Day 83-6: Hope-Simpson Sheds Light on Flu

A retired Scottish doctor has emailed from Buenos Aires, Argentina, to tell me that answers to my questions about flu transmission have been staring me in the face for months. “You need to go back and look into who discovered the role Vitamin D plays in influenza. Follow your own links!”

That’s all he said.

So I’ve spent days compiling information about the thoughts of a deceased English doctor named R. Edgar Hope-Simpson (1908-2003), who spent his final decades challenging and rethinking everything that was known about influenza. A true debunker!

HOPE-SIMPSON'S BELOVED CIRENCESTER, SHORTLY BEFORE HE DIED IN 2003 (Chris Jefferies)

Not that anyone paid much heed. Hope-Simpson’s research was published before the digital age. His papers and his book are out of print. I’ve stumbled on the Gene Clark of viral research, a once-famous man whose greatest work is ignored.

Devoted readers will recall my Round One post about Vitamin D, wherein I noted that flu epidemics correspond to seasonal declines in exposure to sunlight. I failed to digest a Scott McPherson blog entry about Hope-Simpson’s work way back in 2007. Apart from abstract summaries of Hope-Simpson papers once presented in Britain’s Journal Of Hygiene (now Epidemiology & Infection, which has published more recent research on it, too), Hope-Simpson’s work is best accessed via the Vitamin D Council’s excellent and intriguing summation of the actual papers.

R. Edgar Hope-Simpson was a country doctor who riveted the medical world by proving on his own in 1965 that childhood chickenpox virus reactivates in adults as the painful condition called shingles. The British establishment was charmed and impressed that a general practitioner could conceive, research, and demonstrate something important that had eluded research labs and universities. (It brought Nobel prizes to others who followed his work, though a shingles vaccine that hit the market in 2006 isn’t selling because it costs too much.)

Hope-Simpson could have spoken at banquets for the rest of his life, the establishment’s pet exception to the rule that proper research is conducted in well-heeled institutions.

So Who Does Spread Influenza?

He was just getting started on another virus he suspected lurked in seemingly healthy people, as he had shown chickenpox does. While maintaining his practice, Hope-Simpson spent the rest of his life arguing that seasonal flu isn’t spread by sick people!

That’s no misprint: The good doctor surmised that seasonal influenza is activated by an unidentified force that circulates among people whose paths don’t need to cross during flu season. People who are not only symptomless—but entirely well. (Hinting at the mystery is a New York Times story on the peculiarities of swine flu transmission in a Pennsylvania community.)

Like all great thinkers, Hope-Simpson started with good questions.

What makes influenza roar into our lives every year, only to depart abruptly with so many promising subjects yet to be infected? The Black Death didn’t do that. The measles don’t. Disease normally spreads as fast and as far as it can until it runs out of carriers or creatures to infect.

What brings influenza back so regularly? How does it explode across continents and oceans faster—when you consider the necessary incubation period—than jets can carry it? And how did it do this before the Wright Brothers?

Why is the second wave of a pandemic supposed to be worse than the first? How does a disease come to kill more people after it’s made a run through the populace? Shouldn’t people become immune to it?

For that matter, what makes change such a constant feature of all influenza A strains? Why do they inevitably mutate—evolve away from our control—so that health authorities have to guess which varieties to fight against in each new vaccine?

Hope-Simpson began by noting that his hometown in Southwest England came down with epidemic influenza at the same time every year as Prague. (They share the same latitude.) He pored over ancient church registers showing that influenza spread just as quickly back when Britain’s roads were impassible.

He further observed that tropical flu breaks out in the rainy season, when the inhabitants' sun exposure plummets. This was confirmed in a study published by others the year Hope-Simpson died.

‘Solar Radiation’—Vitamin D

He also detected patterns involving sunspots, which reduce the quality of rays that reach us. He surmised that a drop in solar radiation levels triggered seasonal flu in Europe’s dark months and in tropical rainy seasons. Vitamin D’s immunological properties weren’t known yet.

Essentially, Hope-Simpson concluded that epidemics spring up as Vitamin D levels plunge in the population, activating symptomless carriers who caught flu the previous year and then repressed it with natural antibodies.

He also said the flu vanishes broadly every year because carriers stop being infectious after six to eight weeks.

