Bad news and good news about Novel H1N1

oramar · Jun 20, 2009

The bad news is that it continues to spread and has killed 87 people. The good news is that it seem no worse that normal seasonal flu. You have to qualify that by saying we don't know what the future brings. Also, normal seasonal flu can be pretty nasty at times.

indigo girl · Jun 21, 2009

uk: bracing for up to 50% attack rate

http://afludiary.blogspot.com/2009/06/uk-bracing-for-up-to-50-attack-rate.html

...what the h1n1 `swine' flu will bring over the next 2, 3, or even 5 years is anyone's guess. the `working assumption' on attack rates (the percentage of the population that gets sick during a pandemic) is usually pegged around 30% - which is about what we saw in the 1918 spanish flu.
why 70% of the population didn't get sick is unknown.
some may have had a prior exposure to a similar virus, assuming they'd been alive before 1889. but a great many, despite exposure, never developed any illness. it is assumed they had asymptomatic, or sub-clinical infections.
so most pandemic plans have used the 30% attack rate. now, in the uk, planners are cautioning that the attack rate of the h1n1 virus could be higher. ...they are advising that the country prepare for up to 50% to fall ill over the next year.
primary care trusts are now being briefed to expect that the pandemic could affect as much as 40 per cent of the workforce before the end of the year, with many worried that there could be a surge of cases in the autumn, according to health industry sources.
...the workforce could be reduced by 15-20 per cent at the pandemic's peak. in the unlikely event that every school closed, this could rise to 35 per cent." he said it was impossible to predict when the pandemic would peak, but added: "as part of ongoing planning, the nhs is being asked to ensure that antiviral collection points could, if needed, be put into action in a week."
keen to avoid panic, the government is careful to present official statistics showing "laboratory-confirmed" cases, which currently stand at 2,244. yet the true scale of infections is far higher than headline figures suggest. the total number of cases either confirmed by laboratory tests or "clinically presumed" currently stands at 3,725.
£42bn losses are predicted to hit britain as a result of a three per cent fall in gross domestic product (gdp) due to the swine flu pandemic, according to a new report from the oxford economics think tank, due to be released tomorrow. researchers claim that swine flu could threaten already fragile businesses and put further strains on financial markets in what could become a "vicious cycle that postpones the recovery".
deflation is a "significant risk" as a result of the pandemic's impact on the economy - putting back economic recovery by two years, says the report. the predictions are based on a 30 per cent infection rate, should a pandemic begin in october and last for six months.
a $2.5 trillion cut in global gdp is a possibility - with a flu outbreak in the autumn hitting the world economy just as it starts to recover from the credit crunch.

indigo girl · Jun 21, 2009

riding the influenza pandemic wave

http://www.virology.ws/

one notable characteristic of the four previous influenza pandemics is that they occurred in multiple waves. the 1918 pandemic began with outbreaks of low mortality in the spring and summer, followed by a more lethal wave in the winter. this pattern has fueled speculation that the current h1n1 pandemic strain will undergo mutation that leads to the emergence of a more lethal virus. what is the evidence that pandemic waves of increasing virulence are a consequence of viral mutation?
the only virus available from the 1918 pandemic was rescued from an alaskan influenza victim who was buried in permafrost in november of that year, when higher mortality was already evident. this makes it impossible to correlate any genetic changes in the virus with increased virulence. furthermore, as discussed on promedmail,
...there are many different ways of interpreting these differences other than more virulent virus. some of these are differences in populations affected, more circulation of pneumococci and staphylococci during cold weather, more circulation of other viral pathogens, more virulence and larger inocula with the crowding and cold air inhaled.
the november 1918 influenza virus certainly has genetic and phenotypic properties expected of a virulent virus. these include the ability to multiply in the absence of trypsin*, lethality in mice and embryonated chicken eggs, and efficient replication in human bronchial epithelial cells. but we don't know if these properties were absent from the virus that circulated in the spring of 1918.
do the pandemics of 1957 and 1968, which also occurred in waves of increasing lethality, provide any information? viruses are available from different stages of these pandemics, but to my knowledge the virulence studies have not been done.
this uncertainty makes it impossible to conclude that the 2009 h1n1 pandemic strain will become more virulent. nevertheless, speculation is rampant, and accompanied the recent release of the brazilian isolate. another example is an amino acid change in the viral pb2 protein observed in some 2009 h1n1 isolates. according to recombinomics,
acquisition of e627k is a concern because it allows for optimal replication at 33 c, the temperature of a human nose in the winter, in contrast to e627, which is in the avian version of pb2 and allows for optimal replication at 41 c, the body temperature of birds. the appearance of e627k raises concerns that the level of swine flu with e627k will markedly increase in colder months. in 1918, the flu in the spring was mild, but the fall version of the virus, which had e627k, was much more virulent and targeted young, previously healthy adults...
if the amino acid at 627 is an important determinant of virulence, we would expect to find e627 in viruses isolated early in the 1918 pandemic - but such viruses are not available. therefore the role of this amino acid change in virulence in humans cannot be tested. further complicating the situation is that other amino acids in the viral pb2 protein can influence viral replication at low temperatures.
fortunately, new h1n1 isolates are obtained every week, which provide a very accurate sampling of the entire pandemic. should the new h1n1 strain become more virulent, it will be a relatively straightforward task to determine the genetic changes that accompany this property. finally we will be able to determine if pandemic waves of increasing virulence are a consequence of specific changes in the viral rna.