China
Africa
Explore chapters and articles related to this topic
Interaction of Herpesviruses and Retroviruses
Published in Fred Rapp, Oncogenic Herpesviruses, 2019
As indicated in the preceding section, mixed infections with herpes- and retroviruses have been studied in recent years by several investigators under both natural and experimental conditions. In studies of MD in chickens, it was noted that the severity of the disease was influenced by the presence or absence of an avian leukosis virus (ALV). Mortality and gross tumor development were enhanced in chickens inoculated with MD herpesvirus (MDV) contaminated with ALV compared to those exposed to either virus alone.26,29 Furthermore, interference with the growth of MDV was observed in cell cultures; small compact foci were formed when MDV stocks contained ALV, whereas large foci developed when MDV stocks without ALV were used.30,31 Other avian retroviruses, including reticuloendotheliosis virus (REV), also had an effect on the response of chickens to MDV.32,33 However, evidence of pseudotype virions was not reported in these studies.
Erythroleukemia Cell Secretion and Erythroid Cell Differentiation-Inhibiting Factors
Published in Velibor Krsmanović, James F. Whitfield, Malignant Cell Secretion, 2019
Velibor Krsmanović, Jean-Michel Biquard
Experiments with temperature-sensitive mutants of AEV have shown that the v-erbB oncogene is essential for the induction of erythroleukemia.36-40 The v-erbB oncogene action interferes with the differentiation of early target erythroid precursors, such as BFU-E, which are blocked at a stage of differentiation close to the following CFU-E stage.5,41-43 The resulting erythroleukemia cells acquire, or preserve, a long-term self-renewing capacity in vitro and cannot synthesize hemoglobin.36,44,45 However, erythroid cells rendered erythroleukemic by a tsv-erbB mutant of AEV can be induced to synthesize hemoglobin and differentiate when the temperature is shifted from a permissive 36°C to a restrictive 42°C in the presence of erythropoietin.36,43,46 Erythroleukemia cells can also be generated with the avian leukosis virus (ALV), which does not harbor an oncogene, but specifically inserts itself into the host cell’s c-erbB protooncogene.47,48 Activation of the remaining proto-oncogene coding sequence by the viral LTR results in the production of a truncated, spontaneously signaling, EGF receptor, resembling, but slightly different from, the v-erbB product. An overview of the structural and biochemical properties of both v-erbB oncogene and c-erbB proto-oncogene can be found in Chapter 2.
Strategies to Accomplish Targeted Gene Delivery Employing Tropism-Modified Adenoviral Vectors
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
Joanne T. Douglas, David T. Curiel
Retroviral retargeting has also been achieved by genetic modifications to the envelope which introduce ligands directed to specific cell receptors. In experiments with avian leukosis virus (ALV), Valsesia-Wittmann et al. (28) substituted small segments of the variable regions of the receptor-binding domain of the envelope glycoprotein with a 16 amino acid ligand for cell surface integrin receptors. Some of these minimally modified envelope proteins were correctly processed and incorporated into virions. Moreover, the chimeric envelope proteins permitted the infection of target mammalian cells expressing the integrin receptor but resistant to wild-type ALV. Other groups have made larger modifications in fusing a ligand to the retroviral envelope protein for cell-specific targeting. The first success was reported by Kasahara et al. (29), who deleted a portion of the gene encoding the amino-terminal 150 amino acids of the envelope protein of ecotropic MoMLV and replaced it with sequences encoding the same number of amino acids from the blood protein erythropoietin (EPO). Retroviruses coated with this chimeric envelope protein in addition to wild-type ecotropic envelope protein were then generated from a producer cell line. Incorporation of the chimeric EPO-envelope proteins into intact virions was demonstrated by the fact these viruses were recognized by both anti-EPO and antienvelope antisera. The viruses carrying the EPO-envelope hybrid were shown to infect an EPO receptor-containing murine cell line with a greater than sixfold increase in efficiency over the parental wild-type retrovirus. The increase in infection was abolished by the addition of soluble EPO peptide at the time of infection, demonstrating that it was mediated by specific targeting of the EPO receptor by the EPO-envelope hybrid. The modified retrovirus also became specifically infectious for human cells carrying the EPO receptor while failing to infect other human cells. The same group subsequently applied this strategy for the retroviral targeting of human breast cancer cells via the peptide ligand heregulin (30). They showed that the modified ecotropic murine MoMLV viruses could cross species to specifically infect human breast cancer cells which overexpress receptors for heregulin, while cell lines with low or basal levels of these receptors were not infected.
Taishan Pinus massoniana Pollen Polysaccharides Enhance Immune Responses in Chickens Infected by Avian Leukosis Virus Subgroup B
Published in Immunological Investigations, 2018
Shifa Yang, Guiming Li, Zengcheng Zhao, Zhongli Huang, Jian Fu, Minxun Song, Shuqian Lin, Ruiliang Zhu
Serum ALV-B specific antibody was detected by ELISA. Approximately 0.5 mL of peripheral blood was collected weekly from Group I–V, respectively. Serum was separated and tested using Avian Leukosis Virus Antibody (ALV-A/B) Test Kit (IDEXX, USA). The absorbance of each sample at 630 nm was determined on an automated ELISA reader. All experiments were performed in replicate.
