Monthly Archives: May 2026

There seems to be a public perception that the COVID pandemic is over and has turned into just another upper respiratory disease. That’s simply not the case as is evidenced in data such as wastewater, excess mortality, pediatric hospitalizations, and the prevalence of long COVID.

Earlier, I’ve addressed the false notion that the omicron strain is mild. It isn’t, However, it’s fair to ask why hospitalizations are down. There are a number of reasons for this that work synergistically together.

Evolution

First, we haven’t had a major new variant emerge in some time (genetic shift, such as delta and the first round of omicron). What has been occurring are small genetic changes in omicron (genetic drift). However, even drift can create havoc as evidenced by the resurgence in Manaus, Brazil early in the pandemic. Much of the population had been infected with the original strain of the virus only to be reinfected by the gamma variant (P.1), leading to the need for mass graves. This was also an early warning that herd immunity, pushed by both some in the current administration (Dr. Jay Bhattacharya at the NIH and Dr. Vinay Prasad who briefly held a role at the FDA) as well as in the Great Barrington Declaration, wouldn’t work, thus ending the notion of natural herd immunity as a useful approach to the end of the pandemic, in spite of the extensive disease and death that would cause in the process.

While it doesn’t bring the pandemic to an end, the result of that is immune systems among the population that either have some residual immune response either to infection or vaccination. However, it’s important to keep in mind that the robustness of that response fades over time.

The genetic drift has been relatively slow changes to the omicron strain over time since it emerged. When the virus proteins stay relatively stable, that allows whatever residual response in the immune system to more readily identify the virus and react. That could easily change with BA.3.2 (Cicada), which has over 30 mutations to the spike protein alone, but this is still framed as risk, not certainty as an outcome.

Immunity

The immune response reduces susceptibility more than infectiousness, but it provides some of both. If the immune system already has neutralizing antibodies and primed memory B/T cells, the virus faces an immediate immune response. This is why it’s better to get vaccinated as opposed to relying on disease driven immunity. Getting a disease to gain some immune protection from that disease is insanity.

There are a few outcomes from a primed immune response:

• It shortens the period of high viral replication
• It reduces peak viral load
• It reduces the duration of viral shedding
• It reduces the chance of severe inflammatory cascades, such as a cytokine storm

It should also be noted that the waning of immunity varies. For example, mucosal immunity wanes the fastest and T-cell memory lasts the longest. This has implications for both infection and vaccine derived immunity related to how recently either occurred. Immune imprinting could also play a role in response to new variants because it biases the immune system to prefer updating old defenses rather than creating new ones from scratch, which is a risk for those who get COVID vaccines frequently.

Severity

When the immune system is primed, the virus will have less time to replicate before the adaptive immune system fully activates. This reduces the chances of a number of factors that contribute to the severity of disease and need for hospitalization:

• Tissue damage (the virus binds to ACE-2 receptors, which are found in most tissues except most immune cells, red blood cells, bone marrow stem cells, and the lens of the eye).
• Inflammatory response
• Major complications (hypoxia, blood clots, and organ damage/failure)

The take home is that omicron’s intrinsic virulence hasn’t meaningfully changed; what has changed is its effective virulence in a population with widespread immune priming, which makes the same virus appear less severe than it actually is.

An Exponential Illustration

It’s estimated that it takes between 100-1,000 infectious SARS-CoV-2 virions to cause infection to 50% of human hosts. When a viral particle infects a human cell, depending on the type of cell, it creates 1,000-100,000 infectious particles when the cell ruptures. That should clearly illustrate why reducing the number of infected cells early on is so important. Each of those newly produce viruses goes on to infect other cells in the body until the immune system can get it under control. When the immune system has been primed, it has a head start on doing so. That leads to less virus being produced, thereby less tissue damage and less viral load, meaning less spread to others.

For example, I’ll use the midpoint of each range to illustrate the consequences of a few generations of infection within the body without the benefit of an immune response.

• Initial infection: 500 viruses.
• First generation: 500 x 50,000 = 25,000,000
• Second generation: 25 million x 50,000 = 1.25 trillion

Given that the human body has about 30-40 trillion cells, it’s a good thing that we have immune system to stop this kind of exponential growth. It’s also worth mentioning that many of the virions produced in the cell won’t be infectious, but that doesn’t change the mathematical illustration.

Most importantly, SARS-CoV-2 replicates in a period of about 8-12 hours, so that exponential illustration occurs in under one day, thus adding to the importance of preventing infection or vaccination to help mitigate it.

Summary

Hopefully that explains why hospitalizations and infections are down. It’s a combination of repeat infections, vaccinations, and little viral mutation recently. As alluded to earlier, BA.3.2 could change this quickly given its potential for immune escape. That doesn’t bode well for either the vaccinated, the recently infected, or for healthcare capacity. Reduced hospitalizations do not mean reduced risk, they mean the immune system is doing more of the work that hospitals used to do.

We still don’t have enough data to really understand this variant and its impact on humans, but the smartest thing to do is to continue to work upstream from getting infected in the first place by using the various nonpharmaceutical interventions (NPIs), such as respiratory protection, air filtration, and ventilation.

