Relevant bibliographies by topics / VIH (virus) – Reproduction (biologie)

Academic literature on the topic 'VIH (virus) – Reproduction (biologie)'

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Published: 7 October 2023

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Journal articles on the topic "VIH (virus) – Reproduction (biologie)"

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Lamoril, J., and M. Bogard. "La quantification en biologie moléculaire: application à l'étude de la charge virale du virus VIH-1." Immuno-analyse & Biologie Spécialisée 11, no. 5 (January 1996): 325–32. http://dx.doi.org/10.1016/0923-2532(96)88207-x.

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Kim, Keun Il, Ming Yan, Oxana Malakhova, Jiann-Kae Luo, Mei-Feng Shen, Weiguo Zou, Juan Carlos de la Torre, and Dong-Er Zhang. "Ube1L and Protein ISGylation Are Not Essential for Alpha/Beta Interferon Signaling." Molecular and Cellular Biology 26, no. 2 (January 15, 2006): 472–79. http://dx.doi.org/10.1128/mcb.26.2.472-479.2006.

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ABSTRACT The expression of ubiquitin-like modifier ISG15 and its conjugation to target proteins are highly induced by interferon (IFN) stimulation and during viral and bacterial infections. However, the biological significance of this modification has not been clearly understood. To investigate the function of protein modification by ISG15, we generated a mouse model deficient in UBE1L, an ISG15-activating enzyme. Ube1L−/− mice did not produce ISG15 conjugates but expressed free ISG15 normally. ISGylation has been implicated in the reproduction and innate immunity. However, Ube1L−/− mice were fertile and exhibited normal antiviral responses against vesicular stomatitis virus and lymphocytic choriomeningitis virus infection. Our results indicate that UBE1L and protein ISGylation are not critical for IFN-α/β signaling via JAK/STAT activation. Moreover, using Ube1L/Ubp43 double-deficient mice, we showed that lack of UBP43, but not the increase of protein ISGylation, is related to the increased IFN signaling in Ubp43-deficient mice.
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Oludoun, Olajumoke, Olukayode Adebimpe, James Ndako, Michael Adeniyi, Oluwakemi Abiodun, and Babatunde Gbadamosi. "The impact of testing and treatment on the dynamics of Hepatitis B virus." F1000Research 10 (September 17, 2021): 936. http://dx.doi.org/10.12688/f1000research.72865.1.

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Despite the intervention of WHO on vaccination for reducing the spread of Hepatitis B Virus (HBV), there are records of the high prevalence of HBV in some regions. In this paper, a mathematical model was formulated to analyze the acquisition and transmission process of the virus with the view of identifying the possible way of reducing the menace and mitigating the risk of the virus. The models' positivity and boundedness were demonstrated using well-known theorems. Equating the differential equations to zero demonstrates the equilibria of the solutions i.e., the disease-free and endemic equilibrium. The next Generation Matrix method was used to compute the basic reproduction number for the models. Local and global stabilities of the models were shown via linearization and Lyapunov function methods respectively. The importance of testing and treatment on the dynamics of HBV were fully discussed in this paper. It was discovered that testing at the acute stage of the virus and chronic unaware state helps in better management of the virus.
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Barker, Colin T., and Naveen K. Vaidya. "Modeling HIV-1 infection in the brain." PLOS Computational Biology 16, no. 11 (November 19, 2020): e1008305. http://dx.doi.org/10.1371/journal.pcbi.1008305.

