scholarly journals Development of human dendritic cells and their role in HIV infection: antiviral immunity versus HIV transmission

2013 ◽  
Vol 4 ◽  
Author(s):  
Yasuko Tsunetsugu-Yokota ◽  
Mahmod Muhsen
2005 ◽  
Vol 79 (18) ◽  
pp. 11598-11606 ◽  
Author(s):  
Scott E. VanCompernolle ◽  
R. Jeffery Taylor ◽  
Kyra Oswald-Richter ◽  
Jiyang Jiang ◽  
Bryan E. Youree ◽  
...  

ABSTRACT Topical antimicrobicides hold great promise in reducing human immunodeficiency virus (HIV) transmission. Amphibian skin provides a rich source of broad-spectrum antimicrobial peptides including some that have antiviral activity. We tested 14 peptides derived from diverse amphibian species for the capacity to inhibit HIV infection. Three peptides (caerin 1.1, caerin 1.9, and maculatin 1.1) completely inhibited HIV infection of T cells within minutes of exposure to virus at concentrations that were not toxic to target cells. These peptides also suppressed infection by murine leukemia virus but not by reovirus, a structurally unrelated nonenveloped virus. Preincubation with peptides prevented viral fusion to target cells and disrupted the HIV envelope. Remarkably, these amphibian peptides also were highly effective in inhibiting the transfer of HIV by dendritic cells (DCs) to T cells, even when DCs were transiently exposed to peptides 8 h after virus capture. These data suggest that amphibian-derived peptides can access DC-sequestered HIV and destroy the virus before it can be transferred to T cells. Thus, amphibian-derived antimicrobial peptides show promise as topical inhibitors of mucosal HIV transmission and provide novel tools to understand the complex biology of HIV capture by DCs.


2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.


2020 ◽  
Vol 6 (1) ◽  
pp. 5-11
Author(s):  
Bala Augustine Nalah ◽  
Azlinda Azman ◽  
Paramjit Singh Jamir Singh

Harmful cultural practices have psychosocial implications on stigmatization and vulnerability to HIV infection among HIV positive living in North Central Nigeria. To understand this, we conducted qualitative interviews with purposively selected 20 diagnosed HIV positive to explore how culture influences stigmatization and HIV transmission. Data was collected using audio-recorder, transcribed, and analyzed through thematic analysis using ATLAS.ti8 software to code and analyze interview transcripts. The coded data were presented using thematic network analysis to visualize the theme, sub-themes, and quotations in a model. The findings reveal that lack of education was a significant determinant for the continual practice of harmful cultural rites, thereby increasing the risk of HIV infection and stigmatization. Hence, six cultural facilitators have been identified to include female genital mutilation, lack of education, tribal marks and scarification, postpartum sexual abstinence during breastfeeding, sexual intercourse during menstruation, and gender inequality, polygamy, and inheritance law. We conclude that educational teachings and advocacy campaigns be organized in rural schools and public places on the implications of harmful cultural practice to health and psychological well-being. We recommend that the social workers and behavioral scientists should collaborate with other agencies to employ a behavioral-based intervention in eliminating cultural practices and HIV stigma.


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