TY - JOUR
T1 - NB protein does not affect influenza B virus replication in vitro and is not required for replication in or transmission between ferrets
AU - Elderfield, Ruth A.
AU - Koutsakos, Marios
AU - Frise, Rebecca
AU - Bradley, Konrad
AU - Ashcroft, Jonathan
AU - Miah, Shanhjahan
AU - Lackenby, Angie
AU - Barclay, Wendy S.
N1 - Publisher Copyright:
© 2015 The Authors.
PY - 2016/3
Y1 - 2016/3
N2 - The influenza B virus encodes a unique protein, NB, a membrane protein whose function in the replication cycle is not, as yet, understood. We engineered a recombinant influenza B virus lacking NB expression, with no concomitant difference in expression or activity of viral neuraminidase (NA) protein, an important caveat since NA is encoded on the same segment and initiated from a start codon just 4 nt downstream of NB. Replication of the virus lacking NB was not different to wild-type virus with full-length NB in clonal immortalized or complex primary cell cultures. In the mouse model, virus lacking NB induced slightly lower IFN-α levels in infected lungs, but this did not affect virus titres or weight loss. In ferrets infected with a mixture of viruses that did or did not express NB, there was no fitness advantage for the virus that retained NB. Moreover, virus lacking NB protein was transmitted following respiratory droplet exposure of sentinel animals. These data suggest no role for NB in supporting replication or transmission in vivo in this animal model. The role of NB and the nature of selection to retain it in all natural influenza B viruses remain unclear.
AB - The influenza B virus encodes a unique protein, NB, a membrane protein whose function in the replication cycle is not, as yet, understood. We engineered a recombinant influenza B virus lacking NB expression, with no concomitant difference in expression or activity of viral neuraminidase (NA) protein, an important caveat since NA is encoded on the same segment and initiated from a start codon just 4 nt downstream of NB. Replication of the virus lacking NB was not different to wild-type virus with full-length NB in clonal immortalized or complex primary cell cultures. In the mouse model, virus lacking NB induced slightly lower IFN-α levels in infected lungs, but this did not affect virus titres or weight loss. In ferrets infected with a mixture of viruses that did or did not express NB, there was no fitness advantage for the virus that retained NB. Moreover, virus lacking NB protein was transmitted following respiratory droplet exposure of sentinel animals. These data suggest no role for NB in supporting replication or transmission in vivo in this animal model. The role of NB and the nature of selection to retain it in all natural influenza B viruses remain unclear.
UR - http://www.scopus.com/inward/record.url?scp=84960462075&partnerID=8YFLogxK
U2 - 10.1099/jgv.0.000386
DO - 10.1099/jgv.0.000386
M3 - Article
C2 - 26703440
AN - SCOPUS:84960462075
SN - 0022-1317
VL - 97
SP - 593
EP - 601
JO - Journal of General Virology
JF - Journal of General Virology
IS - 3
ER -