The reason experts are particularly concerned about the flu this year is that many people, especially very young children, may have little or no immunity against the respiratory infection because the masking, social distancing and other behaviors aimed at protecting against COVID have blunted flu's spread, too. Also, the CDC notes, young children would do well to get a flu shot soon because they require two shots one month apart, and it takes time to build up immunity.
Yet the world is vulnerable to the next pandemic, perhaps even more than in 1918, when the pace and frequency of global travel was considerably less than today. As the contributors to this chapter demonstrate, there is still much to be learned from past pandemics that can strengthen defenses against future threats. The chapter begins with a review of the events of 1918, the lessons they offer, and the historical and scientific questions they raise. It describes the epidemiology and symptomology of that deadly viral strain, limited efforts toward prevention and treatment, and the resulting social disruption and its exacerbation by the actions of public officials and the media.
It’s A Little Late For This News To Be Helpful For This Year’s Halloween, But Perhaps For Next Y
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Three extensive outbreaks of influenza within 1 year is unusual, and may point to unique features of the 1918 virus that could be revealed in its sequence. Interpandemic influenza outbreaks generally occur in a single annual wave in the late winter. The severity of annual outbreaks is affected by antigenic drift, with an antigenically modified virus strain emerging every 2 to 3 years. Even in pandemic influenza, while the normal late winter seasonality may be violated, the successive occurrence of distinct waves within a year is unusual. The 1890 pandemic began in the late spring of 1889 and took several months to spread throughout the world, peaking in northern Europe and the United States late in 1889 or early 1890. The second wave peaked in spring 1891 (over a year after the first wave) and the third wave in early 1892 (Jordan, 1927). As in 1918, subsequent waves seemed to produce more severe illness so that the peak mortality was reached in the third wave of the pandemic. The three waves, however, were spread over more than 3 years, in contrast to less than 1 year in 1918. It is unclear what gave the 1918 virus this unusual ability to generate repeated waves of illness. Perhaps the surface proteins of the virus drifted more rapidly than other influenza virus strains, or perhaps the virus had an unusually effective mechanism for evading the human immune system.
One theory that may explain these data concerns the possibility that the virus had an intrinsically high virulence that was only tempered in those patients who had been born before 1889. It can be speculated that the virus circulating prior to 1889 was an H1-like virus strain that provided partial protection against the 1918 virus strain (Ministry of Health, 1960; Simonsen et al., 1998; Taubenberger et al., 2001). Short of this cross-protection in patients older than 29 years of age, the pandemic of 1918 might have been even more devastating (Zamarin and Palese, 2004). A second possibility remains that the high mortality of young adults in the 20 to 40 age group may have been a consequence of immune enhancement in this age group. Currently, however, the absence of pre-1918 human influenza samples and the lack of pre-1918 sera samples for analysis makes it impossible to test this hypothesis.
The sequence of the 1918 HA is most closely related to that of the A/ swine/Iowa/30 virus. However, despite this similarity the sequence has many avian features. Of the 41 amino acids that have been shown to be targets of the immune system and subject to antigenic drift pressure in humans, 37 match the avian sequence consensus, suggesting there was little immunologic pressure on the HA protein before the fall of 1918 (Reid et al., 1999). Another mechanism by which influenza viruses evade the human immune system is the acquisition of glycosylation sites to mask antigenic epitopes. The HAs from modern H1N1 viruses have up to five glycosylation sites in addition to the four found in all avian HAs. The HA of the 1918 virus has only the four conserved avian sites (Reid et al., 1999).
It has previously been demonstrated that all three pandemics of this century were characterized by a shift in the age distribution of deaths (Simonsen et al., 1998). The younger population (in that study, persons under 65 years of age) experienced a sharply elevated mortality risk and accounted for a markedly increased fraction of all influenza-related deaths. As we will discuss below, the 1968 pandemic age shift pattern was exacerbated by the protection of the very elderly by virtue of their experience with H3 antigens as children (Simonsen et al., 2003). For the 1968 pandemic, then, the observed age shift was due to a combination of increased risk among the young and decreased risk among the elderly (Simonsen et al., 2003).
