Effect of PDFGS on different stages of RSV lifecycle. Infective RSV gets into the respiratory tract following exposure to RSV viruses (1). RSV interacts with epithelial receptor proteins such as TLR4, CX3CR1 and HSPG using its RSV-F, RSV-G, and RSV-SH proteins (2). Intact RSV enters the host cytosol in an endosome (3). RSV nucleocapsid is released into the cytoplasm (5). Replication and transcription of RSV genome takes place at the inclusion bodies leading to the production of viral mRNA transcript (6) or full length positive sense antigenomes(7) following regulatory control by RSV M2-2. The positive sense antigenome is used as a template to generate the negative sense viral genome (8). The viral mRNA transcript is translated with the host mRNA translation apparatus (9). The negative sense viral RNA genome is packaged alongside with some viral proteins and other host factors required for RSV infectivity (10) this eventually buds off (11) into the pool of infective RSV. PDFGS reduced the cellular pool of infective RSV, suppressed RSV host receptor interaction as well as inhibited RSV internalization, replication, and transcriptional activities. PDFGS also lowered the levels of RSV mRNA transcripts as well as RSV protein. 18β-GA, 18β-glycyrrhetinic acid; CX3CR1, CX3C chemokine receptor 1; GSP, Grape seed proanthocyanidin; HSPG, Heparan sulfate proteoglycan; RSV, Respiratory syncytial virus; RSV-F, RSV fusion protein; RSV-G, Glycoprotein; RSV-L, RSV RNA-dependent RNA polymerase; RSV-M2-1, RSV matrix M2-1; RSV-M2-2, RSV matrix M2-2; RSV-N, RSV nucleoprotein; RSV-NS1, RSV non-structural protein 1; RSV-NS2, RSV non-structural protein 2; RSV-P, RSV phophoprotein; RSV-SH, RSV hydrophobic protein; TLR4, Toll-like receptor 4; Z. officinale, Zingiber officinale.