectively Block HIV Replication after Cell-to-Cell Transfer

Functional Incompatibility between the Generic NF-κB Motif and a Subtype-Specific Sp1III Element Drives the Formation of the HIV-1 Subtype C Viral Promoter

Activity of α- and θ-Defensins against Primary Isolates of HIV-1

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