Since many people are known to spread influenza without showing symptoms, Hope-Simpson’s claim isn’t as radical as it seems. Until you consider that he also asserted that active influenza sufferers do not transmit seasonal virus as much.

His studies of communities in Wales and England showed that in most families, only one member catches flu in a given season. He opined that this individual becomes the vector that spreads flu to his or her uninfected kin during the next epidemic—not the schoolchildren we customarily blame for transmitting flu.

Seasonal flu hides quietly, evolving inside the previous year’s victims and mutating to trick its way past their immune systems. Then it competes with other active flu strains to infect potential hosts. They all play hopscotch in us, among us, competing to replicate. Each year’s flu victims select the viral variety against which they have the least immunity; the winner becomes the new season’s hit strain. That’s why the medical establishment must gamble on which strains to batch into each annual vaccine.

It’s not clear if carriers can spread seasonal flu in July—or if they simply harbor it in an inactive form until their Vitamin D levels drop low enough to let the virus circulate. So I won’t be selling masks on the beach.

Next: What this means for pandemic flu….

Day 87-9: We’re All Animals on This Leaky Ark

‘BEWARE OF PERVERTS’ (Vitalie Ciubotaru)I’ve aroused a tempest of protest. I’m shocked that the furor wasn’t motivated by my bold and succinct account of Dr. Hope-Simpson’s theses. Readers seem charmingly open-minded about that.

You’ll thus be pleased to learn that someone is sending me some old Hope-Simpson papers. Others are being kindly faxed to me by the kind folks at Epidemiology & Infection, the Cambridge University journal. I can’t wait to read and digest them.

First I must wade through a river of indignant emails about my defense of sexual freedom. I wish I could quote them at length but the exciting ones are, um, unprintable.

I’m not going to turn my blog into a debating forum about sexual aggression. I do, however, deny I’m a pervert. I’m proud not to judge other peoples’ sexuality and I’m danged if I’ll be judged for Ayn Rand’s. Some of you people should take a long look in the mirror, naked. We are all animals.

That’s why we get sick.

Day 90-1: My Baby Wrote Me a ‘Letter’

I received a very strange Valentine’s Day card from Nina. (I presume she knows this is July.) It was beautifully put together, probably with the best creative gear at her bank. The cover read, in splashy colors: “How many Valentines does a man need?”

Inside was a photoshopped image of me biting into a heart, adapted from a photo of me grinning as I opened up for some pie she enjoyed trying to make three months ago. A big bowl next to me was full of juicy cardiac treats. She signed it ‘Heartless.’ That part makes sense.

Day 92-5: Flu Virus ‘Seeds’ Humans

Sorry this took so long to prepare. I want to get it right.

R. Edgar Hope-Simpson was 10 when the 1918 pandemic struck England, so he never had the professional opportunity to observe an influenza strain that crossed directly from another species, the way H1N1 is commonly thought to have done in 1918—and as H5N1 has done.

The pandemics that Hope-Simpson lived through as an adult were minor affairs—strains that conquered the world by mixing genes from preexisting human varieties, as H1N1 swine flu did. Many people had vestigial immunity from exposure to precursor strains.

H5N1 TOOK ITS TIME (CDC: Cynthia Goldsmith, Jacqueline Katz & Sherif R. Zaki)I’m guessing that Hope-Simpson would concede that species-jumping strains are so intense, so virulent, that they can and do leap from the sick to the healthy. Leaving aside the curious, almost incomprehensible resistance in some elderly people, no one has any immunity. These strains rage through the population like fire. We’ve all seen it this year.

I think Hope-Simpson’s theories can explain how and why H5N1 percolated for so long before it went global. The virus had to seed us to reach a kind of biological critical mass.

H5N1 killed most of the Indonesians, Egyptians, Vietnamese, Chinese, Indians, and Africans who caught it from birds or other animals. A minority of victims survived. Many weren’t logged as H5N1 cases. Many survivors probably thought they had outlasted dengue fever or some other tropical disease.

But bird flu had found a home in them, if Hope-Simpson was correct. After falling ill, their bodies suppressed the symptoms and the virus proceeded to lie dormant inside them for a year or two.

