Relevant bibliographies by topics / HIV-1 Nef

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Academic literature on the topic 'HIV-1 Nef'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "HIV-1 Nef"

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Pyeon, Dohun, Vivian Rojas, Lenore Price, Seongcheol Kim, Meharvan Singh, and In-Woo Park. "HIV-1 Impairment via UBE3A and HIV-1 Nef Interactions Utilizing the Ubiquitin Proteasome System." Viruses 11, no. 12 (November 27, 2019): 1098. http://dx.doi.org/10.3390/v11121098.

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Molecular basis of HIV-1 life cycle regulation has thus far focused on viral gene stage-specificity, despite the quintessence of post-function protein elimination processes in the virus life cycle and consequent pathogenesis. Our studies demonstrated that a key pathogenic HIV-1 viral protein, Nef, interacted with ubiquitin (Ub)-protein ligase E3A (UBE3A/E6AP), suggesting that interaction between Nef and UBE3A is integral to regulation of viral and cellular protein decay and thereby the competing HIV-1 and host cell survivals. In fact, Nef and UBE3A degraded reciprocally, and UBE3A-mediated degradation of Nef was significantly more potent than Nef-triggered degradation of UBE3A. Further, UBE3A degraded not only Nef but also HIV-1 structural proteins, Gag, thus significantly inhibiting HIV-1 replication in Jurkat T cells only in the presence of Nef, indicating that interaction between Nef and UBE3Awas pivotal for UBE3A-mediated degradation of the viral proteins. Mechanistic study showed that Nef and UBE3A were specific and antagonistic to each other in regulating proteasome activity and ubiquitination of cellular proteins in general, wherein specific domains of Nef overlapping with the long terminal repeat (LTR) were essential for the observed actions. Further, Nef itself reduced the level of intracellular Gag by degrading a cardinal transcription regulator, Tat, demonstrating a broad role for Nef in the regulation of the HIV-1 life cycle. Taken together, these data demonstrated that the Nef and UBE3A complex plays a crucial role in coordinating viral protein degradation and hence HIV-1 replication, providing insights as to the nature of pathobiologic and defense strategies of HIV-1 and HIV-infected host cells.
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Toyoda, Mako, Yoko Ogata, Macdonald Mahiti, Yosuke Maeda, Xiaomei T. Kuang, Toshiyuki Miura, Heiko Jessen, et al. "Differential Ability of Primary HIV-1 Nef Isolates To Downregulate HIV-1 Entry Receptors." Journal of Virology 89, no. 18 (July 15, 2015): 9639–52. http://dx.doi.org/10.1128/jvi.01548-15.

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ABSTRACTHIV-1 Nef downregulates the viral entry receptor CD4 as well as the coreceptors CCR5 and CXCR4 from the surface of HIV-infected cells, and this leads to promotion of viral replication through superinfection resistance and other mechanisms. Nef sequence motifs that modulate these functions have been identified viain vitromutagenesis with laboratory HIV-1 strains. However, it remains unclear whether the same motifs contribute to Nef activity in patient-derived sequences and whether these motifs may differ in Nef sequences isolated at different infection stages and/or from patients with different disease phenotypes. Here,nefclones from 45 elite controllers (EC), 46 chronic progressors (CP), and 43 acute progressors (AP) were examined for their CD4, CCR5, and CXCR4 downregulation functions. Nef clones from EC exhibited statistically significantly impaired CD4 and CCR5 downregulation ability and modestly impaired CXCR4 downregulation activity compared to those from CP and AP. Nef's ability to downregulate CD4 and CCR5 correlated positively in all cohorts, suggesting that they are functionally linkedin vivo. Moreover, impairments in Nef's receptor downregulation functions increased the susceptibility of Nef-expressing cells to HIV-1 infection. Mutagenesis studies on three functionally impaired EC Nef clones revealed that multiple residues, including those at novel sites, were involved in the alteration of Nef functions and steady-state protein levels. Specifically, polymorphisms at highly conserved tryptophan residues (e.g., Trp-57 and Trp-183) and immune escape-associated sites were responsible for reduced Nef functions in these clones. Our results suggest that the functional modulation of primary Nef sequences is mediated by complex polymorphism networks.IMPORTANCEHIV-1 Nef, a key factor for viral pathogenesis, downregulates functionally important molecules from the surface of infected cells, including the viral entry receptor CD4 and coreceptors CCR5 and CXCR4. This activity enhances viral replication by protecting infected cells from cytotoxicity associated with superinfection and may also serve as an immune evasion strategy. However, how these activities are maintained under selective pressurein vivoremains elusive. We addressed this question by analyzing functions of primary Nef clones isolated from patients at various infection stages and with different disease phenotypes, including elite controllers, who spontaneously control HIV-1 viremia to undetectable levels. The results indicated that downregulation of HIV-1 entry receptors, particularly CCR5, is impaired in Nef clones from elite controllers. These functional impairments were driven by rare Nef polymorphisms and adaptations associated with cellular immune responses, underscoring the complex molecular pathways responsible for maintaining and attenuating viral protein functionin vivo.
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Fujiwara, Mamoru, and Masafumi Takiguchi. "HIV-1–specific CTLs effectively suppress replication of HIV-1 in HIV-1–infected macrophages." Blood 109, no. 11 (June 1, 2007): 4832–38. http://dx.doi.org/10.1182/blood-2006-07-037481.

