tetano
Editor, Senior Moderator
mBio
. 2024 Jan 11:e0220323.
doi: 10.1128/mbio.02203-23. Online ahead of print. Inhibiting influenza virus transmission using a broadly acting neuraminidase that targets host sialic acids in the upper respiratory tract
Mila B Ortigoza[SUP] 1 2 [/SUP], Catherina L Mobini[SUP] 2 [/SUP], Hedy L Rocha[SUP] 1 [/SUP], Stacey Bartlett[SUP] 1 [/SUP], Cynthia A Loomis[SUP] 3 [/SUP], Jeffrey N Weiser[SUP] 2 [/SUP]
Affiliations
Influenza virus transmission studies have historically focused on viral mutations that alter hemagglutinin binding to sialic acid (SA) receptors in vitro. However, SA binding preference does not fully account for the complexities of influenza A virus transmission in humans. Our previous findings reveal that viruses that are known to bind α2,6-SA in vitro have different transmission kinetics in vivo, suggesting that diverse SA interactions may occur during their life cycle. In this study, we examine the role of host SA on viral replication, shedding, and transmission in vivo. We highlight the critical role of SA presence during virus shedding, such that attachment to SA during virion egress is equally important as detachment from SA during virion release. These insights support the potential of broadly acting neuraminidases as therapeutic agents capable of restraining viral transmission in vivo. Our study unveils intricate virus-host interactions during shedding, highlighting the necessity to develop innovative strategies to effectively target transmission.
Keywords: DAS181; Streptococcus pneumoniae; infant mouse model; influenza; neuraminidase; shedding; sialic acid; transmission.
. 2024 Jan 11:e0220323.
doi: 10.1128/mbio.02203-23. Online ahead of print. Inhibiting influenza virus transmission using a broadly acting neuraminidase that targets host sialic acids in the upper respiratory tract
Mila B Ortigoza[SUP] 1 2 [/SUP], Catherina L Mobini[SUP] 2 [/SUP], Hedy L Rocha[SUP] 1 [/SUP], Stacey Bartlett[SUP] 1 [/SUP], Cynthia A Loomis[SUP] 3 [/SUP], Jeffrey N Weiser[SUP] 2 [/SUP]
Affiliations
- PMID: 38206008
- DOI: 10.1128/mbio.02203-23
Influenza virus transmission studies have historically focused on viral mutations that alter hemagglutinin binding to sialic acid (SA) receptors in vitro. However, SA binding preference does not fully account for the complexities of influenza A virus transmission in humans. Our previous findings reveal that viruses that are known to bind α2,6-SA in vitro have different transmission kinetics in vivo, suggesting that diverse SA interactions may occur during their life cycle. In this study, we examine the role of host SA on viral replication, shedding, and transmission in vivo. We highlight the critical role of SA presence during virus shedding, such that attachment to SA during virion egress is equally important as detachment from SA during virion release. These insights support the potential of broadly acting neuraminidases as therapeutic agents capable of restraining viral transmission in vivo. Our study unveils intricate virus-host interactions during shedding, highlighting the necessity to develop innovative strategies to effectively target transmission.
Keywords: DAS181; Streptococcus pneumoniae; infant mouse model; influenza; neuraminidase; shedding; sialic acid; transmission.