Now, according to Hope-Simpson, the microbes were desperate to replicate. This entailed further evolution so they could jump past their carriers’ immune systems to infect other people. When their recovered hosts’ Vitamin D ran low, H5N1 would power up, mutate, and attack new subjects.

At this stage, H5N1 became a human disease: An avian virus that had learned to survive in one human being became capable to spreading to other human beings. This explains the early cases in which no animal or human vector—a sick chicken or person or cat—was identified. One person had encountered another who harbored freshly minted human H5N1. Without symptoms.

Each low-light season (rainy season, in the tropics) would bring a wavelet of human cases that would recede after spreading just a bit more. I begin to wonder about the rumors of experimental H5N1 vaccines based on human survivor antibodies. Could they have helped it circulate?

The ‘First’ Flu Wave is Second … or Fourth

I’ve also located strong evidence that the so-called springtime inaugural wave of the 1918 pandemic wasn’t the first. A noted U.K. microbiologist named Dr. John S. Oxford makes a very good case that British soldiers garrisoned in Étaples, France, were felled by what looks to have been pre-pandemic flu in December 1916. They turned blue.

Mortality studies from New York City at the start of 1918 indicate an undetected pandemic wave that took the young, spared the old. Helen Branswell published an article that raised similar questions during the swine flu pandemic.

Did the spring 1918 pandemic follow a series of herald waves that no one noticed? Each would have left more carriers embedded in a seemingly healthy populace. One wave’s survivors would quietly inspire the next until the tide of illness rose so high that it could be ignored only by monarchs and politicians bent on world conquest.

If I’m right, we can catch H5N1 from just about anyone. We could catch it from sick people because pandemic influenza trumps the seasonal pattern. We might get it, per Hope-Simpson, from recovered latent carriers. Or it can be spread, as everyone knows, from infected people who aren’t yet showing symptoms.

This may explain why the first wave of pandemic flu is weaker than a later one. The second and third waves are spread by both freshly sickened carriers and by seemingly healthy veterans from earlier waves. Sources of contagion abound. Because the virus is mutating to leap from recovered victims, later waves are likelier to entail evolutionary gains in virulence as the unstable RNA virus tries new tricks.

Which could in theory render any vaccines generated from a first-wave virus obsolete!

No one is safe until the deadly strain loses its punch. We knew that, didn’t we? Now we know why.

Day 96-7: Ulcers Are for Hecklers, not ‘Crackpots’

My relentless correspondent (no, not Nina, whose emailed accusations mount like the snows in her native South Dakota) reports that the LES DIY is still holding well-attended meetings and that morale is strong. She suggests I shuck off my “romantic egotism” and attend a meeting tomorrow night. Drink is pledged afterward, even for “snotty self-indulgent Randian nonmembers.”

If ‘Evelyn’ had promised to reveal herself at said meeting, I’d be sure to attend. But I don’t think she goes to these things. So instead of driving Anna to tears again, I’ll just hope she’s feeling better—sunbathing, swimming, cooking tasty grub for her friends,

HOPE-SIMPSON: LONG-LIVED, VISIONARY REBELI’ll head upstate early in the morning to find refuge. It’s what Crusoe would do. Now that I think the earth is well sprinkled with human H5N1 survivor ‘bots colonized by virions, Round Two should really suck.

 I’ll post sporadically until I’m settled. I’ve arranged for someone to fill orders for personal protection equipment that come in while I’m gone.

A final note regarding the fabulous Dr. Hope-Simpson (for those who email that he and I are crackpots): When a couple of Australian doctors, J. Robin Warren and Barry J. Marshall, tried to tell the world that peptic ulcers were caused by a bacterium named Heliobacter pylori—and not booze, spices, and insufferable spouses—they were scorned for years. That must have made winning the Nobel Prize more fun.

Hope-Simpson took lots of honors, but never that one. Two scientists who separately followed up on his work with chickenpox (varicella zoster virus) and herpes zoster each won a Nobel.

Hope-Simpson was a gutsy man whose Quaker faith made him resist fighting in World War II. He was lively enough to remarry in his 90s. His obituary shows a balding, bespectacled man with an amiable expression. It bespeaks that he maintained a good sense of humor and professed to love life, even as he was leaving it.