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AbstractBoth CD4+ T cells and macrophages are major reservoirs of HIV-1. Previous study showed that HIV-1–specific cytolytic T lymphocytes (CTLs) hardly recognize HIV-1–infected CD4+ T cells because of Nef-mediated HLA class I down-regulation, suggesting that HIV-1 escapes from HIV-1–specific CTLs and continues to replicate in HIV-1–infected donors. On the other hand, the CTL recognition of HIV-1–infected macrophages and the effect of Nef-mediated HLA class I down-regulation on this recognition still remain unclear. We show a strong HIV-1 antigen presentation by HIV-1–infected macrophages. HIV-1–specific CTLs had strong abilities to suppress HIV-1R5 virus replication in HIV-1–infected macrophages and to kill HIV-1R5–infected macrophages. Nef-mediated HLA class I down-regulation minimally influenced the recognition of HIV-1–infected macrophages by HIV-1–specific CTLs. In addition, HIV-1–infected macrophages had a stronger ability to stimulate the proliferation of HIV-1–specific CTLs than HIV-1–infected CD4+ T cells. Thus, the effect of Nef-mediated HLA class I down-regulation was less critical with respect to the recognition by HIV-1–specific CTLs of HIV-infected macrophages than that of HIV-1–infected CD4+ T cells. These findings support the idea that the strong HIV-1 antigen presentation by HIV-1–infected macrophages is one of the mechanisms mediating effective induction of HIV-1–specific CTLs in the acute and early chronic phases of HIV-1 infection.
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Kruize, Zita, Ad C. van Nuenen, Stan W. van Wijk, Arginell F. Girigorie, Karel A. van Dort, Thijs Booiman, and Neeltje A. Kootstra. "Nef Obtained from Individuals with HIV-1 Vary in Their Ability to Antagonize SERINC3- and SERINC5-Mediated HIV-1 Restriction." Viruses 13, no. 3 (March 6, 2021): 423. http://dx.doi.org/10.3390/v13030423.

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Nef is a multifunctional viral protein that has the ability to downregulate cell surface molecules, including CD4 and major histocompatibility complex class I (MHC-I) and, as recently shown, also members of the serine incorporator family (SERINC). Here, we analyzed the impact of naturally occurring mutations in HIV-1 Nef on its ability to counteract SERINC restriction and the clinical course of infection. HIV-1 Nef sequences were obtained from 123 participants of the Amsterdam Cohort Studies and showed multiple amino acid variations and mutations. Most of the primary Nef proteins showed increased activity to counteract SERINC3 and SERINC5 as compared to NL4-3 Nef. Several mutations in Nef were associated with either an increased or decreased infectivity of Bal26-pseudotyped HIV-1 produced in the presence of SERINC3 or SERINC5. The 8R, 157N and R178G Nef mutations were shown to have an effect on disease progression. Survival analysis showed an accelerated disease progression of individuals infected with HIV-1 carrying arginine or asparagine at position 8 or 157 in Nef, respectively, or the R178G Nef mutation. Here, we observed that naturally occurring mutations in Nef affect the ability of Nef to counteract SERINC3- and SERINC5-mediated inhibition of viral infectivity. The majority of these Nef mutations had no significant effect on HIV-1 pathogenesis and only the 8R, 157N and R178G mutations were associated with disease course.
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Stove, Veronique, and Bruno Verhasselt. "Modelling Thymic HIV-1 Nef Effects." Current HIV Research 4, no. 1 (January 1, 2006): 57–64. http://dx.doi.org/10.2174/157016206775197583.

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Foster, John L., and J. Victor Garcia. "HIV-1 Nef: at the crossroads." Retrovirology 5, no. 1 (2008): 84. http://dx.doi.org/10.1186/1742-4690-5-84.

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Harris, Mark, Sandra Talbot, Panagiotis Patsilinacos, and James C. Neil. "The HIV-1 nef gene product." Biochemical Society Transactions 20, no. 2 (May 1, 1992): 517–20. http://dx.doi.org/10.1042/bst0200517.

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Jokiaho, R., N. Síren, L. Lehtikari, and N. von Weymarn. "Crystallization of recombinant HIV-1 Nef." Acta Crystallographica Section A Foundations of Crystallography 61, a1 (August 23, 2005): c236. http://dx.doi.org/10.1107/s0108767305089932.

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Nunes-Alves, Cláudio. "HIV-1 Nef targets restriction factors." Nature Reviews Microbiology 13, no. 11 (October 12, 2015): 661. http://dx.doi.org/10.1038/nrmicro3573.

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Vérollet, Christel, Shanti Souriant, Emilie Bonnaud, Paul Jolicoeur, Brigitte Raynaud-Messina, Cassandre Kinnaer, Isabelle Fourquaux, et al. "HIV-1 reprograms the migration of macrophages." Blood 125, no. 10 (March 5, 2015): 1611–22. http://dx.doi.org/10.1182/blood-2014-08-596775.

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Key PointsHIV-1 Nef reprograms human macrophage migration favoring the mesenchymal mode, which translates in vivo to macrophage tissue accumulation. Nef enhances mesenchymal migration by influencing podosome organization and function via the phagocyte-specific kinase Hck and WASP.
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Dissertations / Theses on the topic "HIV-1 Nef"

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Chen, Nan. "The role of HIV-1 Nef gene in HIV-mediated pathogenesis." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404289.

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Rahim, Mir Munir Ahmed 1975. "Pathogenesis of HIV-1 nef in adult mice." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115698.

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Development of a suitable animal model of AIDS is much needed in AIDS research to study infection and pathogenesis as well as to evaluate methods of prevention and treatment of HIV infection. Small animals such as rodents are attractive candidates for AIDS research due to the availability of various inbred and genetically engineered strains, extensive knowledge or their immune system, especially in mice, and the relative ease of breeding and maintaining animal colonies. Transgenic small animal models carrying entire HIV genome or selected genes have been instrumental to understand functions of HIV genes in vivo and their role in HIV pathogenesis. The type of cells in which HIV genes are expressed seems to be an import prerequisite for the study of HIV gene functions in transgenic mice. Mice constitutively expressing the entire HIV-1 genome or HIV-1 nef gene in CD4 + T cells and in the cells of macrophage/dendritic lineage develop an AIDS-like disease very similar to AIDS disease in humans. Similarly, expression of Nef in adult mice, using inducible system, results in the AIDS-like disease. This disease is characterized by thymic atrophy, impaired thymocyte maturation, loss of CD4+ T cells, increased activation and turnover of T cells, which can occur in the absence of lymphypenia, and non-lymphoid organ disease involving the lungs and kidneys. Susceptibility of adult mice to the pathological effects of Nef suggests that the AIDS-like disease in the constitutively expressing Nef Tg mice is not due to developmental defects caused by early expression of Nef. This model highlights the important role of Nef in HIV-1 pathogenesis. The high similarity in the disease in these Tg mice with human AIDS strongly suggest that these mice are a relevant model to study AIDS. This study further evidence that mouse cells can support functions of Nef and these Tg mice represent a unique model to study Nef functions in vivo in the context of the primary immune system. Moreover, the inducible Nef Tg model has given us the ability to control the level and time of expression of Nef which was impossible to do in the previously reported constitutive Nef Tg mouse models. These mice will be useful to study immune reconstitution since Nef expression can be turned off after withdrawal from dox.
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Chuah, Lay Khim Marinee. "Role of nef in HIV-1 gene regulation." Doctoral thesis, Universite Libre de Bruxelles, 1992. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212893.

