Understanding The Market System of Human Trafficking

The crime of human trafficking is a phenomenon that practically affects every part of the world. The crime is generally influenced by various political as well as socio-economic factors. Oftentimes, victimization, causal factors, and policy response receive the most attention in human trafficking studies, while other aspects like the market system or supply and demand in human trafficking are given little focus. Hence, the objective of this paper is to analyze the market system and the intrinsic elements that influence the supply and demand in human trafficking, with a reference to the case study of Sabah, Malaysia. The qualitative data for this paper were obtained through personal observation and interviews with public officials from the government enforcement agencies like the Royal Malaysian Police, Immigration Department of Malaysia, as well as former traffickers, ex-victims, and academicians. Besides, various reports from the government, non-governmental organizations, and news media helped to collate and provide a comprehensive analysis of the subject matter. Using perspectives from the economics of crime, this paper examined the macro and micro-level factors that regulate the supply and demand in human trafficking. The findings suggest that the supply of trafficked labour in Sabah is influenced by macro-level factors like globalization, unequal economic development, demographic factors, and domestic conflict, while the demand for trafficked labour is amplified by the factors such as consumers, exploiters, socio-culture, and the state. These elements are essential in regulating the market system of supply and demand in human trafficking. An inclusive understanding of supply and demand in human trafficking is important as it has implications for knowledge development as well as policy responses to disrupt the market forces that sustain the crime

The current biotechnology outlook in Malaysia

Blessed with extremely rich biodiversity, Malaysia is all geared up to explore new high technology to utilize the advantage it possesses whilst to protect its environment. Biotechnology has been identified as an appropriate driver that can deliver economic gains through research and development, improvement of food security, creation of entrepreneurial opportunities for industrial growth, health and environmental sustainability. This paper attempts to address the evolution of biotechnology institutions and the stumbling blocks in developing the Malaysian biotechnology industry. This paper identifies three main impediments in the current Malaysian biotechnology, namely lack of skilled human capital; weak industrial base; and lack of commercialization effort. Besides, a set of strategies are discussed with aim to further improve and strengthen the Malaysian biotechnology industry. In general, the arguments are presented by mapping out the symbiotic relationship between data from elite interviews, archival data and observations.Malaysian biotechnology industry, human capital, industrial base, commercialization

An Integrated Model To Analyse Policy Process: A Case Study Of Malaysia’s National Biotechnology Policy

Biotechnology is one of the major technologies of the twenty-first century and in fact is the fastest growing sectors in the world. It is a fascinating field that has been identified as the next engine of growth for Malaysia, one that will deliver economic gains through research and development, creation of entrepreneurial opportunities for industrial growth, improvement of food security, health and environmental sustainability. Realising the important contributions of biotechnology to the country, this research seeks to examine the policymaking process of National Biotechnology Policy, which is aimed to provide a structured guideline in developing the industry

Simian varicella virus infects enteric neurons and α4β7 integrin-expressing gut-tropic T-cells in nonhuman primates

The pathogenesis of enteric zoster, a rare debilitating complication of reactivation of latent varicella-zoster virus (VZV) in the enteric nervous system (ENS), is largely unknown. Infection of monkeys with the closely related Varicellovirus simian varicella virus (SVV) mimics VZV disease in humans. In this study, we determined the applicability of the SVV nonhuman primate model to study Varicellovirus infection of the ENS. We confirmed VZV infection of the gut in latently infected adults and demonstrated th

Current in vivo models of varicella-zoster virus neurotropism

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. Varicella-zoster virus (VZV), an exclusively human herpesvirus, causes chickenpox and establishes a latent infection in ganglia, reactivating decades later to produce zoster and associated neurological complications. An understanding of VZV neurotropism in humans has long been hampered by the lack of an adequate animal model. For example, experimental inoculation of VZV in small animals including guinea pigs and cotton rats results in the infection of ganglia but not a rash. The severe combined immune deficient human (SCID-hu) model allows the study of VZV neurotropism for human neural sub-populations. Simian varicella virus (SVV) infection of rhesus macaques (RM) closely resembles both human primary VZV infection and reactivation, with analyses at early times after infection providing valuable information about the extent of viral replication and the host immune responses. Indeed, a critical role for CD4 T-cell immunity during acute SVV infection as well as reactivation has emerged based on studies using RM. Herein we discuss the results of efforts from different groups to establish an animal model of VZV neurotropism

Simian varicella virus infection of Chinese rhesus macaques produces ganglionic infection in the absence of rash