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While highly active antiretroviral therapy (HAART) is successful in controlling the replication of Human Immunodeficiency Virus (HIV-1) in many patients, currently there is no cure for HIV-1, presumably due to the presence of reservoirs of the virus. One of the least studied viral reservoirs is the brain, which the virus enters by crossing the blood-brain barrier (BBB) via macrophages, which are considered as conduits between the blood and the brain. The presence of HIV-1 in the brain often leads to HIV associated neurocognitive disorders (HAND), such as encephalitis and early-onset dementia. In this study we develop a novel mathematical model that describes HIV-1 infection in the brain and in the plasma coupled via the BBB. The model predictions are consistent with data from macaques infected with a mixture of simian immunodeficiency virus (SIV) and simian-human immunodeficiency virus (SHIV). Using our model, we estimate the rate of virus transport across the BBB as well as viral replication inside the brain, and we compute the basic reproduction number. We also carry out thorough sensitivity analysis to define the robustness of the model predictions on virus dynamics inside the brain. Our model provides useful insight into virus replication within the brain and suggests that the brain can be an important reservoir causing long-term viral persistence.
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Diao, Feifei, Chenlong Jiang, Yangyang Sun, Yanni Gao, Juan Bai, Hans Nauwynck, Xianwei Wang, Yuanqi Yang, Ping Jiang, and Xing Liu. "Porcine reproductive and respiratory syndrome virus infection triggers autophagy via ER stress-induced calcium signaling to facilitate virus replication." PLOS Pathogens 19, no. 3 (March 27, 2023): e1011295. http://dx.doi.org/10.1371/journal.ppat.1011295.

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Calcium (Ca2+), a ubiquitous second messenger, plays a crucial role in many cellular functions. Viruses often hijack Ca2+ signaling to facilitate viral processes such as entry, replication, assembly, and egress. Here, we report that infection by the swine arterivirus, porcine reproductive and respiratory syndrome virus (PRRSV), induces dysregulated Ca2+ homeostasis, subsequently activating calmodulin-dependent protein kinase-II (CaMKII) mediated autophagy, and thus fueling viral replication. Mechanically, PRRSV infection induces endoplasmic reticulum (ER) stress and forms a closed ER–plasma membrane (PM) contacts, resulting the opening of store operated calcium entry (SOCE) channel and causing the ER to take up extracellular Ca2+, which is then released into the cytoplasm by inositol trisphosphate receptor (IP3R) channel. Importantly, pharmacological inhibition of ER stress or CaMKII mediated autophagy blocks PRRSV replication. Notably, we show that PRRSV protein Nsp2 plays a dominant role in the PRRSV induced ER stress and autophagy, interacting with stromal interaction molecule 1 (STIM1) and the 78 kDa glucose-regulated protein 78 (GRP78). The interplay between PRRSV and cellular calcium signaling provides a novel potential approach to develop antivirals and therapeutics for the disease outbreaks.
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Veit, Michael, Mohamed Rasheed Gadalla, and Minze Zhang. "Using Alphafold2 to Predict the Structure of the Gp5/M Dimer of Porcine Respiratory and Reproductive Syndrome Virus." International Journal of Molecular Sciences 23, no. 21 (October 30, 2022): 13209. http://dx.doi.org/10.3390/ijms232113209.

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Porcine reproductive and respiratory syndrome virus is a positive-stranded RNA virus of the family Arteriviridae. The Gp5/M dimer, the major component of the viral envelope, is required for virus budding and is an antibody target. We used alphafold2, an artificial-intelligence-based system, to predict a credible structure of Gp5/M. The short disulfide-linked ectodomains lie flat on the membrane, with the exception of the erected N-terminal helix of Gp5, which contains the antibody epitopes and a hypervariable region with a changing number of carbohydrates. The core of the dimer consists of six curved and tilted transmembrane helices, and three are from each protein. The third transmembrane regions extend into the cytoplasm as amphiphilic helices containing the acylation sites. The endodomains of Gp5 and M are composed of seven β-strands from each protein, which interact via β-strand seven. The area under the membrane forms an open cavity with a positive surface charge. The M and Orf3a proteins of coronaviruses have a similar structure, suggesting that all four proteins are derived from the same ancestral gene. Orf3a, like Gp5/M, is acylated at membrane-proximal cysteines. The role of Gp5/M during virus replication is discussed, in particular the mechanisms of virus budding and models of antibody-dependent virus neutralization.
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Chadsuthi, Sudarat, and Surapa Wichapeng. "The Modelling of Hand, Foot, and Mouth Disease in Contaminated Environments in Bangkok, Thailand." Computational and Mathematical Methods in Medicine 2018 (June 3, 2018): 1–8. http://dx.doi.org/10.1155/2018/5168931.