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Craig, Heather Marie. "Alterations of intracellular protein sorting by HIV-1 nef /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9970642.

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Jennelle, Lucas Trent. "Contribution of Calnexin to HIV-1 Nef effects on ABCA1." Thesis, The George Washington University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3557581.

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HIV-infected patients are at increased risk of developing atherosclerosis, in part due to an altered HDL profile exacerbated by downmodulation and impairment of ATP-Binding Cassette Transporter A1 (ABCA1) activity by the HIV-1 protein Nef. Nef has been shown to increase delivery of cholesterol to lipid rafts, sites of viral assembly and egress, by inhibition of ABCA1 cholesterol efflux functionality and reduction of ABCA1 protein levels through lysosomal degradation. Important mechanistic details of ABCA1 inactivation and degradation by Nef, and whether these two processes are intimately linked or separable are still to be defined. The studies presented here were designed to identify cellular co-factors for ABCA1-mediated cholesterol efflux that may be targeted by Nef to achieve ABCA1 inactivation. In these studies, a novel cellular factor, the ER-resident lectin chaperone calnexin, was shown to be involved in a physical interaction with ABCA1 that is disrupted by Nef. Nef was found to bind and redistribute calnexin and reduce binding and co-localization of ABCA1 with calnexin. In vitro knockdown of calnexin via RNAi reproduced several previously described biochemical effects of Nef, including redistribution of ABCA1, increased ABCA1 membrane localization, and reduced ABCA1 recycling. Importantly, knockdown of calnexin also resulted in reduced ABCA1-mediated cholesterol efflux, but without the Nef-mediated reduction in ABCA1 protein levels, suggesting that Nef utilizes a bipartite mechanism to inactivate and degrade ABCA1 and that these functions may be separable. Despite the lack of effect of calnexin knockdown on ABCA1 protein levels, interference with the ABCA1-calnexin interaction was critical for Nef-mediated functional impairment of ABCA1. This was shown with a Nef mutant defective in interaction with calnexin which was incapable of preventing ABCA1-calnexin interaction and was also defective in impairing ABCA1-mediated cholesterol efflux activity. Thus, these studies identified a novel mechanism by which HIV-1 Nef impairs functional activity of cholesterol transporter ABCA1 by blocking its interaction with calnexin. Calnexin acts as an ABCA1 functional chaperone, limiting total and cell surface ABCA1 expression while increasing ABCA1-mediated cholesterol efflux. Combined with the demonstration that Nef increases delivery of ABCA1 to lysosomes, these results suggest the Nef-mediated impairment of ABCA1 function involves reduced interaction with calnexin followed by delivery of ABCA1 to lysosomes for degradation.

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Dai, Weiwei. "SERINC5: Its Sensitivity to Nef and Restriction of HIV-1." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/984.

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The accessory protein Nef of human immunodeficiency virus type 1 (HIV-1) has long been known to enhance the infectivity of HIV-1 progeny virions. The multipass transmembrane proteins serine incorporator 3 (SERINC3) and SERINC5 were recently identified as novel antiviral proteins that restrict HIV-1 infectivity. Nef enhances HIV-1 infectivity by removing SERINCs from the plasma membrane, which prevents their incorporation into progeny HIV-1 virions. To exploit this potent intrinsic antiretroviral factor for potential therapy development, it is critical to explore the determinants in SERINC5 that govern its downregulation by Nef and its restriction on HIV-1 infectivity. Here I report that the ability to inhibit HIV-1 infectivity is conserved among vertebrate SERINC5 proteins, whereas the sensitivity to downregulation by Nef is not. However, a Nef-resistant SERINC5 became Nef-sensitive when its intracellular loop 4 (ICL4) was replaced by that of Nef-sensitive human SERINC5. Conversely, human SERINC5 became resistant to Nef when its ICL4 was replaced by that of a Nef-resistant SERINC5. In general, ICL4 regions from SERINCs that exhibited resistance to a given Nef conferred resistance to the same Nef when transferred to a sensitive SERINC, and vice versa. I demonstrate that human SERINC5 can be modified to restrict HIV-1 infectivity even in the presence of Nef. Moreover, by generating chimeras between SERINC5 and SERINC2, which does not exhibit antiretroviral activity, I demonstrate that SERINC5’s inhibitory function, unlike the sensitivity to Nef, requires the participation of more than one region. Helix 4 and extracellular loop 5 (ECL5) of SERINC5 are both required for the potent restriction of HIV-1 infectivity. In contrast, a large amino-terminal portion of SERINC5 is not required for its antiretroviral activity of SERINC5. The determinants in ECL5 disperse throughout the loop. Furthermore, the ECL5 of SERINC5 is a hotspot region that determines the Env-dependent antiretroviral activity of SERINC5.
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Ramalho, Eduardo Dias. "Variabilidade genética de NEF em amostras de HIV-1 circulantes." reponame:Repositório Institucional da UnB, 2006. http://repositorio.unb.br/handle/10482/2319.

