You are in luck!
"Original antigenic sin postulates that the virus sub-type that one is first exposed to in childhood will provide the greatest immunity in later years." ( source)
This is an H1 virus. Those born between 1918 and 1957 first sinned with H1.
Immunity isn't near 100% but those born before '57 are safer. In Australia the median age of death was 56--half the cases were older, half younger. In normal flu seasons there the median age is 83.
My mom and her twin turned 90 this year. They were in utero when the worst wave of the 1918 pandemic hit. My grandmother told me about it. Everyone was sick she said. But she wasn't and pregnant woman were in the highest risk group.
Interesting read... :-)
Relevance to the current H1N1pdm pandemic
Impact of the first A/H1N1pdm pandemic wave, Apr-Aug 2009.
Since April 2009, most countries have reported laboratory-confirmed cases of H1N1pdm. It is also clear that these counts would greatly underestimate the total burden of the first pandemic wave, as most cases would not have been confirmed. For example, CDC had discouraged physicians from laboratory testing due to overwhelmed laboratory system a few weeks into the outbreak. Consequently, the count of ~100K cases in late July was known to be severely undercounted; instead, CDC estimated that over 1M persons had been infected in the US.
The 1st wave of H1N1pdm in summer 2009 can be characterized as mild, relative to the mortality impact of severe winter-seasonal influenza epidemics. However the H1N1pdm outbreak is associated with the “signature age shift” that is typical for influenza pandmics. Morbidity and mortality have tended to occur in adults aged 20-50 years [8], with some deaths in children, and largely sparing of seniors. Both of these features – a mild summer wave with elevated mortality in young adults resembles the pattern of the 1918 pandemic, in which a first spring wave in the US [32] or summer wave in Europe [33] was associated with unusual deaths in young adults. The subsequent catastrophic wave in autumn 1918 killed about 2% of the population world-wide, with a dramatic mortality elevation in young adults [28]. Of note, the 1st wave of the H1N1pdm virus has had a very different morbidity impact in various US cities and regions, something that cannot easily be explained by contemporary mathematical models. For example, about 7% of persons living in NY City are thought to have been infected this summer, while other cities did not see much of an elevation in influenza illness [34]. Similarly, while Argentina has been experiencing an emergency situation, surrounding countries like New Zealand have had far less of an impact [35]. Such variability of impact have previously been noted for 1918-20 pandemic and attributed to differences in access to care and overall risk of dying in developing countries [27].
The early phases of recognition of emerging infections almost always show a high case fatality rate due to the dramatic ascertainment of cases and the unknown extent of infections that have already occurred. Media and public health alarm bells are frequently sounded until there is a clearer understanding of the degree of background infections are measured as well as transmission rates. Limited laboratory diagnostic tests and uncertain definitions of disease during the early phase lead to frequent misunderstandings. With improved sensitive and specific diagnostics and population based surveys, a clearer picture emerges.
The uncertainly about the number of people infected (=denominator for case fatality rate) is critical when it comes to ascertaining the case fatality ratio and thus getting a stronger sense of the severity of this pandemic. It is extremely difficult to gauge how many people have been infected thus far, based on passive surveillance data available, which consists mostly of deaths, hospitalizations, or influenza-like-illnesses. The proportion of symptomatic cases who seek care and are captured by existing surveillance systems remains unclear is is bound to vary across countries and settings, and with media addition as the pandemic progresses. So far, estimates of the case fatality rate range between 1 per 10,000 for Acute Respiratory Distress Syndrom (see [36]) to 1 per 2,000 for all influenza-related deaths. These estimates come with large cofnidence intervals and are likely to change over time. Of note, the case fatality rate for seasonal influenza is 1 per 1,000 on average, which appears more severe than H1N1pdm, however one has to remembers that it is mostly driven by a high proportion of deaths among seniors. By contrast, H1N1pdm-related deaths are concentrated in people under 60 yrs, a population typically at low risk of influenza-related deaths.
