Host protein linked to a shared step in respiratory virus spread
A study published in Nature reports that the host protein myoferlin is involved in a late step used by several enveloped RNA viruses to move their genetic cargo inside infected cells. The findings focus on how viruses traffic viral ribonucleoprotein (vRNP) complexes—packages of viral RNA and proteins—towards the cell surface before they are assembled into new virus particles and released.
Important respiratory viruses, including influenza A virus (IAV) and respiratory syncytial virus (RSV), are known to take advantage of the Rab11 endosomal recycling pathway. In polarized epithelial cells, this pathway can support the delivery of viral components to the apical surface, aiding the exit of newly formed viruses.
Rab11 vesicles and remodelling late in infection
Late in infection, Rab11-containing vesicles are described as transporting vRNP complexes towards the cell surface, where packaging and budding occur. The study notes that virus-infected cells do not simply rely on standard Rab11-positive recycling endosomes. Instead, during IAV infection, cells generate remodelled Rab11-containing vesicles suited to viral transport.
While Rab11 is a recognised part of this process, the authors state that additional host factors shared across different viruses’ vRNP trafficking vesicles have been unclear.
Myoferlin found with vRNPs and Rab11 during late stages
The researchers report that myoferlin associates with IAV vRNPs in the cytoplasm and that myoferlin is observed colocalising with Rab11 during late stages of infection. This places myoferlin within the cellular transport system used to deliver viral material to the cell surface.
The study further reports that the same role is conserved in other viruses that use similar intracellular logistics. Along with influenza, myoferlin is described as participating in late-stage vRNP trafficking for RSV and Sendai virus (SeV).
Potential link to endosomal biogenesis proteins
The authors also connect myoferlin to the recruitment of EHD family proteins, which are involved in endosomal biogenesis. In the study’s account, myoferlin likely helps bring EHD proteins to the distinct Rab11-containing endosomes that carry vRNPs, supporting the formation or function of these virus-adapted trafficking vesicles.
Overall, the study describes myoferlin as a crucial host factor that supports the movement of viral genetic cargo to the cell surface, contributing to the replication and spread of influenza, RSV and Sendai virus. The researchers highlight the shared dependence on this host component as a potential common vulnerability that could inform future antiviral strategies.