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Dissertação (mestrado)—Universidade de Brasília, Instituto de Ciências Biológicas, Departamento de Biologia Celular, 2006.
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Em 2005, cerca de 40 milhões de pessoas viviam com HIV/AIDS no mundo. Desse total, aproximadamente 600 mil residiam no Brasil. Em vista do elevado percentual de infecções pelo HIV-1, o desenvolvimento de vacinas contra esse vírus é uma das prioridades no que se refere à saúde pública mundial. Entretanto, apesar dos estudos sobre esse vírus, pouco se conhece sobre a importância da sua diversidade genética para a eficácia de potenciais vacinas. Assim, conhecer a variabilidade do HIV-1 em diferentes partes do mundo, bem como o seu perfil antigênico, pode ser de fundamental importância para a aplicação dessas. Uma das proteínas mais imunogênicas do HIV-1 é Nef, que desempenha diversas funções importantes durante a infecção viral in vivo, como, por exemplo, aumentar a infectividade e a replicação viral e modular negativamente proteínas presentes na superfície celular. Por essas características, Nef pode ter papel importante na imunização contra o vírus. O presente trabalho teve como objetivo principal analisar amostras de uma série histórica de isolados do HIV-1 circulantes no Distrito Federal e no estado de Rondônia e, desse modo, contribuir para a caracterização desses vírus, pela descrição da variabilidade do gene nef. Além disso, foram avaliados motivos e resíduos importantes para as atividades biológicas de Nef. Para isso, 33 amostras, 17 do Distrito Federal e 16 de Rondônia, foram amplificadas por nested-PCR para o gene nef e seqüenciadas. Todas foram caracterizadas como pertencentes ao subtipo B. Pela dedução da seqüência de aminoácido foi possível observar que duas amostras apresentaram códons de parada prematuros, devido a mutações que levaram a mundança na fase de leitura do gene. Os motivos e resíduos associados às atividades biológicas de Nef também foram analisados. Os sítios de miristoilação, fosforilação por PKA e reconhecimento de Nef pela protease viral encontraram-se conservados em 100%, 66,6% e 69,7% das amostras, respectivamente. Em relação à modulação de CD4 por Nef, 36,4% das amostras apresentaram todos os motivos e resíduos conservados. Os motivos e resíduos associados à modulação negativa de MHC de classe I estiveram conservados em 57,6% das amostras analisadas, enquanto 54,5% dos isolados apresentaram os motivos envolvidos na modulação de MHC de classe II. Quanto à modulação de CD1d, 45,4% das amostras apresentaram a totalidade de motivos e resíduos associados a essa atividade conservados, enquanto aqueles associados à modulação de CD28 estiveram conservados em 81,8%. Enquanto 93,9% das amostras apresentaram o motivo e o resíduo associados à sinalização para apoptose celular conservados. Em relação às alterações em vias de sinalização celular, 63,6% das amostras apresentaram os motivos e resíduos responsáveis pela interação de Nef com domínios SH3 conservados, enquanto 84,8% mostraram-se conservadas para aqueles necessários para a interação de Nef com proteínas Pak. Quanto aos epitopos de Nef reconhecidos por linfócitos T CD4, 18 dos 29 já descritos na literatura foram observados, sendo que o mais freqüente foi encontrado em 75,8% das amostras. Em relação aos epitopos de Nef reconhecidos por linfócitos T citotóxicos considerados ótimos, o mais freqüente foi observado em 84,8% das amostras. Pelo fato de Nef ser uma das regiões imunodominantes do HIV-1, bem como ser uma proteína da fase precoce da infecção, vacinas que utilizem suas porções antigênicas encontram-se em desenvolvimento. Dessa forma, a caracterização da variabilidade do gene nef pode ser de grande importância para o desenvolvimento de estratégias de utilização de potenciais vacinas anti-HIV-1 futuramente no Distrito Federal e em Rondônia. __________________________________________________________________________________________ ABSTRACT
Nearly forty million people around the world were living with HIV/AIDS in 2005, about six hundred thousand in Brazil. Thus, the development of vaccines against this virus is a world public health priority. However, despite several studies concerning this virus, little is known about the relevance of its genetic variability to the efficacy of potential vaccines. Consequently, knowing the HIV-1 variability in different parts of the world, and also its antigenic profile, may be of high importance for the applicability of those vaccines. Nef is one of the most immunogenic proteins of HIV-1, it performs many important functions during the viral infection in vivo, such as increase the viral infectivity and replication, and downmodulate proteins of the cell surface. For these characteristics, Nef may have an important role in the immunization against the virus. The present study had as main objective the analysis of samples from a historical series of isolates of HIV-1 circulating in Federal District and Rondônia, and the contribution to the characterization of this virus, by the description of the variability of the nef gene. Additionally, the conservation of important motifs and residues related to the biological activities of Nef were also analyzed. With this purpose, thirty-three samples, seventeen from Federal District and sixteen from Rondônia, were amplified by nested-PCR for the nef gene and sequenced. All of them clustered with subtype B references isolates in the philogenetic analysis. The motifs and residues associated to Nef biological activities were also analyzed. The miristoilation, fosforilation by PKA and recognition of Nef by the viral protease sites were conserved in 100%, 66,6% and 69,7% of the samples, respectively. Considering the CD4 modulation by Nef, 36,4% of the samples presented all the motifs and residues conserved. 57,6% and 54,5% of the samples had all motifs and residues associated to the down-modulation of MHC class I and to the modulation of MHC class II conserved, respectively. Considering the downmodulation of CD1d, 45,4% of the samples had all the motifs and residues associated to this activity, while 81,8% had those associated to the modulation of CD28. 93,9% of the samples had the motif and the residue associated to the signalization of cell apoptosis conserved. Considering Nef effects on cell signalization pathways, 63,6% of the samples presented the motifs and residues responsible for the interaction of Nef with SH3 domains, while 84,8% had those necessary to the interaction of Nef with Pak proteins. Considering the Nef epitopes recognized by T CD4 lymphocytes eighteen of the twenty-nine previously described were observed, the most frequent one occurred in 75,8% of the samples. Considering the Nef epitopes recognized by T cytotoxic lymphocytes, the most frequent one was observed in 84,8% of the samples. Because Nef is one of the most immunodominant regions of HIV-1 virus, as well one early phase protein, vaccines that use its antigenic regions are in development. In this way, the characterization of the variability of the nef gene may be of high importance to the development of utilization strategies for the potential anti-HIV-1 vaccines in Federal District and Rondônia in the future.
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Chaudhuri, Rittik. "The mechanism of HIV-1 Nef-mediated downregulation of CD4." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/224775.

