Beth writes:
I’ve followed with interest the discussions about polio in the weekly clinical updates and TWIV.
It seems to me that given the huge number of people in the NYC area, the constant influx of international travelers, and the likelihood of oral polio vaccine resulting in contagious infections, that vaccine-derived polio should be actively circulating in the metro area most of the time. Yet the municipal wastewater analysis page reports only one positive concerning sample in Rockland county in 2024. Does that mean that the wastewater surveillance system is not capturing a complete picture? Or is it more or less accurate and polio is not currently circulating in New York?
Thanks for your thoughts.
VR answer:
Before answering I would like to clarify what a negative result means. A negative result does not mean that there is no poliovirus RNA in the sample, it simply means that the amount of poliovirus specific RNA is beneath the level of detection.
Wastewater sampling for the detection of poliovirus in the United States is tightly controlled and restricted. This decision is based on the idea that wild type 2 poliovirus has been eradicated as defined by the WHO in 2016, and which I have previously mentioned on TWiV several times.
To prevent the re-introduction of wild type type 2 poliovirus in the world, WHO issued guidelines that stipulate that any form of type 2 poliovirus must be handled and transported under the global action plan for poliovirus containment guidelines (GAP III/IV). This document outlines procedures required to address/maintain the biosecurity and biocontainment of type 2 polioviruses. For instance, anyone exposed or infected with type 2 poliovirus must be quarantined and their stool must be collected and tested for the presence of infectious virus. Only after 2 consecutive stool tests are negative is the person taken out of quarantine. It is also because of these guidelines that it can never be proven that the administration of remdesivir cured the chronic excreter as the last stool samples could not be transported to the appropriate facility for analysis.
Because US has agreed to follow these WHO endorsed guidelines for type 2 poliovirus containment, several issues arise. Specifically, how does one place a community under containment if type 2 poliovirus is found within their environment? While the guidelines laid out in GAPIII/IV documents can be applied to laboratories and laboratory workers, they cannot be applied to geographical areas or large populations. Furthermore, since most poliovirus infections are asymptomatic, it is most difficult to identify patient zero.
With these caveats in mind, the US CDC decided that wastewater sampling should only be performed in communities with known transmission of poliovirus. Transmission is defined as the identification of a case of paralytic poliomyelitis. Therefore, there is no wastewater sampling in most entry points. In 2022 wastewater sampling was performed in communities that were known to associate with the Jewish community in Rockland where the patient was identified. This explanation is why wastewater collected from sheds in Dutchess county were tested.
This policy also states that wastewater sampling can cease after 6 weeks of negative sampling results. Consequently few wastewater sheds are continuously tested or tested at all for the presence of poliovirus.
John writes:
Drs. TWiV,
As of this week I can now count four people I’ve known, one quite well, that are now COVID stats. The virus got the first two before there were any vaccines. The latter two I suspect were unvaccinated if not outright anti-vaxxers.
Also this week my fully-vaccinated son got it for the second time. As an attorney with the Public Defender’s office, he’s probably often in the presence of the less-than-vaccinated. That aside, he’s feeling better now, but texted me that he’d hate to imagine how he would feel if he hadn’t been vaccinated.
And with that, this popped into my head. Remember Sy Syms, the purveyor of surplus stock men’s clothing warehouses? The slogan was, “An educated consumer is our best customer.”
So to paraphrase Sy Syms, I replied to my son: “An educated immune system is your best friend.”
Otherwise, in 1077, besides the science I was quite interested in hearing Sana Naderi’s story and how it is in Iran. Thanks for asking her about that.
Best wishes from a gray Greater Braddock that got little snow from yesterday’s event and stayed between 33 and 36F all day.
John
Michael writes:
I recently listened to episode 1075 about Marek’s disease virus in chickens. As discussed in the episode, the virus became more pathogenic in the early 1900’s after the advent of industrial chicken farming and the higher pathogenicity is associated with higher viral replication. It seems to me that in pre-industrial farming, a faster replicating but more pathogenic virus would have had a higher chance of killing the small flock it infected before being moved into another flock. But the rise of industrial farms with thousands of birds crammed into small spaces opened a new niche for faster replicating, more pathogenic viruses – it didn’t matter that they killed their hosts faster because there were so many hosts around. I’m not sure how you would test that hypothesis, but for the sake of argument let’s assume it’s true.