Mechanism of Infection and the Cruise Ship

I had been thinking about hantavirus recently just before the recent reports of three deaths from hantavirus aboard a cruise ship are extremely unusual. 149 people remain on board and have not been allowed ashore, and the boat hasn’t been allowed to dock.

As is illustrated above, the normal route of transmission of the virus to people is through the feces and body fluids of infected rodents. In the US, most of the activity has been centered in the Four Corners region (the area where Arizona, Colorado, New Mexico, and Utah meet).

In a worst-case scenario, infection can lead to hantavirus pulmonary syndrome (HPS), which can have a 35% mortality rate. In the US, the median age of patients with HPS (n=890 since 1993) is 38 and about 2/3 of them are male.

There is some behavioral explanation for this. It’s thought that many exposures have to do with going to cabins, barns, sheds, and outbuildings in the spring to clean them for summer use. This can involve sweeping up rodent droppings and dust contaminated with dried urine and saliva from rodents who used the structure for shelter during the winter. In addition, this also may be due to handling firewood or stored materials where deer mice have nested.

That’s what makes this cruise ship outbreak so unusual. The three who died are passengers, so their exposure to rodent infested areas on a cruise ship seems far less likely than that of the crew. However, it’s also worth noting that the Andes hantavirus (the most likely South American one – ANDV) does have a documented human-to-human transmission chain, although that doesn’t happen efficiently. This also could mean that the exposures happened before embarkation in Argentina.

It’s most likely that the rodents or contaminated materials came on board in Argentina. However, it will be interesting to see if there are hantavirus problems on St. Helena in the near future, given there has never been reported cases there. If that happens, one could conclude that an infected rodent left the ship at that port, which would mean that it was a rodent infestation problem on the ship before it left Argentina as opposed to contaminated materials being brought onboard. This is all conjecture though as a thought experiment.

El Niño and Unexpected Ecological Context for Rodent-Borne Viruses

The cruise ship wasn’t what originally put hantavirus back on my radar — climate models did. The trigger for my thinking is both European and US models for El Niño. About 15 years ago I wrote something on ProMED about the interaction between El Niño, West Nile Virus, and hantavirus and how that could lead to an outbreak of HPS in the Four Corners region, as occurred in 1993. My conclusions were what got me interested in the health impacts of climate change.

During El Niño, some parts of the US have more rain as seen in this map from NOAA, including areas near the Four Corners Region. The simplest description is the southwestern and southern US.

Hantavirus

Extra moisture in the southwest would cause far more production of grasses, which would have the seeds to help support a larger deer mouse population. Deer mice are prolific breeders. They breed year around, but peak during fall and spring (ie, when there is more grain and other food sources). Females produce 2-4+ litters each year and can become pregnant about a month after birth. This means that given enough food, exponential growth of rodent populations can happen quickly (ie, 10-20 fold in a single season), increasing the chances of spreading hantavirus into human structures.

West Nile Virus (WNV)

WNV is primarily spread by the Culex mosquitos, which have a range across most of the US. They simply need a stagnant source of water (used tires, clogged gutters, buckets, bird baths, flower pots, etc.) to breed, even better if there is some organic material in it. Think about that in context of more moisture in the southern US, particularly in late winter/early spring, when birds would be migrating north.

Corvids (crows, jays, and magpies) are the birds that often die quickly from WNV due to high viral loads. That’s not very important in relation to deer mice though. Owls and hawks are often infected through predation, either on infected rodents or consuming the carcasses of other infected birds.

The Perfect Climate/Biological Storm

That creates a perfect storm of high deer mice populations due to increased grain production from El Niño moisture and increased Culex mosquito (and WNV prevalence) due to the increased moisture, depleting raptor populations that would otherwise help control deer mice populations.

Cruise Ship Parting Thoughts

Cruise ships puzzle me. I’ve described them as prisons with better tasting food that has a chance of making you really sick or killing you. They simply are not for me. When I was searching for information about the cruise ship incident, I came across a much better quote about them. “I do not understand why people want to visit a floating petri dish disguised as a 1990s mall built inside a terrible hotel. Is it the buffet?“

This is even more puzzling to me during an ongoing pandemic, which leads me to my other thought about this event and a possible contributor. Even though COVID vaccines are no longer mandated by the cruise industry for passengers or crew, I wonder if the crew are more likely to keep up on vaccines and take precautions on their own due to what happened in the cruise industry earlier in the pandemic. Passengers who would choose to go on a cruise right now certainly throw caution to the wind and I suspect would have been repeatedly infected. The crew are aboard for their livelihood.

That might account for why it’s been passengers that have died even though I can’t figure out how they would have more likely been exposed than crew. It might have much more to do with less cautious people with repeated COVID infections having damaged immune systems, thereby being more likely to become diseased with a lower viral load than among a similar immunocompetent cohort.

A Bigger Perfect Storm

Hopefully this provides some context as to why the interaction of climate and zoonotic disease is so important. Toss in climate refugees and crowding and the problems become even larger than this simple discussion around two viruses and climate. The path we are on is pretty bleak.