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Nef, an accessory protein of HIV-1, is a critical determinant of viral pathogenicity. The pathogenic effects of Nef are in large part dependent on its ability to decrease the amount of CD4 on the surface of infected cells. Early studies suggested that Nef induces downregulation by linking the cytosolic tail of CD4 to components of the host-cell protein-trafficking machinery. However, the specific sorting pathway that Nef uses to modulate CD4 expression remained uncertain. According to one model, Nef was thought to interfere with the transport of newly synthesized CD4 from the TGN to the cell-surface. Another model claimed that Nef facilitated the removal of CD4 from the plasma membrane. The primary goal of this thesis was to determine which of these models was correct. To accomplish this objective, a novel Nef-CD4 system was developed in Drosophila S2 cells. Nef was not only able to downregulate human CD4 in S2 cells, but it did so in a manner that was phenotypically indistinguishable from its activity in human cells. An RNAi screen targeting protein-trafficking genes in S2 cells revealed a requirement for clathrin and the clathrin-associated, plasma membrane-localized AP-2 complex in the Nef-mediated downregulation of CD4. In contrast, depletion of the related AP-1 and AP-3 complexes, which direct transport from the TGN and endosomes, had no effect. The requirement for AP-2 was subsequently confirmed in a human cell line. Yeast three-hybrid and GST pull-down assays were then used to demonstrate a robust, direct interaction between Nef and AP-2. This interaction was found to depend on a [D/E]xxxL[L/I]-type dileucine motif, located in the C-terminal loop of Nef, that is essential for CD4 downregulation. While mapping the binding site of AP-2 on Nef, a second determinant of interaction in the C-terminal loop was identified. Mutation of this motif, which conforms to a consensus [D/E]D diacidic sequence, prevented Nef from binding to AP-2 and down-regulating CD4. However, the same mutations did not affect the ability of Nef to interact with either AP-1 or AP-3, providing further evidence that these complexes are not required for the modulation of CD4 expression. Additional experiments indicated that the Nef diacidic motif most likely binds to a basic patch on AP-2 α-adaptin that is not present in the homologous AP-1 γ and AP-3 δ subunits. As with the Nef diluecine and diacidic motifs, the α-adaptin basic patch was shown to be necessary for CD4 downregulation. Moreover, all three of these motifs were needed for the cooperative assembly of a CD4-Nef-AP-2 tripartite complex, which was observed here for the first time using a yeast four-hybrid system. The data in this thesis uniformly support an endocytic model of Nef-mediated CD4 downregulation. Indeed, there is now strong evidence that Nef simultaneously binds CD4 and AP-2, thereby connecting the receptor to the cellular endocytic machinery and promoting its rapid internalization from the plasma membrane. In addition, the identification of novel motifs required for this process has provided new insights on endocytosis, and may facilitate the development of pharmacological inhibitors of Nef function.
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Chang, Alex Hongsheng. "Intracellular inhibition of immune dysfunction induced by HIV-1 Nef protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/NQ56524.pdf.

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Cosma, Antonio. "Use of the regulatory protein Nef for vaccination against HIV-1." Diss., kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/8329/.

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Books on the topic "HIV-1 Nef"

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Rottmann, Erik. His name is John!: The story of John the Baptist : Luke 1:5-80, Mark 1:1-8 for children. St. Louis, MO: Concordia Pub. House, 2007.

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Donais, Rosalie M. As many as received Him, to them gave He power: To become the sons of God, even to them that believe on His name, John 1:12. Tremont, IL (P.O. Box 151, Tremont 61568): Apostolic Christian Church Foundation, 1987.

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ill, Converse James, ed. God builds his church: Stories of God and his people from Acts, Galatians, 1 and 2 Thessalonians, 1 and 2 Corinthians, Romans, Philippians, Colossians, Ephesians, Philemon, 1 and 2 Timothy, Titus, Hebrews, Jude, James, 1 and 2 Peter, 1, 2, and 3 John, and Revelation. Scottdale, Pa: Herald Press, 1987.

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Following in His steps: Suffering, community, and christology in 1 Peter. Atlanta, Ga: Scholars Press, 1998.

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John, White. The ancient history of the Māori, his mythology and traditions: V. 1-3: Horo-Uta or Taki-Tumi Migration; v. 4-6: Tai-Nui. Christchurch [N.Z.]: Kiwi Publishers, 1997.

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God, his servant, and the nations in Isaiah 42:1-9: Biblical theological reflections after Brevard S. Childs and Hans Hübner. Tübingen: Mohr Siebeck, 2014.

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Alward, Donna, and Soraya Lane. Little Cowgirl on His Doorstep / Mission: Soldier to Daddy: 2 in 1. Harlequin Mills & Boon, Limited, 2013.

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Majid, Adrian, and Bruce L. Gilliam. Future Antiretrovirals, Immune-Based Strategies, and Therapeutic Vaccines. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0023.

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Highly active antiretroviral therapy remains the mainstay of treatment for patients chronically infected with HIV. Novel drugs, both within existing classes and new ones, are in various stages of development and testing. New medications within existing classes of antiretroviral agents are in clinical trials and will likely offer activity against resistant HIV-1 strains and provide alternatives for combination pill therapy. Novel therapeutics including oral attachment inhibitors and monoclonal antibody treatments continue to show efficacy against HIV-1 and progress in clinical trials. Tenofovir alafenamide is a prodrug that produces higher intracellular levels of tenofovir diphosphate with likely less renal and bone toxicity. Among traditional classes of HIV treatment, both doravirine (a non-nucleoside reverse transcriptase inhibitor) and cabotegravir (an integrase strand inhibitor) are newer agents with activity against resistant virus. Maturation inhibitors are a new class of treatment that block protease cleavage, leading to the release of an immature virion.
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Bernstein, Jeffrey A. Baruch Spinoza. Edinburgh University Press, 2018. http://dx.doi.org/10.3366/edinburgh/9781474423632.003.0022.