Around the 40 minute mark, Vincent states that a less fit virus is one that doesn’t replicate as much and that “over time you select for higher viral replication”. But if it’s true that industrial farming created a new niche for faster replicating viruses, that’s not entirely the case. Because faster replication is associated with higher virulence in the host in this particular virus, the faster replicating viruses are only more fit *in the new niche created by industrial farming*. And if you somehow transported a modern high virulence virus to the past, it would kill too many hosts and burn out before it could become more widely established. In that pre-industrial environment, a faster replicating but more pathogenic virus is more fit from an in-host viral replication standpoint but it’s less fit from an evolutionary standpoint because it’s too virulent to efficiently move between host populations.
I’m not a virologist, but it seems weird that fitness is just focused on viral replication without taking into consideration how that replication affects a virus’s ability to infect new hosts. A virus that kills its hosts too quickly to spread seems less fit regardless of how many copies it makes of itself.
Best regards,
Michael
—————————————–
Michael Skvarla, Ph.D.
Assistant Research Professor of Arthropod Identification
Department of Entomology
Penn State University
Matt writes:
First off, big fan of the TWIV podcast. I was turned on to TWIV by a random swim parent who said, in the early pandemic, you sound like these guys I listen to every week…have you ever heard of TWIV? She didn’t understand half of what you said but learned a lot anyway. I’m an NIH researcher (cardiovascular/eicosanoids mostly) and I enjoy the “in the weeds” coverage weekly. We’ve actually tested a drug to battle the host-response phase of COVID but we kind of had 1 shot at it, and after seeing the data we realized how bad a model the K18-hACE2 mouse really is. Way too harsh. Good for vaccine and RNA analog testing, bad if you think you might have something that offers mild improvement IMO.
I typically hate hearing my words read back on a podcast but I have a question I’m not sure anyone knows the answer to and that may be of general interest. Maybe you could paraphrase. My son caught some crud that some would call a ‘common cold’ before Christmas (no diagnosis of the crud, non COVID per Ab test, he got a flu shot this year, it seemed viral not bacterial). 2+ weeks later he still has a moderate lingering cough. To me the COVID data was revelatory in that the host-response phase isn’t just after the viral phase it seems post-viral (minimal remaining virus, minimal contagiousness). In hACE2-mice, viral copies drop 100-fold from day 2 to 4 (Winkler 2000 data) and mice start dying of practically sterile pneumonia on day 6-7. I’m wondering if we (you/they) have any idea about the length of viral phase vs host response phase for other viruses? Is there any data or a sensible common rule (5-days?) of isolation or masking to follow for common cold, flu, etc before one emerges back into the world? I sent him back to school 13 days after the first symptoms and I feel comfortable with that despite mild coughing. Another son and my wife are on a similar trajectory. Was I wrong to send him back to school?
Sorry if you’ve covered this, I’ve only listened to the past 200 shows or so :-).
Thanks,
Matt
Jonathan writes:
Traveling to rural Africa and just got the recommended 2-dose rabies pre-exposure shots, but can’t get a straight answer from my doctor on the true benefits. She said it “reduces the severity of the disease,” but since the ultimate symptom of rabies is almost always death, does that mean that the PrEP is sufficient on its own to render rabies survivable sans post-exposure treatment? She said I should seek treatment ASAP after an exposure, which seems logical, but since I’d be doing that anyway, what is the benefit of getting the PrEP at all?
Thank you!
Jonathan
Sonrisa writes:
Hi everyone,
I haven’t been listening to all your episodes, so not sure if someone has already shared this as a pick, but if not…. I couldn’t think of a better group of people to share this with 💕
Happy new year!
Sonrisa
Anonymous writes:
Wow! Human Cells Vibrate With Resonant Frequency and It’s Technically Audible