The discovery and development of IP3 receptor modulators: an update
Published in Expert Opinion on Drug Discovery, 2021
Jessica Gambardella, Marco B. Morelli, Xujun Wang, Vanessa Castellanos, Pasquale Mone, Gaetano Santulli
In 1993, two potent agonists of IP3Rs, adenophostins A and B, were isolated from the culture broth of Penicillium brevicompactum SANK 11991 and SANK 12177 [22]. In particular, they were more effective (nearly 10-fold) then the endogenous ligand, showing their potent action on all three IP3R subtypes. The structure of adenophostin A and B (Figure 1B) inspired many groups in synthesizing new ligands with additional modifications and properties. For instance, 3″-dephospho-AdA is an analog of AdA-A that lacks a phosphate group (5ʹ-P), as shown in Figure 1C. This synthetic compound was tested in DT40 cells (chicken B cell line derived from an avian leukosis virus-induced bursal lymphoma) devoid of native IP3R and stably expressing single subtypes of mammalian IP3Rs, showing that this analog is effective as the parental compound, and does not have a selective action for a specific IP3R subtype [23,24]. To better understand the role of the different phosphate groups and of the adenosine-motif in the interaction and activation of IP3Rs, another group synthesized all three possible bisphosphate analogs of AdA [25]. The study provided new information on the functional role of the chemical groups in the IP3 structure. In particular, the compound harboring 4,5 bisphosphates displayed an efficacy only 4-fold less potent than IP3; the 5-dephospho (1,4 bisphosphates) conserved an optimal activity, in line with the previous study on 3″-dephospho-AdA [23]. This evidence challenges the paradigm that the two vicinal bisphosphate groups (4,5) are critical for IP3-like activity. Conversely, the compound that was lacking the 2ʹ-AMP was 400-fold weaker than endogenous ligand [25]. This finding strongly suggests that adenosine has a key role in determining the affinity and the interaction with IP3R, while only two phosphates groups (even not adjacent) are enough to ensure the interaction. This brilliant investigation offered new and precious information for designing new compounds as potent IP3R agonists. Another potent IP3R ligand was synthesized conjugating an aromatic group at the 5ʹ-position of AdA, and this addition was well tolerated in the receptor binding [26]. The parental structure of AdA was also modified by replacing adenine with a triazole ring, without compromising the overall compound potency [27].
New strategies for treatment of COVID-19 and evolution of SARS-CoV-2 according to biodiversity and evolution theory
Published in Egyptian Journal of Basic and Applied Sciences, 2020
This article explains why plasma from COVID-19 recovering patients is used, as well as the use of some plants to treat COVID-19. The blood plasma contains antibodies and also contains antivirus microRNA as a result of infection previously. Plants and food also contain antioxidants, as well as microRNA, which play an important role as an anti-virus. Avian infectious bronchitis virus (IBV) is a coronavirus which infects chickens and causes severe economic losses to the poultry industry worldwide. MicroRNAs are important intracellular regulators and play a pivotal role in viral infections. It was found that overexpressed gga-miR-30d inhibited IBV replication [13]. In poultry, viral infections (e.g., Marek’s disease virus, avian leukosis virus, influenza A virus, and so on) can cause devastating mortality and economic losses. Because viruses are solely dependent on host cells to propagate, they alter the host intracellular microenvironment. MicroRNAs are crucial post-transcriptional regulators of gene expression in a wide spectrum of biological processes, including viral infection. Recently, microRNAs have been identified as key players in virus–host interactions [14]. RNA interference (RNAi)-based tools are used in multiple organisms to induce antiviral resistance through the sequence-specific degradation of target RNAs by complementary small RNAs. In plants, highly specific antiviral RNAi-based tools include artificial microRNAs (amiRNAs) and synthetic trans-acting small interfering RNAs (syn-tasiRNAs). syn-tasiRNAs have emerged as a promising antiviral tool allowing for the multi-targeting of viral RNAs through the simultaneous expression of several syn-tasiRNAs from a single precursor [15]. Multiple interplays between viral and host factors are involved in influenza virus replication and pathogenesis. Several small RNAs have recently emerged as important regulators of host response to viral infections., a critical role of Y-class small RNA and hsa-miR-1975 in host’s defense against influenza virus was demonstrated [16]. The interferon-inducible microRNA (miR) miR-128, a novel antiviral mediator that suppresses the expression of the host gene TNPO3, is known to modulate HIV-1 replication. Notably, they observed that anti-miR-128 partly neutralizes the IFN-mediated block of HIV-1. Elucidation of the mechanisms through which miR-128 impairs HIV-1 replication may provide novel candidates for the development of therapeutic interventions [17].