Varicella-zoster virus (VZV) causes varicella (chickenpox), becomes latent in ganglia along the entire neuraxis, and may reactivate to cause herpes zoster (shingles). VZV may infect ganglia via retrograde axonal transport from infected skin or through hematogenous spread. Simian varicella virus (SVV) infection of rhesus macaques provides a useful model system to study the pathogenesis of human VZV infection. To dissect the virus and host immune factors during acute SVV infection, we analyzed four SVV-seronegative Chinese rhesus macaques infected intratracheally with cell-associated 5 × 103 plaque-forming units (pfu) of SVV-expressing green fluorescent protein (n = 2) or 5 × 104 pfu of wild-type SVV (n = 2). All monkeys developed viremia and SVV-specific adaptive B- and T-cell immune responses, but none developed skin rash. At necropsy 21 days postinfection, SVV DNA was found in ganglia along the entire neuraxis and in viscera, and SVV RNA was found in ganglia, but not in viscera. The amount of SVV inoculum was associated with the extent of viremia and the immune response to virus. Our findings demonstrate that acute SVV infection of Chinese rhesus macaques leads to ganglionic infection by the hematogenous route and the induction of a virus-specific adaptive memory response in the absence of skin rash

Simian Varicella Virus Infection of Rhesus Macaques Recapitulates Essential Features of Varicella Zoster Virus Infection in Humans

Simian varicella virus (SVV), the etiologic agent of naturally occurring varicella in primates, is genetically and antigenically closely related to human varicella zoster virus (VZV). Early attempts to develop a model of VZV pathogenesis and latency in nonhuman primates (NHP) resulted in persistent infection. More recent models successfully produced latency; however, only a minority of monkeys became viremic and seroconverted. Thus, previous NHP models were not ideally suited to analyze the immune response to SVV during acute infection and the transition to latency. Here, we show for the first time that intrabronchial inoculation of rhesus macaques with SVV closely mimics naturally occurring varicella (chickenpox) in humans. Infected monkeys developed varicella and viremia that resolved 21 days after infection. Months later, viral DNA was detected only in ganglia and not in non-ganglionic tissues. Like VZV latency in human ganglia, transcripts corresponding to SVV ORFs 21, 62, 63 and 66, but not ORF 40, were detected by RT-PCR. In addition, as described for VZV, SVV ORF 63 protein was detected in the cytoplasm of neurons in latently infected monkey ganglia by immunohistochemistry. We also present the first in depth analysis of the immune response to SVV. Infected animals produced a strong humoral and cell-mediated immune response to SVV, as assessed by immunohistology, serology and flow cytometry. Intrabronchial inoculation of rhesus macaques with SVV provides a novel model to analyze viral and immunological mechanisms of VZV latency and reactivation

Simian Varicella Virus DNA in Saliva and Buccal Cells After Experimental Acute Infection in Rhesus Macaques

Simian varicella virus (SVV) infection of non-human primates is the counterpart of varicella zoster virus (VZV) infection in humans. To develop non-invasive methods of assessing SVV infection, we tested for the presence of SVV DNA in saliva, as has been documented in human VZV infection, and in buccal cells to determine whether epithelial cells might provide a more reliable source of material for analysis. Five rhesus macaques intratracheally inoculated with SVV all developed varicella with viremia and macular-papular skin rash in 1–2 weeks, which resolved followed by establishment of latency. DNA extracted from longitudinal blood peripheral blood mononuclear cells (PBMCs), saliva and buccal samples collected during acute infection and establishment of latency were analyzed by real-time qPCR. After intratracheal inoculation, viremia was observed, with peak levels of 101–102 copies of SVV DNA in 100 ng of PBMC DNA at 4 and 7 days post inoculation (dpi), which then decreased at 9–56 dpi. In saliva and buccal cells at 7 dpi, 101–104 copies and 101–105 copies of SVV DNA in 100 ng of cellular DNA, respectively, were detected in all the five monkeys. At 9 dpi, saliva samples from only two of the five monkeys contained SVV DNA at 102–103 copies/100 ng of saliva DNA, while buccal cells from all five monkeys showed 100–103 copies of SVV DNA/100 ng of buccal cell DNA. Similar to viremia, SVV DNA in saliva and buccal cells at 11–56 dpi was lower, suggesting clearance of viral shedding. SVV DNA levels were generally higher in buccal cells than in saliva. Our findings indicate that SVV shedding into the oral cavity parallels acute SVV infection and underscore the relevance of both saliva and buccal cell samples to monitor acute varicella virus infection