Pneumoviral Protein Expression Vectors
Pneumovirus includes respiratory syncytial virus. The respiratory syncytial viral protein expression vectors are derived from NCBI reference sequence NC_001803.1. All of the expression vectors are codon optimized for mammalian cell expression. Choose to add a GFP or his tag to the C terminal end of any protein. A CMV promoter is used for mammalian cell expression and the backbone contains a selection marker for Geneticin (G418). All non-tagged glycoprotein expression vectors have been functionally validated using pseudotyped viral particles.
Respiratory syncytial virus (RSV) is a filamentous enveloped, negative sense, and single stranded RNA virus that causes infections of the respiratory tract in people of all ages. However, RSV is more commonly found in children and older adults as it is responsible for 1 in every 50 deaths among children who are 5 years or younger. In those groups of people, RSV infection could lead to more serious illnesses such as bronchitis, pneumonia, or coup. RSV is divided into two antigenic subtypes (A & B) based on the reactivity of the F and G surface proteins to monoclonal antibodies. Subtype A is more prevalent and more virulent because it has higher viral loads and faster transmission time. RSV genome contains 10 genes encoding 11 proteins. There are four nucleocapsid proteins (nucleoprotein N, phosphoprotein P, large polymerase subunit L, transcription anti-termination factor M2-1), three membranous envelope glycoproteins (fusion F, attachment G, and small hydrophobic SH), two nonstructural proteins (NS1 and NS2), one viral assembly factor (the matrix protein M), and an RNA regulatory factor M2-2. RSV infects the target cell via the attachment of G protein, followed by fusion of the virus and host cell membrane mediated by F protein, resulting in release of the genomic RNA into the cytoplasm. There are several ways in which the G protein attaches to the host cells (epithelial cells). One way includes the G protein binding to glycosaminoglycans, such as heparan sulfate, on the surface of host cells. Another way is through the binding of the CX3C fractalkine-like motif in the G protein to the chemokine receptor 1 (CX3CR1) on the surface of ciliated bronchial host cells. After attachment, the F protein, which exists in multiple conformational forms, undergoes conformational changes, and enables the protein to insert itself into the host cell membrane, leading to the fusion of viral and host cell membranes.