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Hand, foot, and mouth disease (HFMD) has spread widely in a continuing endemic in Thailand. There are no specific vaccines or antiviral treatments available that specifically target HFMD. Indirect transmission via free-living viruses from the environment may influence HFMD infections because the virus can survive for long periods in the environment. In this study, a new mathematical model is proposed to investigate the effect of indirect transmission from contaminated environments and the impact of asymptomatic individuals. By fitting our model to reported data on hospitalized individuals of HFMD endemic in Bangkok, Thailand, 2016, the basic reproduction number was estimated as 1.441, which suggests that the disease will remain under current conditions. Numerical simulations show that the direct transmission from asymptomatic individuals and indirect transmission via free-living viruses are important factors which contribute to new HFMD infections. Sensitivity analysis indicates that the basic reproduction number is sensitive to the transmission rate of asymptomatic and symptomatic subgroups and indirect transmission. Our findings suggest that cleaning the environment frequently and healthcare precautions which include the reduction of direct transmission rates should be promoted as effective control strategies for preventing the HFMD spread.
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Castelo Branco, Anna Cláudia, Luanda Mara da Silva Oliveira, Fábio Seiti Yamada Yoshikawa, Anna Julia Pietrobom, Amaro Nunes Duarte Neto, and Maria Notomi Sato. "Evaluation of human placental villi inflammation via TLR4 activation during Zika virus infection." Placenta 83 (August 2019): e92. http://dx.doi.org/10.1016/j.placenta.2019.06.292.

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Zhang, Lin, Lu Zhang, Yu Pan, Junxin Gao, Yunfei Xu, Xi Li, Zhijun Tian, Hongyan Chen, and Yue Wang. "Downregulation of miR-218 by porcine reproductive and respiratory syndrome virus facilitates viral replication via inhibition of type I interferon responses." Journal of Biological Chemistry 296 (January 2021): 100683. http://dx.doi.org/10.1016/j.jbc.2021.100683.

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Ling, Xiaoya, Zhigang Cao, Panpan Sun, Hua Zhang, Yaogui Sun, Jia Zhong, Wei Yin, et al. "Target Discovery of Matrine against PRRSV in Marc-145 Cells via Activity-Based Protein Profiling." International Journal of Molecular Sciences 24, no. 14 (July 16, 2023): 11526. http://dx.doi.org/10.3390/ijms241411526.

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Porcine reproductive and respiratory syndrome (PRRS) seriously endangers the sustainable development of the pig industry. Our previous studies have shown that matrine can resist porcine reproductive and respiratory syndrome virus (PRRSV) infection. This study aimed to explore the anti-PRRSV targets of matrine in Marc-145 cells. Biotin-labeled matrine 1 and 2 were used as probes. MTT assay was used to determine the maximum non-cytotoxic concentration (MNTC) of each probe in Marc-145 cells. The anti-PRRSV activity of each probe was evaluated via MTT, qPCR and Western blot, and its anti-inflammatory activity was evaluated via qPCR and Western blot. The targets of matrine in Marc-145 cells were searched using activity-based protein profiling (ABPP), and compared with the targets predicted via network pharmacology for screening the potential targets of matrine against PRRSV. The protein–protein interaction networks (PPI) of potential targets were constructed using a network database and GO/KEGG enrichment analysis was performed. ACAT1, ALB, HMOX1, HSPA8, HSP90AB1, PARP1 and STAT1 were identified as potential targets of matrine, and their functions were related to antiviral capacity and immunity. Matrine may play an anti-PRRSV role by directly acting on ACAT1, ALB, HMOX1, HSPA8, HSP90AB1, PARP1 and STAT1.
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Dissertations / Theses on the topic "VIH (virus) – Reproduction (biologie)"

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Gonzales, Baptiste. "Etudes des facteurs cellulaires et lipidiques déterminant la localisation du site d'assemblage et de bourgeonnement du VIH-1." Electronic Thesis or Diss., Tours, 2019. http://www.theses.fr/2019TOUR3811.

