Background
Influenza A virus (IAV) neuraminidase (NA) cleaves sialic acids (Sias) from glycans. Inhibiting NA with oseltamivir suppresses both viral infection, and viral release from cultured human airway epithelial cells. The role of NA in viral exit is well established: it releases budding virions by cleaving Sias from glycoconjugates on infected cells and progeny virions. The role of NA in viral entry remains unclear. Host respiratory epithelia secrete a mucus layer rich in heavily sialylated glycoproteins; these could inhibit viral entry by mimicking sialylated receptors on the cell surface. It has been suggested that NA allows influenza to penetrate the mucus by cleaving these sialylated decoys, but the exact mechanism is not yet established.

/pdf/influenza-a-penetrates-host-mucus-by-cleaving-sialic-acids-3who9588ar.pdf

Influenza A penetrates host mucus by cleaving sialic acids with neuraminidase

Gene transfer to the lung: lessons learned from more than 2 decades of CF gene therapy.

The pig represents a useful, large experimental model for biomedical research. Recently, it has been used in different areas of biomedical research. The aim of this study was to review the basic anatomical structures of the head region in the pig in relation to their use in current research. Attention was focused on the areas that are frequently affected by pathological processes in humans: the oral cavity with teeth, salivary gland, orbit, nasal cavity and paranasal sinuses, maxilla, mandible and temporomandibular joint. Not all of the structures have an equal morphology in the pig and human, and these morphological dissimilarities must be taken into account before choosing the pig as an experimental model for regenerative medicine.

https://journals.sagepub.com/doi/pdf/10.1258/la.2012.012062

The pig as an experimental model for clinical craniofacial research

Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene that encodes a cAMP-regulated anion channel. Although CF is a multi-organ system disease, most people with CF die of progressive lung disease that begins early in childhood and is characterized by chronic bacterial infection and inflammation. Nearly 90% of people with CF have at least one copy of the ΔF508 mutation, but there are hundreds of CFTR mutations that result in a range of disease severities. A CFTR gene replacement approach would be efficacious regardless of the disease-causing mutation. After the discovery of the CFTR gene in 1989, the in vitro proof-of-concept for gene therapy for CF was quickly established in 1990. In 1993, the first of many gene therapy clinical trials attempted to rescue the CF defect in airway epithelia. Despite the initial enthusiasm, there is still no FDA-approved gene therapy for CF. Here we discuss the history of CF gene therapy, from the discovery of the CFTR gene to current state-of-the-art gene delivery vector designs. While implementation of CF gene therapy has proven more challenging than initially envisioned; thanks to continued innovation, it may yet become a reality.

https://ir.uiowa.edu/cgi/viewcontent.cgi?article=1026&context=pediatrics_pubs

Cystic Fibrosis Gene Therapy: Looking Back, Looking Forward.

Adeno-associated virus (AAV) was fi rst discovered as a contaminant of adenovirus stocks in the 1960s. The development of recombinant AAV vectors (rAAV) was facilitated by early studies that generated infectious molecular clones, determined the sequence of the genome, and defi ned the genetic elements of the virus. The refi nement of methods and protocols for the production and application of rAAV vectors has come from years of studies that explored the basic biology of this virus and its interaction with host cells. Interest in improving vector performance has in turn driven studies that have provided tremendous insights into the basic biology of the AAV lifecycle. In this chapter, we review the background on AAV biology and its exploitation for vectors and gene delivery.

Adeno-Associated Virus

Differences between rodent and human airway cell biology have made it difficult to translate recombinant adeno-associated virus (rAAV)-mediated gene therapies to the lung for cystic fibrosis (CF). As new ferret and pig models for CF become available, knowledge about host cell/vector interactions in these species will become increasingly important for testing potential gene therapies. To this end, we have compared the transduction biology of three rAAV serotypes (AAV1, 2 and 5) in human, ferret, pig and mouse-polarized airway epithelia. Our results indicate that apical transduction of ferret and pig airway epithelia with these rAAV serotypes closely mirrors that observed in human epithelia (rAAV1> rAAV2 ≅ rAAV5), while transduction of mouse epithelia was significantly different (rAAV1 > rAAV5 ≫ rAAV2). Similarly, ferret, pig and human epithelia also shared serotype-specific differences in the polarity (apical vs basolateral) and proteasome dependence of rAAV transduction. Despite these parallels, N-linked sialic acid receptors were required for rAAV1 and rAAV5 transduction of human and mouse airway epithelia, but not ferret or pig airway epithelia. Hence, although the airway tropisms of rAAV serotypes 1, 2 and 5 are conserved better among ferret, pig and human as compared to mouse, viral receptors/co-receptors appear to maintain considerable species diversity.

Comparative biology of rAAV transduction in ferret, pig and human airway epithelia.

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Comparative biology of rAAV transduction in ferret, pig and human airway epithelia.