In addition, an important quantity to gauge disease severity is the proportion of asymptomatic cases, which remains largely unknown (for H1N1pdm as well as for seasonal influenza viruses). The proportion of asymptomatic cases can only be measured by costly prospective studies combining serological outcomes to measure evidence of infection, with a clinical follow-up of patients to monitor symptoms. Such studies were conducted in the 1940-1970s in US and British households and proved instrumental in monitoring the impact of past pandemics (eg, [22]). So far, there has not been such studies for H1N1pdm, although some may be under way.
In the meantime, to monitor trends in H1N1pdm burden over time or across age groups, we can rely on existing passive surveillance systems which are insensitive to the ascertainment issues – for example, CDCs 122 mortality system, which showed only a moderate elevation of mortality during the 1st wave in summer in the US [37]. Thus, at least in the US, it is clear that the 1st wave was not associated with a measurable amount of excess mortality above the seasonal baseline. This is not to say that severe outcomes and deaths have not occurred; CDCs pediatric surveillance system shows that influenza related hospitalizations and deaths occurred nationwide; however, the numbers were definitely lower than that attributed to seasonal influenza during the last 4 influenza seasons.
But some other countries have reported high hospitalization impact. For example, in the Southern hemisphere where the influenza season is normally during May-September, the impact has been reported to be “the worst in the last decade” in New Zealand and Argentina, with ICUs filled. But also the UK had an intense first wave, despite high use of antivirals for prophylaxis and treatment. In Mexico, adults aged 20-50 had a clearly elevated hospitalization rate than for a comparison period in previous years [8].
Clearly, more data are urgently needed to assess the mortality and morbidity burden of the first wave of H1N1pdm, and quantify variation across countries and age groups.
What will happen in the 2nd wave expected this autumn?
Even though the similarities of the epidemiology of H1N1pdm and the 1918 pandemic are concerning, there is no way of knowing whether the current H1N1pdm virus will cause a more severe 2nd wave in the coming fall. The virus may or may not acquire virulence mutations and become a more pathogenic state in successive waves.
There are some unique differences in this pandemic from prior pandemics. As noted earlier, A(H1) viruses have previously circulated in the population, and may have conferred some level of protection to older age groups, who are relatively spared against morbidity and mortality [8][38]
Evolution dictates that success of transmission and ability to compete with other evolving viruses will determine the characteristics of future strains. There have been historic examples of mild, moderate or severe waves followed in previous pandemics [24]. However, even if this pandemic is at the mild end of scale, it is worth keeping in mind the age shift of severe disease to younger populations, warranting increased attention to populations not normally thought about at greater risk.
While there is no way to predict the course of this pandemic, careful statistical measurements of age-specific morbidty and mortality data, combined with information on virus activity and genetic characteritics, allows for an assessment of pandemic impact, and is crucial in the first two years of a new virus circulation [39][26].
Factors that may affect H1N1pdm impact in the waves to come
On the positive side, some factors could attenuate the mortality impact of subsequent waves of H1N1pdm, possibly in the fal, in particular effective pandemic vaccination. In addition, immunity acquired from exposure to H1N1pdm in summer 2009 could protect a fraction of the population against subsequent outbreaks of similar or related viruses in fall [40]. Other factors include antiviral and antibiotic use (to mitigate primary viral infection and secondary bacterial infections), school closings, and effective social mitigation strategies.
On the negative side, other factors could lead to a worsening situation in the coming months. These include winter-seasonal factors in the Northern Hemisphere, including presence of bacterial pathogens such as S.pneumo and MRSA, who are responsible for a large fraction of influenza-triggered deaths in seasonal epidemics and past pandemics [41]. As discussed previously, viral acquisition of virulence factors by mutation would be unfortunate, as would acquisition of antiviral resistance determinants.
Age has it’s rewards? :(