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There is currently a paucity of literature relating to Agamben’s philosophical treatment of Spinoza (Julie Klein, Dimitris Vardoulakis and Miguel Vatter being notable exceptions).1 There has certainly been no attempt to show how Agamben’s manifold references to the seventeenth-century Dutch-Jewish philosopher form a constellation in his thought. In this chapter, I will attempt to bring those references together under the categorial headings of (1) ‘Living in the Middle Voice’ and (2) ‘The Contemplative Life as Inoperativity’. I choose these categories because Agamben’s key concern (as I read him) involves radically rethinking the figures of ‘life’ and ‘living’ as well as providing a new apologia for contemplation. First, however, a few methodological remarks.
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Cox, Josephine H., Stuart Z. Shapiro, Liza Dawson, Cynthia Geppert, Andrew M. Siegel, and M. Patricia D’Souza. Vaccines for The Prevention and Treatment of HIV Infection. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0032.

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While the HIV/AIDS pandemic continues, the overall incidence of HIV infections has fallen through use of antiretroviral therapy (ART) and multiple prevention modalities. To achieve a durable end to the pandemic and avoid the requirement for daily antiretroviral medication over a lifetime, a safe and effective prophylactic vaccine remains essential. This chapter reviews current advances in prophylactic and therapeutic HIV-1 vaccine strategies and the challenges that lie ahead. Recent success in isolation of potent broadly neutralizing antibodies (bnAbs) from infected individuals, the discovery of mechanisms of bnAb induction, and progress in understanding mechanisms of CD8 T-cell killing of HIV-infected cells and the structure of the HIV envelope trimer have opened new strategies for HIV vaccine design. On the therapeutic front, the persistence of HIV reservoirs remains a formidable obstacle to achieving sustained virological remission in HIV-infected individuals after ART is discontinued. Development of a new generation of immune-based therapeutic agents might contribute to a curative intervention. The chapter closes with an overview of ethical challenges in vaccine development and clinical testing.
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Book chapters on the topic "HIV-1 Nef"

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Heigele, Anke, Daniel Sauter, Jan Münch, and Frank Kirchhoff. "HIV-1 Accessory Proteins: Nef." In Methods in Molecular Biology, 115–23. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-670-2_10.

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Gombert, F. O., R. Schaude, W. Tröger, G. Jung, H. Rübsamen-Waigmann, W. Blecha, S. Pfeifer, et al. "Complete epitope fine-mapping of HIV-1 Nef-protein." In Peptides 1990, 872–75. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3034-9_359.

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Venkatesan, Sundararajan, Steven M. Holland, Nafees Ahmad, Paul Wingfield, Ratan K. Maitra, and H. Clifford Lane. "Molecular Functional Studies of HIV-1 REV and NEF Proteins." In Advances in Molecular Biology and Targeted Treatment for AIDS, 189–201. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5928-9_17.

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Brack-Werner, Ruth, Thomas Görblich, Thomas Werner, Francesca Chiodi, Lutz Gürtler, Josef Eberle, Annemarie Schön, and Volker Erfle. "Sequence Analysis of Neuroinvasive and Blood-Derived HIV-1 nef Genes." In Technical Advances in AIDS Research in the Human Nervous System, 189–204. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1949-2_15.

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Spohn, Renate, Jente Brünjes, Filomena Rossi, Frank O. Gombert, and Günther Jung. "Conformational analysis of the HIV-1 Nef protein using theoretical and experimental methods." In Peptides 1992, 894–95. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1470-7_410.

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Ratner, Lee, Thomas M. J. Niederman, Homer Lozeron, and Martin Bryant. "Structure and Function of HIV and SIV Nef Proteins." In Advances in Molecular Biology and Targeted Treatment for AIDS, 203–16. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5928-9_18.

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Guy, B., M. P. Kieny, Y. Riviere, M. Girard, L. Montagnier, and J. P. Lecocq. "Does HIV NEF Protein Belong to the G-Protein Family?" In The Guanine — Nucleotide Binding Proteins, 285–88. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2037-2_28.

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Nieva, José L., Aitziber Agirre, Tatiana Suárez, and Félix M. Goñi. "Membrane topology of the HIV-1 fusion peptide." In Spectroscopy of Biological Molecules: New Directions, 381–82. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4479-7_170.

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Pegoretti, Anna. "Lo “studium” e la biblioteca di Santa Maria Novella nel Duecento e nei primi anni del Trecento (con una postilla sul Boezio di Trevet)." In The Dominicans and the Making of Florentine Cultural Identity (13th-14th centuries) / I domenicani e la costruzione dell'identità culturale fiorentina (XIII-XIV secolo), 105–39. Florence: Firenze University Press, 2020. http://dx.doi.org/10.36253/978-88-5518-046-7.09.

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Building on recent scholarship, this article sketches the development of the Florentine studium of Santa Maria Novella in the thirteenth century, before it became a studium generale between 1305 and 1311. The catalogue of Santa Maria Novella’s library and the information regarding works which were conceived there are collected and analysed to outline the core of the ancient library. The first quire of the manuscript Florence, Biblioteca Nazionale Centrale, Conv. soppr. G 3.451 (cc. 1-8) constitutes a notable case study for the learning interests of Dominican friars. Finally, this article discusses the controversial letter written by Nicholas Trevet to the dedicatee of his commentary on Boethius’ Consolatio Philosophiae and re-assesses its disputed connec- tion with the Florentine environment.
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A., Zulema, Giorgio Mangino, Valentina Gallo, Maria Vincenza, Gianna Fiorucci, Giovanna Romeo, and Elisabetta Affabris. "HIV-1 Nef Transfer and Intracellular Signalling in Uninfected Cells." In HIV-Host Interactions. InTech, 2011. http://dx.doi.org/10.5772/21623.

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Conference papers on the topic "HIV-1 Nef"

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Almodovar, Sharilyn, Melanie Hakar, Amanda A. Allshouse, Serena Fong, Mehrdad Arjomandi, Priscilla Y. Hsue, Laurence Huang, and Sonia C. Flores. "HIV-1 NEF In HIV-Associated Pulmonary Hypertension: Are There Lung-Specific Nef Signature Sequences?" In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6260.

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Corrêa, Lucília Zeymer Alves, Carlos Eduardo M. Salvador, and Carlos Kleber Z. Andrade. "New molecules containing the 1,2,3-triazole moiety as potential HIV-1 Nef inhibitors." In 14th Brazilian Meeting on Organic Synthesis. São Paulo: Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/chempro-14bmos-r0249-1.

