H5N1 samples from dairy cows in California and swine in Oregon have revealed the virus is not only infecting unexpected mammalian hosts.
It’s also mutating in ways that should set off alarms.
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S110N has been previously associated with changes in receptor specificity.
It means potentially enabling the virus to interact with alpha-2,6 receptors.
This is the evolutionary groundwork for a host range expansion.
A prerequisite for efficient human-to-human transmission.
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The fact that this mutation is found in dairy cows, a host not traditionally associated with influenza virus replication, raises critical questions about adaptation.
Dairy cows do not have the dense networks of alpha-2,3 receptors typically required for H5N1 replication.
The virus may be altering its binding preferences or utilizing alternative pathways to establish infection.
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The H5N1 outbreaks in the U.S. are no longer isolated incidents 🧵
Human cases in California and Missouri appear to share the same clade, B3.13.
This link raises the possibility of a novel transmission pathway.
Milk products.
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Both cases are classified as “unknown origin” since there is no evidence of direct exposure to poultry, which is the traditional reservoir for H5N1 in humans.
This lack of an avian connection points to a new, potentially mammalian host.
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The detection of B3.13 in two states separated by over 1,500 miles points to a virus that may already be circulating beyond localized clusters.
The virus is not limited to isolated spillover events from birds but could be spreading through a shared pathway.
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H5N1 is no longer a distant threat confined to birds.
It’s becoming a clear and present danger to humanity.
It’s closing the gap between animal-to-human transmission and the one thing we all dread:
Sustained human-to-human spread.
🧵
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The findings on H5N1’s 2022 strain are a brutal warning.
Rhis virus is becoming more adept at targeting humans.
It binds to cells in the human respiratory tract with greater efficiency than H5N1 from 2005, and even rivals the attachment and replication ability of H3N2.
Which caused the deadly 1968 pandemic.
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We’ve seen this play out before.
In 1918, an avian-origin H1N1 virus mutated to spread between humans.
It killed an estimated 50 million people worldwide.
The 1968 H3N2 pandemic killed over a million people.
Both started with zoonotic viruses slowly adapting to human hosts.
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The teenager in British Columbia is a preview of what pandemic risk truly looks like 🧵
A single critical case, no clear source, and the absence of a transmission chain.
It’s a script we know too well, and one we’re doing nothing to rewrite.
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A single human infected with H5N1, a virus notorious for its catastrophic mortality in avian and human hosts, now lies in airborne isolation, lungs failing, held alive by machines.
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The case has already revealed two mutations in the virus.
One making it better at binding to human cells, the other driving infection deep into the lungs.
They are evidence of a virus edging closer to a species barrier it was never supposed to cross.
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