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Lack of transmission of a human influenza virus with avian receptor specificity between ferrets is not due to decreased virus shedding but rather a lower infectivity in vivo.
J Gen Virol. 2011 Aug; 92(Pt 8):1822-31.JG

Abstract

Influenza virus attaches to host cells by sialic acid (SA). Human influenza viruses show preferential affinity for α2,6-linked SA, whereas avian influenza viruses bind α2,3-linked SA. In this study, mutation of the haemagglutinin receptor-binding site of a human H3N2 influenza A virus to switch binding to α2,3-linked SA did not eliminate infection of ferrets but prevented transmission, even in a co-housed model. The mutant virus was shed from the noses of ferrets directly inoculated with virus in the same amounts and for the same length of time as wild-type virus. Mutant virus infection was localized to the same anatomical regions of the upper respiratory tract of directly inoculated animals. Interestingly, wild-type virus was more readily neutralized than the mutant virus in vitro by ferret nasal washes containing mucus. Moreover after inoculation of equal doses, the mutant virus grew poorly in ex vivo ferret nasal turbinate tissue compared with wild-type virus. The dose of mutant virus required to establish infection in the directly inoculated ferrets was 40-fold higher than for wild-type virus. It was concluded that minimum infectious dose is a predictor of virus transmissibility and it is suggested that, as virus passes from one host to another through stringent environmental conditions, viruses with a preference for α2,3-linked SA are unlikely to inoculate a new mammalian host in sufficient quantities to initiate a productive infection.

Authors+Show Affiliations

Department of Virology, Imperial College London, St Mary's Campus, London W2 1PG, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21508186

Citation

Roberts, Kim L., et al. "Lack of Transmission of a Human Influenza Virus With Avian Receptor Specificity Between Ferrets Is Not Due to Decreased Virus Shedding but Rather a Lower Infectivity in Vivo." The Journal of General Virology, vol. 92, no. Pt 8, 2011, pp. 1822-31.
Roberts KL, Shelton H, Scull M, et al. Lack of transmission of a human influenza virus with avian receptor specificity between ferrets is not due to decreased virus shedding but rather a lower infectivity in vivo. J Gen Virol. 2011;92(Pt 8):1822-31.
Roberts, K. L., Shelton, H., Scull, M., Pickles, R., & Barclay, W. S. (2011). Lack of transmission of a human influenza virus with avian receptor specificity between ferrets is not due to decreased virus shedding but rather a lower infectivity in vivo. The Journal of General Virology, 92(Pt 8), 1822-31. https://doi.org/10.1099/vir.0.031203-0
Roberts KL, et al. Lack of Transmission of a Human Influenza Virus With Avian Receptor Specificity Between Ferrets Is Not Due to Decreased Virus Shedding but Rather a Lower Infectivity in Vivo. J Gen Virol. 2011;92(Pt 8):1822-31. PubMed PMID: 21508186.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lack of transmission of a human influenza virus with avian receptor specificity between ferrets is not due to decreased virus shedding but rather a lower infectivity in vivo. AU - Roberts,Kim L, AU - Shelton,Holly, AU - Scull,Margaret, AU - Pickles,Raymond, AU - Barclay,Wendy S, Y1 - 2011/04/20/ PY - 2011/4/22/entrez PY - 2011/4/22/pubmed PY - 2011/9/20/medline SP - 1822 EP - 31 JF - The Journal of general virology JO - J. Gen. Virol. VL - 92 IS - Pt 8 N2 - Influenza virus attaches to host cells by sialic acid (SA). Human influenza viruses show preferential affinity for α2,6-linked SA, whereas avian influenza viruses bind α2,3-linked SA. In this study, mutation of the haemagglutinin receptor-binding site of a human H3N2 influenza A virus to switch binding to α2,3-linked SA did not eliminate infection of ferrets but prevented transmission, even in a co-housed model. The mutant virus was shed from the noses of ferrets directly inoculated with virus in the same amounts and for the same length of time as wild-type virus. Mutant virus infection was localized to the same anatomical regions of the upper respiratory tract of directly inoculated animals. Interestingly, wild-type virus was more readily neutralized than the mutant virus in vitro by ferret nasal washes containing mucus. Moreover after inoculation of equal doses, the mutant virus grew poorly in ex vivo ferret nasal turbinate tissue compared with wild-type virus. The dose of mutant virus required to establish infection in the directly inoculated ferrets was 40-fold higher than for wild-type virus. It was concluded that minimum infectious dose is a predictor of virus transmissibility and it is suggested that, as virus passes from one host to another through stringent environmental conditions, viruses with a preference for α2,3-linked SA are unlikely to inoculate a new mammalian host in sufficient quantities to initiate a productive infection. SN - 1465-2099 UR - https://www.unboundmedicine.com/medline/citation/21508186/Lack_of_transmission_of_a_human_influenza_virus_with_avian_receptor_specificity_between_ferrets_is_not_due_to_decreased_virus_shedding_but_rather_a_lower_infectivity_in_vivo_ L2 - http://jgv.microbiologyresearch.org/pubmed/content/journal/jgv/10.1099/vir.0.031203-0 DB - PRIME DP - Unbound Medicine ER -