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Almodovar, Sharilyn, Amanda Allshouse, Rob Knight, Sarah Roemer, Norbert F. Voelkel, Priscilla Hsue, Marc J. C. Humbert, and Sonia Flores. "HIV-1 Nef Signature Sequences Are A Feature Of HIV-related Pulmonary Hypertension: A Genetic Translational Tool?" In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5209.

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REN, F., S. OGISHIMA, and H. TANAKA. "A NEW ALGORITHM FOR ANALYSIS OF WITHIN-HOST HIV-1 EVOLUTION." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2000. http://dx.doi.org/10.1142/9789814447362_0057.

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Nishimura, R. H. V., F. T. Toledo, and G. C. Clososki. "Preparation of New Magnesium Carbenoids Aiming Inhibitors of HIV-1 Protease Synthesis." In 15th Brazilian Meeting on Organic Synthesis. São Paulo: Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/chempro-15bmos-bmos2013_2013913171326.

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Greenberg, Jared A., Xian Fan, and David M. Guidot. "THE HIV-1 PROTEIN TAT DECREASES NRF-2 EXPRESSION IN RAT ALVEOLAR EPITHELIAL CELLS." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5223.

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Andonie, Razvan, Levente Fabry-Asztalos, Lukas Magill, and Sarah Abdul-Wahid. "A New Fuzzy ARTMAP Approach for Predicting Biological Activity of Potential HIV-1 Protease Inhibitors." In 2007 IEEE International Conference on Bioinformatics and Biomedicine (BIBM 2007). IEEE, 2007. http://dx.doi.org/10.1109/bibm.2007.9.

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Szczyrba, Igor, Martin Burtscher, and Rafal Szczyrba. "A Proposed New Brain Injury Tolerance Criterion Based on the Exchange of Energy Between the Skull and the Brain." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-171967.

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The Head Injury Criterion limit, HIC1000T = 1000, was developed based on skull fracture data (short time intervals T) and longer duration head translations that lead to Closed Head Injuries (CHI). However, recent results imply that the HIC limits depend on the time interval T and the victim’s age [1]. Since the HIC lacks a clear physical interpretation, it is difficult to compare (verify) the new HIC limits with data from non-translational motions, e.g., to link these limits with the Diffuse Axonal Injury (DAI) criterion developed for head rotations [2]. The recent Head Impact Power (HIP) criterion can be applied to arbitrary motions, but it requires determining six parameters experimentally [3].
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Desmyter, J. "AIDS 1987." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644751.

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AIDS virus (HIV) transmission by transfusions and blood products has been essentially halted in industrialized countries which haye introduced systematic anti-HIV screening of donations in 1985. New anti-HIV screening assays, based in part on the replacement of disrupted HIV virions by defined DNA recombinant HIV antigens, have improved specificity; sensitivity has been improved as to dectect seroconversion at an earlier stage. Confirmatory assays and (self-)exclusion of risk groups from blood donation do remain mandatory. HIVAg can be detected in some infections before antibody conversion, and HIVAg is more likely to be found in those anti-HIV positives who proceed to disease. However, there is no justification so far for routine parallel HIVAg and anti-HIV screening. There is continued uncertainty how many HIV carriers have not (yet) developed antibody, but their numbers may have been overestimated. Studies to determine how many HIV transmitters have escaped blood bank detection, and why, need to be undertaken in spite of formidable logistic difficulties.The risk of developing AIDS is now estimated at 25-50 % within 10 years after the infectious contact. It is not clear whether the risk should be estimated differently in different groups or persons. In cities in Central Africa, 5-20 % of men and women are confirmed anti-HIV positives. At least 75 % of this HIV carrier rate is due to heterosexual transmission. Heterosexual transmission has been slower in Western countries, but factors precluding slow evolution to high figures by the same route outside Africa have not been identified. Therefore, countries have no choice in advocating behaviour changes in the general population, and not only in the classical risk groups. Initial hesitations toward extended voluntary and confidential screening are dwindling. Well-conceived confidential screening may be the only way to avoid strong-armed government intervention. The latter is certain to be divisive, and is likely to be counterproductive on balance.An efficacious vaccine remains remote, but an antiviral which prolongs life by at least several months in AIDS patients, but not all of them, is now available. Zidovudine (AZT), however, is toxic and mere prolongation of life without cure will impose an additional burden on AIDS economics.A novel virus (HIV-2) has been identified and is already widespread in West-Africans. It causes AIDS, but the present ratio of AIDS cases in those infected seems lower than with HIV(-l); this feature may be transient. HIV-2 antibodies are either detected or missed by anti-HIV-1 screens; if found, they can be distinguished from anti-HIV-1 only by special confirmatory technique. New screening assays showing equal sensitivity for HIV-1 and HIV-2 in a single test should be devised. At present, HIV-2 is very rare in Western countries compared to HIV-1.
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Hansen, Laura, Manu O. Platt, Roy L. Sutliff, and Rudolph L. Gleason. "The Mechanical and Structural Changes in Murine Arteries due to the Antiretroviral Drug Azidothymidine (AZT)." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80799.

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With over 33 million people infected with the human immunodefeciency virus (HIV-1), HIV-1 and autoimmune deficiency syndrome (AIDS) is a worldwide epidemic [1]. However, the development and widespread use of highly active antiretroviral therapy (HAART) has helped transform HIV-1 infection from a terminal disease leading to AIDS to a manageable chronic condition. With the increase in life expectancy, a new set of non-AIDS related complications has emerged including dyslipidemia, lipodystrophy, insulin resistance, diabetes mellitus, and cardiovascular disease (CVD) specifically high risks for myocardial infarction[2] and increased incidence of atherosclerosis [3]. Additionally, patients exhibit markers of subclinical atherosclerosis including endothelial dysfunction [4], carotid artery intima-media thickening [5], and arterial stiffening [4, 6].
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Reports on the topic "HIV-1 Nef"

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HEFNER, Robert. IHSAN ETHICS AND POLITICAL REVITALIZATION Appreciating Muqtedar Khan’s Islam and Good Governance. IIIT, October 2020. http://dx.doi.org/10.47816/01.001.20.

