Professional Representations of Collaboration in the Response to Intimate Partner Violence.

Purpose: Due to the complexity of intimate partner violence (IPV) and the many actors involved in its social and legal responses, there is a broad consensus that collaboration is essential if IPV is to be overcome. Few studies, however, have provided details as to how these collaborations occur. Rather, research on collaboration in IPV has typically focused on a series of factors facilitating and hindering it. However, these factors are rarely articulated in a systemic, comprehensive, and integrated way. Method: To gain a better understanding of the socio-judicial response to IPV, we conducted a case study in an administrative region in the Province of Quebec, Canada. We conducted individual interviews with 37 key informants who work with people experiencing IPV. The data were subjected to deductive thematic coding as well as to intra- and inter-role matrices that cross-referenced the themes. Result: According to our findings, interagency referrals and information sharing were the most common collaborative practices reported by participants which leading us to characterize the region studied in this article as poorly integrated. Factors facilitating and hindering collaboration are discussed in relation to previous studies. Conclusion: Recommendations for cross-sectoral training, organizational policy development, and opportunities to leverage the expertise of specialized actors in IPV response systems are made.

The perceptions of judicial and psychosocial interveners of the consequences of dropped charges in domestic violence cases.

Many domestic violence cases do not go to trial because the victim refuses to testify. This article presents a qualitative study exploring the dismissal of criminal charges in domestic violence cases. The 22 judicial and psychosocial professionals interviewed in Montreal, Canada, discussed various consequences of the legal decision to dismiss the charges on victims, perpetrators, justice system professionals, and society as a whole. Respondents clearly did not view the withdrawal of charges as a failure of the criminalization of domestic violence.

Cholera toxin inhibits HIV-1 replication in human colorectal epithelial HT-29 cells through adenylate cyclase activation.

Mixed feeding, combining breast milk and nonhuman milk and/or solid food, is a common practice in developing countries that increases the risk of vertical HIV-1 transmission. It also enhances the risk of infection by waterborne microorganisms such as Vibrio cholerae, a diarrhoea-causing pathogen that frequently infects children below 18 months of age. Although both HIV-1 and V. cholerae affect young children and target intestinal epithelial cells, no information is currently available on possible interactions between these two pathogens. In this study, we show for the first time that cholera toxin (CTx), at a concentration as low as 100 pg/ml, inhibits HIV-1 infection of HT-29, a human colorectal epithelial cell line. The CTx-mediated inhibitory effect does not result from a down-regulation of receptor/co-receptor expression or a modulation of viral transcription. Nevertheless, additional experiments indicate that a yet to be identified early step in the virus life cycle is targeted by CTx since the enterotoxin similarly reduces infection of HT-29 cells with AMLV-I, HTLV-I and HIV-1 pseudotyped viruses while exerting no effect on infection with VSV-G pseudotypes. Furthermore, our results indicate that the CTx-dependent suppression is not due to the cholera toxin subunit B but linked instead to the action of cholera toxin subunit A (CTA). Altogether our data indicate that the CTA subunit of CTx is negatively affecting an early event in HIV-1 replication in human colon cancer HT-29 cells.

Interleukin-4 inhibits an early phase in the HIV-1 life cycle in the human colorectal cell line HT-29.

Intestinal epithelial cells are continuously in contact with the gut-associated lymphoid tissues (GALT). Gastrointestinal infection by viruses, bacteria and parasites or the presence of an inflammatory bowel disease may influence the GALT cytokine network. However, the effect of the different cytokines on susceptibility of human intestinal epithelial cells to HIV-1 infection remains undefined. We demonstrate here that IL-4 inhibits infection with reporter HIV-1 viruses pseudotyped with NDK-Env without affecting integrated proviral DNA. Furthermore, IL-4 also inhibits, in a dose-dependent manner, infection of HT-29 cells with HIV-1-based AMLV, HTLV-I and VSV-G pseudotypes. A fusion assay showed that this event is not affected by IL-4, thus suggesting that a post-fusion step is affected. A reduction in the completion of DNA retrotranscription indicates that IL-4 may affect this step, or any prior event. Altogether our data indicate that IL-4 is negatively affecting an early post-fusion step in the HIV-1 replication cycle in HT-29 cells.

Ingestion of the malaria pigment hemozoin renders human macrophages less permissive to HIV-1 infection.

Few studies have investigated the pathophysiologic mechanisms responsible for what seems to be a possible interaction between Plasmodium falciparum, the causative agent of malaria, and HIV-1 in dually infected patients. It has been shown that Plasmodium parasites detoxify heme molecules into a pigment called hemozoin (HZ), which can significantly modulate the immune system. The primary objective of this study was to determine whether exposure of human primary monocyte-derived macrophages (MDMs) to the malaria pigment influences the process of HIV-1 infection. We report here that HIV-1 replication is significantly diminished in HZ-loaded MDMs. The HZ-mediated reduction in virus replication is due to a block at a step in the virus life cycle occurring between the completion of full-length reverse transcripts and integration of viral DNA within the host chromosome. Understanding the pathological mechanisms involved in P. falciparum and HIV-1 co-infection is of high importance because of possible therapeutic ramifications.