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La formation des particules du VIH-1 résulte de l'assemblage des précurseurs Gag sur le feuillet interne de la membrane plasmique (MP) des cellules infectées. Les protéines Gag sont spécifiquement adressées à la MP grâce à des interactions entre le domaine MA et le PI(4,5)P2. Cette étude décrit le rôle des phosphadidylinosito1-4-phosphate 5-kinase de type 1 (PIP5K1alpha, beta et sigma) au cours des étapes tardives du VIH-1 dans le modèle celllulaire HeLa. Nous avons démontré que la PIP5K1alpha est l'enzyme principalement impliquée dans la production du PI(4,5P2. En suivant le trafic de Gag à la MP. Leur inhibition respective induit l'accumulation des précurseurs viraux dans les compartiments intracellulaires distincts et diminue la libération des pseudo-particules Gag dans les deux cas. L'ensemble de nos résultats démontre pour la première fois l'importance de l'activité des PIP5K1alpha et sigma dans l'assemblage et le bourgeonnement du VIH-1 et fournit de nouveaux éléments utiles à la compréhension des étapes tardives du cycle de multiplication viral
The production pocesses of HIV-1 particle of HIV-1 particles results from the assembly of Gag Precursors at the inner leaflet of the plasma membrane (PM) of infected cells. Gag proteins are specifically targeted to PM through interactions between MA domain and PI(4,5)P2. This study describes the role of phosphatidylinositol-4-phosphate 5-kinase type 1 (PIP5K1alpha, beta et sigma) in the late stages of HIV-1 in the context of HeLa cells. We determined that PIP5K1alpha is the principal producer of cellular PI(4,5)P2. By using a confocal microscopy approach, we followed the Gag proteins trafficking and showed that only alpha and y isoforms are required for the correct targeting of Gag to PM. Their respective inhibition leads to the accumulation of viral precursors at distinct intracellular comprtements, and decreases the release of Gag pseudoparticles in both cases. Altogether, our results highlight for the first time the crucial role PIP5K1alpha and sigma in the HIV-1 assembly and budding and provide new insights for a better understanding of the late stages of the virus replication cycle
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Escaich, Sonia. "Étude quantitative et qualitative de la réplication du VIH-1 au cours des différents stades de l'infection : applications au pronostic et au suivi de traitement antiviral." Lyon 1, 1992. http://www.theses.fr/1992LYO1T023.

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Cheynet, Valérie. "De la détection du virus VIH-1 : protéines recombinantes et modèles cellulaires d'infection." Lyon 1, 1994. http://www.theses.fr/1994LYO1T211.

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Rakotobe, Dina. "Étude de la fonction de la protéine cellulaire EED dans le cycle viral du virus VIH-1." Lyon 1, 2007. http://www.theses.fr/2007LYO10092.

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La protéine EED (Embryonic Ectoderm Development) appartient à la famille des Polycomb Group agissant comme répresseurs épigénétiques. EED interagit avec la matrice du VIH (MA) et Nef. Nous avons mis en évidence qu'EED se lie aussi à l'intégrase (IN), et forme un complexe ternaire EED-MAIN. Ce ‘ménage-à-trois' est retrouvé aux pores nucléaires (NPC) et dans le noyau des cellules MT4 infectées par le VIH entre 1. 5 et 6h après l'infection. A la phase tardive du cycle viral, EED provoque un effet negatif important sur la production de VIH (~ 2 log). Nef restaure la production virale, et joue le rôle d'antagoniste d'EED. EED et Nef se relocalisent dans une fraction cellulaire insoluble, différente des microdomaines membranaires (ou ‘lipid rafts'). L'imagerie cellulaire révèle qu'EED induit la localisation aberrante de NPC dans le cytoplasme des cellules 293T. Ces NPC ectopiques pourraient séquestrer ou/et perturber le trafic cellulaire des génomes viraux, et donc l'assemblage des virions
Human protein EED (Embryonic Ectoderm Development) belongs to the Polycomb Group family, which act as gene silencers. EED interacts with the matrix protein of HIV-1 (MA) and Nef. We found that EED also binds to integrase (IN), and forms a ternary complex with MA and IN. This ‘menage-a-trois’ EEDIN- MA was found at the nuclar pore complexes (NPC) and in the nucleus of HIV-infected MT4 cells at early times post-infection (1. 5-6h pi). Overexpression of EED in transfected 293T cells resulted in a strong negative effect on HIV-1 yields (~ 2 log) at late times pi. This late negative effect was antagonized by Nef (and its G2A mutant), and was associated with a relocation of EED and Nef to a non-raft, pelletable cellular fraction. Cellular imaging showed that EED induced an aberrant location of clusters of NPC in the cytoplasm of 293T cells. These ectopic NPC might sequester the viral genomic RNA (gRNA), provoke a mistrafficking of gRNA, and result in a lower efficiency of virion assembly
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Hemonnot, Bénédicte. "Rôle de la phosphorylation des protéines virales dans le cycle de rétrovirus VIH-1 et HTLV-1." Montpellier 2, 2004. http://www.theses.fr/2004MON20143.