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Ours is an age of pervasive political turbulence, and the scale of the challenge requires new thinking on politics as well as public ethics for our world. In Western countries, the specter of Islamophobia, alt-right populism, along with racialized violence has shaken public confidence in long-secure assumptions rooted in democracy, diversity, and citizenship. The tragic denouement of so many of the Arab uprisings together with the ascendance of apocalyptic extremists like Daesh and Boko Haram have caused an even greater sense of alarm in large parts of the Muslim-majority world. It is against this backdrop that M.A. Muqtedar Khan has written a book of breathtaking range and ethical beauty. The author explores the history and sociology of the Muslim world, both classic and contemporary. He does so, however, not merely to chronicle the phases of its development, but to explore just why the message of compassion, mercy, and ethical beauty so prominent in the Quran and Sunna of the Prophet came over time to be displaced by a narrow legalism that emphasized jurisprudence, punishment, and social control. In the modern era, Western Orientalists and Islamists alike have pushed the juridification and interpretive reification of Islamic ethical traditions even further. Each group has asserted that the essence of Islam lies in jurisprudence (fiqh), and both have tended to imagine this legal heritage on the model of Western positive law, according to which law is authorized, codified, and enforced by a leviathan state. “Reification of Shariah and equating of Islam and Shariah has a rather emaciating effect on Islam,” Khan rightly argues. It leads its proponents to overlook “the depth and heights of Islamic faith, mysticism, philosophy or even emotions such as divine love (Muhabba)” (13). As the sociologist of Islamic law, Sami Zubaida, has similarly observed, in all these developments one sees evidence, not of a traditionalist reassertion of Muslim values, but a “triumph of Western models” of religion and state (Zubaida 2003:135). To counteract these impoverishing trends, Khan presents a far-reaching analysis that “seeks to move away from the now failed vision of Islamic states without demanding radical secularization” (2). He does so by positioning himself squarely within the ethical and mystical legacy of the Qur’an and traditions of the Prophet. As the book’s title makes clear, the key to this effort of religious recovery is “the cosmology of Ihsan and the worldview of Al-Tasawwuf, the science of Islamic mysticism” (1-2). For Islamist activists whose models of Islam have more to do with contemporary identity politics than a deep reading of Islamic traditions, Khan’s foregrounding of Ihsan may seem unfamiliar or baffling. But one of the many achievements of this book is the skill with which it plumbs the depth of scripture, classical commentaries, and tasawwuf practices to recover and confirm the ethic that lies at their heart. “The Quran promises that God is with those who do beautiful things,” the author reminds us (Khan 2019:1). The concept of Ihsan appears 191 times in 175 verses in the Quran (110). The concept is given its richest elaboration, Khan explains, in the famous hadith of the Angel Gabriel. This tradition recounts that when Gabriel appeared before the Prophet he asked, “What is Ihsan?” Both Gabriel’s question and the Prophet’s response make clear that Ihsan is an ideal at the center of the Qur’an and Sunna of the Prophet, and that it enjoins “perfection, goodness, to better, to do beautiful things and to do righteous deeds” (3). It is this cosmological ethic that Khan argues must be restored and implemented “to develop a political philosophy … that emphasizes love over law” (2). In its expansive exploration of Islamic ethics and civilization, Khan’s Islam and Good Governance will remind some readers of the late Shahab Ahmed’s remarkable book, What is Islam? The Importance of Being Islamic (Ahmed 2016). Both are works of impressive range and spiritual depth. But whereas Ahmed stood in the humanities wing of Islamic studies, Khan is an intellectual polymath who moves easily across the Islamic sciences, social theory, and comparative politics. He brings the full weight of his effort to conclusion with policy recommendations for how “to combine Sufism with political theory” (6), and to do so in a way that recommends specific “Islamic principles that encourage good governance, and politics in pursuit of goodness” (8).
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Prevalence of sexually transmitted infections among men who have sex with men and injecting drug users and validation of audio computer-assisted self interview (ACASI) technique in Abuja, Lagos, and Ibadan, Nigeria: Technical report. Population Council, 2011. http://dx.doi.org/10.31899/hiv14.1004.

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Most-at-risk populations (MARPS), including men who have sex with men (MSM) and injecting drug users (IDUs), represent 1 percent of Nigeria’s population yet account for 38 percent of new HIV infections. Despite their elevated risk, MSM and IDUs are less likely than the general population to access HIV prevention and sexual health services because of stigmatization. There is a dearth of data on prevalence of HIV and sexually transmitted infections (STIs) among MSM and IDUs because their behaviors make them difficult to be reached programmatically and engaged in research. While the need for HIV and STI prevalence data is clear, there is also a need to improve the quality and reliability of behavioral data collected for national surveillance, where these stigmatized subpopulations may underreport sensitive behaviors that put them most at risk. This technical report provides details of a study that sought to determine the prevalence of HIV and STIs and sexual and injecting risk behaviors in MSM and male IDUs, and determine if Audio Computer-Assisted Self Interviews provide more accurate reporting of risk behaviors than face-to-face interviewing.
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Prevalence of sexually transmitted infections among men who have sex with men and injecting drug users and validation of audio computer-assisted self interview (ACASI) technique in Abuja, Lagos, and Ibadan, Nigeria: Report Fact Sheet. Population Council, 2011. http://dx.doi.org/10.31899/hiv14.1005.

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Most-at-risk populations (MARPS), including men who have sex with men (MSM) and injecting drug users (IDUs), represent only 1 percent of Nigeria’s population yet account for 38 percent of new HIV infections. Despite their elevated risk, MSM and IDUs are less likely than the general population to access HIV prevention and sexual health services because of stigmatization. There is a dearth of data on prevalence of HIV and sexually transmitted infections (STIs) among MSM and IDUs because their behaviors make them difficult to be reached programmatically and engaged in research. While the need for HIV and STI prevalence data is clear, there is also a need to improve the quality and reliability of behavioral data collected for national surveillance, where these stigmatized subpopulations may underreport sensitive behaviors that put them most at risk. As noted in this fact sheet, computer-based interviewing systems are becoming an accepted alternative to face-to-face interviews, providing an efficient and replicable research tool for collecting sensitive behavioral data.
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