During the 1957 A(H2N2) Asian pandemic in the United States, nearly 40 percent of all influenza-related deaths occurred in the younger population under 65 years of age. The proportion of deaths among people under age 65 that occurred during A(H2N2) epidemics dropped to 5 percent by 1968, when circulation of this virus ceased. In the 1968 A(H3N2) pandemic, this proportion was approximately 50 percent, but declined to less than 10 percent over the next decade (Figure 1-6) (Simonsen et al., 2003). The age shift in mortality was even more pronounced in the 1918 A(H1N1) Spanish influenza pandemic (Collins, 1931; Simonsen, 1998; Olson et al., 2004).
To investigate whether this age-specific mortality pattern also describes the international experience, we set out to develop a methodology for measuring pandemic mortality burden based on annual mortality data (Heiman et al., unpublished). Annual age-specific P&I mortality data were provided by WHO for the United States and Japan. We estimated the pandemic excess mortality in 1957 and 1958 by subtracting as background the number of deaths in surrounding years when there was little or no influenza A activity. We validated this approach by comparing these U.S. age-specific excess mortality estimates with those generated using actual seasonal data (Serfling et al., 1967). We found that for Japan, the age pattern of relative impact over the first seasons was very similar to that observed in the United States (Table 1-5). Also, in contrast to the United States where there was no measurable increase in influenza-related mortality until October, P&I mortality in Japan was elevated in the early summer of 1957 (Reichert et al., 2001).
Lamont Library will be open 24/7 during reading and exam periods this year. For more information, see the announcement in the Harvard Gazette. Our decision to make Lamont available for late night study during this time follows a successful trial run of 24-hour operations at the end of the spring semester.
His name was Todd Hodne, and he was perhaps the most dangerous predator ever to play college football. "I have been a prosecutor for nearly 30 years," wrote John B. Collins, who prosecuted one of Hodne's crimes, in a letter to a parole board. "I have prosecuted serial killers and capital cases. Todd Hodne, to this day, remains among the three most dangerous, physically imposing and ruthless excuses for a human being I have ever faced in court."
There was an investigation of the attack. "The police came over," she says. "They were in my apartment for a long time." Karen remembers her attacker going through everything, and now the cops were doing the same. Jean remembers seeing smudges of black all throughout their apartment where police had tried to lift fingerprints. Jean also remembers that when Hodne was arrested, Clyde had reminded her that the three of them had run into him at The Saloon a few weeks before the attack. Karen remembers police finding a footprint outside her window. But 43 years later, what Karen remembers most is the sense she had that the police were investigating her as much as they were investigating what happened to her: "And basically what came out of it was that they told me they didn't have enough information to go to court. And that's what I heard from everyone involved in this: not enough evidence. They had evidence."
Todd Hodne was one of seven players in Paterno's recruiting class of 19 who lettered his freshman year. He played in at least seven games in the 1977 season, including the Fiesta Bowl. One of the few photos that the Daily Collegian ran of spring practice in 1978 shows Joe Paterno giving Hodne the benefit of his personal tutelage, above the caption, "Do it like this." Beyond the announcement of Hodne's suspension from the team, neither the school nor the football program ever made a public statement of any kind about Hodne or the students he attacked. He was, after all, a player of no consequence, involved in an isolated incident. He would leave State College and never be heard from again.
"A normal person shouldn't do this," Hodne says in the statement he gave to Nassau County police about his attack on the 16-year-old girl. "There seems to be two sides of myself lately. When I sit down and think about what I do, it drives me crazy. How could I do something like that? I think I need to see a psychiatrist. If you could arrange it, I think I do. It's not normal for someone to want to do this, and I want to try to straighten out, you know."
Gruber went inside and brought the receiver of his phone outside and handed it to Hodne, who told the dispatcher his name was Steven Hodne, the twin brother of Todd Hodne. As he said later in a parole board hearing, he didn't want the police to judge him unfairly because of Todd Hodne's notoriety. When he gave the phone back, Gruber tried to console him. "Get away from me!" Hodne snapped. For the next 30 seconds, Hodne stood motionless, staring at the cab and at Hirsch. "I'm sick of this s---," he finally said. Then he got in the cab and drove away. 2ff7e9595c
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