Reports of mass death events in sea mammals continue to pour in from around the world. The situation along the coast of Chile is particularly grim as evidenced in the following report.
SERNAPESCA [National Fisheries and Aquaculture Service] reported that
strandings continue to occur along the Chilean coast. In total, 3347
specimens of sea lions, 958 Humboldt penguins, 16 marine otters, 15
porpoises, and 11 Chilean dolphins have already been reported. The
northern macrozone concentrates the highest mortality of these
animals, with the region of Arica and Parinacota leading the ranking
with 1486 dead animals, followed by Antofagasta with 752, Atacama with
623, Tarapacá with 484, and Coquimbo with 412. On the other hand, in
southern Chile, the Biobío region stands out with 200 dead marine
animals, associated with the avian influenza epidemic.
Soledad Tapia, National Director of SERNAPESCA, said that "we have
already recorded 2415% more dead stranded marine animals than last
year [2022] in the country, and this is attributed to the phenomenon
of HPAI that we are facing not only in Chile but also in various
countries in South and North America, Europe, and Asia."
The Humboldt penguin is a protected species, in decline for years, and found only in a limited range. The Chilean government is estimating that about 10% of the total population has died recently from this highly pathogenic Avian Influenza A. The number of dead Sea-lions continues to increase, and new species of sea mammals have been infected and killed, as the virus continues to expand its range of potential victims. Of course we still don’t know if there is spread from one mammal to another, or if all of these sea mammals are infected through their proximity to H5N1 infected birds.
What does H5N1 need to do in order to cause transmission between humans? For starters, the virus needs to replicate in human cells. The RNA polymerase of the virus needs the co-operation of a human enzyme to assist its function. As a result of Gain of Function research from more than a decade ago—which was temporarily halted but now allowed if it passes muster with the Department of HHS—we know that a particular mutation, E627K, of the viral PB2 polymerase enzyme makes this process much more efficient. That mutation was recently confirmed in a human patient infected with H5N1 in South America. Replicating in human cells is one thing, but in order for the virus to be transmissible from one human to another, it needs to acquire mutations which allow its hemagglutinin protein to better latch onto human cell’s sialic acid surface molecules. This is analogous to the SARS2-Cov19 Spike fitting into the lock of our ACE2 molecules. Right now the virus is occasionally able to do that (sporadic human infections prove the point), but the process is not efficient, and requires large exposure to high quantities of virus. That is why the people infected so far have had close contact with infected birds. The last requirement for H5N1 to make the transition to a human adapted virus, is a bit more esoteric but important. As we cough, speak or breath, tiny droplets are expelled containing the virus and other components of our respiratory secretions. If these droplets travel directly into the mouth or eyes of another person, the virus has no difficulty—but when they hang around in the air and begin to evaporate, the acidity in the drop increases and the surface proteins of the virus change shape. That alteration causes the viral surface protein to loose the ability to dock with the critical sialic acid molecules on our cells needed for infection. COVID was so brutally efficient at transmission because the virus remains infectious for hours suspended in minute droplets circulating on air currents. As I have discussed, one of the major errors of our CDC and the WHO, was the failure to acknowledge multiple lines of published evidence from the environmental science and engineering literature demonstrating that COVID was aerosol spread. Pig’s immune systems have some similarity to ours when it comes to resistance to Influenza. They may end up being the canary in the coal mine for evidence of sustained mammalian transmission. H5N1 has passed one of three hurdles on the path toward being a giant human problem. Persisting in saying that, “this is an Avian virus, which just happens to be infecting more and more mammalian species, but represents a low risk for human pandemic”—might just be another major error for CDC and WHO.
In my last post I highlighted the rise of Arcturus XBB.1.16 in India and Southeast Asia. The CDC NowCast data this Friday confirms its rapid ascent in the US. With three data points in hand it appears to me this variant has a doubling time around 10 days. That would put it on track to replace XBB.1.5, “Kraken”, as the dominant COVID within about one month. “Who cares”, is a completely legitimate response. Countering this is the fact that cases are rising in India faster than they have in almost a year. In the US we have largely given up testing, even for illness, let alone exposure—so we have very little guidance on disease burden, until there is an increase in hospitalizations. What we need to be vigilant about at this point, is the arrival of a COVID variant with a bit more bite and increase in severe disease. Arcturus is showing us that even at this late date in the Pandemic, a single mutation in the Spike protein can cause the virus to be significantly more infectious, and cause an increase in re-infections. It would be naive to dismiss the possibility of the virus developing mutations which would confer more rapid and higher level viral replication as a means to increased spread. That could lead to another Delta type surge with increased severity of disease. Let’s hope not, and continue to “Know your enemy”, even as the official public health emergency ends. While it is true that the eventual course of a pandemic is for the new pathogen to become less severe over time, this is not necessarily a linear process.
The last item for consideration today is a recent report of several cases of longer Paxlovid courses being effective in terminating persistent COVID infection in severely immune compromised persons. Remember that about 200 people per day in the US continue to die from the now Endemic, and that’s more than a bad Influenza year. People at very high risk include those that have received treatments for cancers and other diseases which destroy B lymphocytes—the cells that produce antibodies. These 4 case reports show that the patients with months of continuous COVID infection and symptoms were cured with longer (mostly 21 day) courses of Paxlovid. In several cases this was after failure of remdesivir or molnupiravir, and standard short course Paxlovid. Paxlovid has been a very effective agent, even if the short course of 5 days sanctioned by the FDA sometimes was followed by viral relapse. With monoclonal antibodies out of the picture now, Paxlovid is the last viable treatment for some folks in tough situations. Last May the CEO of Pfizer suggested people experiencing a viral relapse after 5 days of Paxlovid could take a second course. He was quickly corrected by the FDA, which said there was no scientific data to support that. More importantly when a drug is allowed by EUA (emergency use authorization), doctors are not allowed to use it “off label”, meaning in any way which deviates from the FDA directive. That of course didn’t stop Dr. Fauci (a guy who knows a thing or two about anti-viral medications) from taking a second course when he relapsed. Now we have some limited data that people with severe immune compromise can be cured from persistent infection with Paxlovid.
Thanks for your attention. Please forward to any sentient creature, mammalian or otherwise, who you think would be interested. Remember the only problem with political jokes…is that they keep getting elected. What we need to remember for the next Pandemic was gifted to us by Ben Franklin, “If we do not hang together, we will most certainly hang separately”.
Could you speak t the calculations made as to risk/benefit ratio on "gain of function" research?