Induction of galectin-1 expression by HTLV-I Tax and its impact on HTLV-I infectivity.

BACKGROUND: Cell-free Human T-cell Leukemia Virus type I (HTLV-I) virions are poorly infectious and cell-to-cell contact is often required to achieve infection. Other factors might thus importantly contribute in increasing infection by HTLV-I. Galectin-1 is a galactoside-binding lectin which is secreted by activated T lymphocytes. Several functions have been attributed to this protein including its capacity to increase cell-to-cell adhesion. Based on previous studies, we postulated that this protein could also accentuate HTLV-I infection. RESULTS: Herein, we demonstrate that galectin-1 expression and release are higher in HTLV-I-infected T cells in comparison to uninfected T cells. Furthermore, galectin-1 expression was activated in various cell lines expressing the wild type viral Tax protein while this induction was minimal upon expression of NF-kappaB activation-defective TaxM22. Cotransfection of these Tax expression vectors with galectin-1 promoter-driven luciferase constructs confirmed that Tax upregulated galectin-1 promoter activity. However, a NF-kappaB-independent mechanism was strongly favoured in this induction of galectin-1 expression as no activation of the promoter was apparent in Jurkat cells treated with known NF-kappaB activators. Using HTLV-I envelope pseudotyped HIV-1 virions, galectin-1 was shown to increase infectivity. In addition, a co-culture assay with HTLV-I-infected cells also indicated an increase in cell fusion upon addition of galectin-1. This effect was not mediated by factors present in the supernatant of the HTLV-I-infected cells. CONCLUSION: These data suggest that HTLV-I Tax increases galectin-1 expression and that this modulation could play an important role in HTLV-I infection by stabilizing both cell-to-cell and virus-cell interactions.

HIV-1 infection of trophoblasts is independent of gp120/CD4 Interactions but relies on heparan sulfate proteoglycans.

Mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1) is the leading cause of HIV infection in infants. Direct infection of trophoblasts--cells forming the placental barrier--may cause this transmission. Entry of HIV-1 into trophoblasts is unusual for this retrovirus, because it is associated with endocytosis. However, given that trophoblasts express no or few receptors/coreceptors required for virus internalization, the mechanism underlying this event remains ambiguous. In the present study, we show that HIV-1 entry and infection of polarized trophoblasts are independent not only of CD4 but also of envelope (Env) glycoproteins gp120 and gp41. Virus internalization, cytoplasmic release, reverse transcription, integration, and HIV-1 gene expression occurred with both fusion-incompetent and Env-deficient viruses. Importantly, fusion-independent infection was observed when we used viruses produced in a natural cellular reservoir (i.e., primary human cells). Finally, HIV-1 requires heparan sulfate proteoglycans for uptake in trophoblasts. Together, our findings illustrate that HIV-1 utilizes an unusual pathway for entering human polarized trophoblasts.

A new sensitive and quantitative HTLV-I-mediated cell fusion assay in T cells.

Similar to several other viruses, human T cell leukemia virus type I (HTLV-I) induces the formation of multinucleated giant cells (also known as syncytium) when amplified in tissue culture. These syncytia result from the fusion of infected cells with uninfected cells. Due to the intrinsic difficulty of infecting cells with cell-free HTLV-I virions, syncytium formation has become an important tool in the study of HTLV-I infection and transmission. Since most HTLV-I-based cell fusion assays rely on the use of non-T cells, the aim of this study was to optimize a new HTLV-I-induced cell fusion assay in which HTLV-I-infected T cell lines are co-cultured with T cells that have been transfected with an HTLV-I long terminal repeat (LTR) luciferase reporter construct. We demonstrate that co-culture of various HTLV-I-infected T cells with different transfected T cell lines resulted in induction of luciferase activity. Cell-to-cell contact and expression of the viral gp46 envelope protein was crucial for this induction while other cell surface proteins (including HSC70) did not have a significant effect. This quantitative assay was shown to be very sensitive. In this assay, the cell fusion-mediated activation of NF-kappaB and the HTLV-I LTR occurred through previously described Tax-dependent signaling pathways. This assay also showed that cell fusion could activate Tax-inducible cellular promoters. These results thus demonstrate that this new quantitative HTLV-I-dependent cell fusion assay is versatile, highly sensitive, and can provide an important tool to investigate cellular promoter activation and intrinsic signaling cascades that modulate cellular gene expression.