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Roulet, Vanessa. "Étude de l'infection du testicule humain par le VIH." Rennes 1, 2005. http://www.theses.fr/2005REN1S191.

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Les résultats obtenus dans le cadre de cette thèse portent sur l'infection du testicule humain par le VIH. Nous avons tout d'abord montré que les celulles de Leydig isolées sont permissives à certaines souches de VIH-2 et de SIV, mais ne sont pas infectées par le VIH-1. Ensuite, nous avons adapté et caractérisé un système de culture organotypique de testicule humain. Ce modèle permet de conserver les interactions cellulaires et moléculaires de l'ensemble des types cellulaires présents au sein des explants et de préserver l'activité métabolique des cellules de Leydig. L'architecture globale des tubes séminifères et l'intégrité du tissu interstitiel sont maintenus jusqu'à 16 jours de culture. Finalement, ce modèle nous a permis d'étudier la réplication d'une souche de VIH-1 R5X4 au sein du tissu testiculaire. La production de particules virales infectieuses a été détectée dans les surnageants de cultures exposées au virus, associée à une augmentation du nombre de copies d'ADN provirales au sein des explants. En conclusion, nos résultats montrent que le testicule infecté de manière productive par le VIH in vitro, représente un réservoir potentiel pour le virus.
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Zazopoulos, Emmanuel. "Étude de la structure et de la fonction de la protéine Nef du virus d'immunodéficience humaine de type 1." Lyon 1, 1993. http://www.theses.fr/1993LYO1T078.

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Vergne, Laurence. "Génotypes et phénotypes du HIV-1 en Afrique : implications biologiques et thérapeutiques de la diversité génétique." Montpellier 2, 2003. http://www.theses.fr/2003MON20114.

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Sirois, Mélissa. "INTERACTIONS VIH-HÔTE : Modulation de l'expression de facteurs cellulaires." Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/28492/28492.pdf.

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Mary, Catherine. "Utilisation séquentielle des sites accepteurs d'épissage lors de l'expression du provirus HIV-1 : analyse par cartographie à la RNAse." Lyon 1, 1994. http://www.theses.fr/1994LYO1T236.

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Books on the topic "VIH (virus) – Reproduction (biologie)"

1

Morrie, Blumberg, Sinding Steven W, and Social Development Center (Chicago, Ill.), eds. Fertility, family planning, HIV/AIDS, and reproductive health: With emphasis on the Third World. Chicago: Social Development Center, 2004.

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M, Hardy Leslie, and Institute of Medicine (U.S.). Committee on Prenatal and Newborn Screening for HIV Infection., eds. HIV screening of pregnant women and newborns. Washington, D.C: National Academy Press, 1991.

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Virus Replication and Genome Interaction. The Company of Biologists Limited, 1987.

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Gender Policy And Hiv In China Catalyzing Policy Change. Springer, 2009.

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HIV Screening of Pregnant Women And Newborns. Natl Academy Pr, 1990.

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