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Order Mononegavirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The subfamily consists of 8 genera with 34 species. Regarding public healthcare, the most important and dangerous members of the orthoparamyxoviruses are Nipah virus of the Henipavirus genus, measles virus of the Morbillivirus genus, and human parainfluenza viruses (PIVs) 1 and 3 belonging to the Respirovirus genus. The orthoparamyxoviruses remain a serious burden of animal and poultry husbandry. Thus, peste des petits ruminants virus (PPRV) of the Morbillivirus genus causes disease affecting goats and sheep with up to 80% mortality rate in acute cases, and members of the Atlantic salmon aquaparamyxovirus species of the Aquaparamyxovirus genus are one of the causes of proliferative gill inflammation of salmons that leads to considerable losses in fishery. Sendai virus of the Respirovirus genus is responsible for a highly transmissible respiratory tract infection in mice and occasionally in pigs. Importantly, the rinderpest, or cattle plague, caused by rinderpest virus (RPV) of the Rinderpest morbillivirus species, genus Morbillivirus, was officially proclaimed by the UN Food and Agriculture Organization as fully eradicated, making it the second eliminated disease after smallpox in world history (A world without rinderpest 2014).
Gene Therapy and Small Molecules Used in the Treatment of Cystic Fibrosis
Published in Yashwant Pathak, Gene Delivery, 2022
Manish P. Patel, Uma G. Daryai, Mansi N. Athalye, Praful D. Bharadia, Jayvadan Patel
Sendai virus is a single-stranded RNA virus which belongs to the family of Paramyxoviridae. This virus is effective at transfecting airway epithelial cells, as sialic acid and cholesterol receptors are present on their apical surface (Burney and Davies, 2012). The key factors that are important for entry of virus into cells are the fusion (F) and hemagglutinin neuraminidase (HN) envelope proteins. The HN protein mediates virus–host cell attachment via sialic acid receptors whereas the F protein is essential in fusing virus and cell membranes, allowing the viral nucleocapsid to be released into the host cell (Griesenbach, Pytel, and Alton, 2015).
Liposome/Viral Hybrid Gene Delivery Systems
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
The next question is will virosomes work in vivo as a gene delivery system? Studies using Sendai virosomes suggest the answer to this question may be yes. Sendai virus (which is also called hemagglutinating virus of Japan; HVJ) is an enveloped virus with two surface proteins required for cell entry (11). An attachment protein mediates initial binding of the viral envelope to sialic acid residues on the cell membrane. A fusion protein mediates interactions between the viral envelope and the plasma membrane at neutral pH and thus introduces the viral genome into the cytoplasm. Sendai virosomes are manufactured in a slightly cruder fashion than RSV virosomes (12). Basically, the virus is propagated in chick eggs, the viral envelope harvested, and then lysed with detergent. Liposomes are prepared separately using various combinations of naturally occurring lipids. Plasmid DNA, the disrupted viral envelopes, and the liposomes are added together and, through physical methods, reconstituted viral envelopes encapsulating DNA are formed. These Sendai virosomes are large (1 μm in diameter) and contain extraneous viral components (but no active virus). In vitro, Sendai virosomes are much more efficient at delivering their payload to the interior of the cell than similarly constructed liposomes without viral envelope components (11).
Comparing respiratory syncytial virus and rhinovirus in development of post-viral airway disease
Published in Journal of Asthma, 2022
Deepika Narayanan, Mitchell H. Grayson
The potential mechanism of RSV and the immune pathway involved has been studied by using Sendai virus (SeV) in murine models; SeV is genetically related to RSV so the mechanism of disease with SeV could be representative of that seen with RSV. When mice are infected with Sendai virus (SeV), airway epithelial cells release type I interferons (IFNα/β), which, although having an antiviral effect, can often lead to epithelial cell death, with the dead epithelial cells being eventually engulfed by macrophages (13). The chemokine, CCL5 (RANTES) protects macrophages from virus-induced death, effectively allowing them to participate in phagocytic viral clearance (14). In propagating acute post-viral disease, CD49d + neutrophils are recruited to the airway, where they are able to induce expression of the high affinity IgE receptor, FcεRI, on lung conventional dendritic cells (DC) (13,15). Next, anti-SeV IgE is produced, which binds to the DC expressed FcεRI, and then can be crosslinked by SeV, leading to release of the chemokine CCL28 (13). CCL28 attracts Th2 cells that then produce IL-13 (16). IL-13 is involved in the propagation of chronic post-viral airway disease (13,17). However, Th2 IL-13 production is not required in the SeV model as IL-13 can be produced by iNKT (invariant natural killer T cells) and then by a subset of activated macrophages (13,17). Macrophage activation requires iNKT production of IL-13, and when macrophages are activated by IL-13 (through IL-13Rα), they produce more IL-13 (17). IL-13 acts on the airway to drive mucous cell metaplasia and airway hyperreactivity (17).
Inner ear gene delivery: vectors and routes
Published in Hearing, Balance and Communication, 2020
Chris Valentini, Betsy Szeto, Jeffrey W. Kysar, Anil K. Lalwani
Viral-mediated gene delivery into the inner ear has been applied to animal models using various viral vectors including adenovirus [3–6], adeno-associated virus [7–10], lentivirus [11–13], herpes simplex virus [14–16], vaccinia virus [16], and Sendai virus [17,18]. These viral vectors have previously been reviewed in detail [19]. While adenovirus (AdV) has high transfection efficiency and can accommodate large gene inserts, AdV-mediated gene therapy results in only transient expression of the transgene [20]. Lentivirus, a retrovirus, can achieve long term gene expression and can also accommodate large gene inserts, but may be immunogenic and ototoxic and carries the danger of random integration into the genome [12]. Herpes simplex virus (HSV), a neurotropic vector, has been used to transduce neurotropin-3 within mice to prevent cisplatin-induced damage [14]. Both HSV and vaccinia virus may elicit strong immune responses within the host. Sendai virus, of the paramyxoviridae family, is a promising vector because of its low pathogenicity, high transduction efficiency, and location exclusively within the cytoplasm [17,18]. However, this vector has been less thoroughly investigated for inner ear gene delivery compared to other viral vectors.
Novel prime-boost vaccine strategies against HIV-1
Published in Expert Review of Vaccines, 2019
Jean-Louis Excler, Jerome H. Kim
Sendai virus (SeV) is a RNA virus that can infect the upper respiratory tract. As a live viral vector that is not pathogenic in humans, SeV is genetically and antigenically related to hPIV-1, SeV antibodies cross-react with hPIV-1 antibodies that are present in most people. Priming with low- or high-dose Sendai (SeV)-Gag given at 0 and 4 months intranasally, an intramuscular Ad35 boost encoding HIV Gag, reverse transcriptase, integrase, and Nef (Ad35-GRIN); priming with Ad35-GRIN and boosting with SeV-Gag; and priming and boosting with a higher-dose SeV-Gag (NCT01705990). Gag-specific IFN-γ ELISpot responses were higher in groups primed with SeV-Gag and boosted with Ad35-GRIN than those after a single dose of Ad35-GRIN or SeV-Gag; responses persisted for ≥8 months after completion of the prime-boost regimen. Functional CD8+ T-cell responses with greater breadth, magnitude, and frequency in a viral inhibition assay were also seen after Ad35-GRIN boost, compared with those who received either vaccine alone. Ad35-GRIN+SeV-Gag did not boost T-cell counts but elicited the highest Gag-specific antibody titers. Mucosal antibody responses were sporadic [109]. This strategy less promising than expected is no longer pursued.