Native Parainfluenza Virus type 3 protein

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Parainfluenza Virus type 3 (PIV-3) is a member of the Paramyxoviridae family primarily affecting the respiratory system. The virus is enveloped with a spherical shape and possesses a genome composed of single-stranded negative-sense RNA. Important structural proteins include the hemagglutinin-neuraminidase (HN) fusion (F) and nucleocapsid (N) proteins facilitating cell entry and replication. The target's molecular mass varies depending on its structural proteins with the HN protein being approximately 66 kDa. PIV-3 predominantly expresses in epithelial cells of the upper and lower respiratory tract resulting in infection primarily affecting the respiratory regions.

Biological function summary

Parainfluenza Virus type 3 infects host cells by binding to sialic acid receptors aided by its hemagglutinin-neuraminidase protein transitioning viruses into the host. Following this the fusion protein facilitates the merging of viral and cellular membranes furthering virus entry. PIV-3 does not function as part of a larger protein complex but works through coordinated action of its proteins to establish infection and evade the host immune response. PIV-3 replicates in host cell cytoplasm where it hijacks the host's cellular machinery for its propagation.

Pathways

Parainfluenza Virus type 3 interacts with cellular pathways involved in viral entry and replication. It significantly engages pathways like the JAK-STAT signaling pathway where it antagonizes host immune response. Disruption in these pathways aids the virus in immune evasion enhancing its infectivity. Related proteins such as interferon regulatory factors are affected as PIV-3 inhibits signaling that would typically activate antiviral responses supporting viral persistence in the host.

Parainfluenza Virus type 3 is a major cause of respiratory illnesses including bronchiolitis and pneumonia particularly in infants and immunocompromised patients. Its presence is often found in conjunction with proteins like IL-6 where persistent viral infection exacerbates inflammatory responses. Conditions such as asthma exacerbations are also linked to PIV-3 with the virus contributing to airway hyperreactivity linking it to chronic airway obstruction. Due to these associations research into this target remains integral for the development of effective therapeutics and preventive strategies against respiratory infections.