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ROTTERDAM, THE NETHERLANDS-Locked up in the bowels of the medical faculty building here and accessible to only a handful of scientists lies a man-made flu virus that could change world history if it were ever set free.
In an old post (http://www.newfluwiki2.com/diary/3672/is-crowding-a-factor-for-influenza-mortality-rates) it was discussed if crowding would somehow be a factor implyed in influenza mortality. Recently an article published in PLoS ONE addressed this question and put forward the hypothesis that the difference seen in mortality between epidemic waves
may have been due to the number of simultaneous contacts a susceptible individual had with infectious ones. The higher the number of simultaneous contacts, in a brief period of time, the higher the infectious dose at which, in average, a susceptible individual was exposed to. It is proposed that there is a background mortality rate due to mild disease. But as the number of infectious individuals with mild disease increases there is a proportion of severe cases, for which the mortality is higher, that build up.
In the end the Case-fatality rate is just the average between mortality due to mild and severe influenza disease. According to this hypothesis non-pharmaceutical measures may be more important to reduce mortality then incidence. In fact, non-pharmaceutical measures are known to delay the spread of the epidemic. If the number of infectious individuals is lower at each time less severe cases build up and thus mortality will be kept at lower rates.
There has been a lot of discussion in this forum about the impact of UV light, schools, malls, vitamin D and the temperature of the nasal mucous membrane on influenza transmission. But what about the environmental temperature and humidity? Before going further let me clear I don't know anything about the impact of temperature and humidity on pandemic H1N1 (commonly know as swine flu). But I have read and studied enough about OTHER influenza stains, that I currently believe that temperature and humidity impacts whether influenza is transmitted just by contact, by contact and droplets or by contact, droplet and airborne routes. Why is this important? Well if it is just by contact you can literally wash your hands of influenza. If it is contact and droplet, you wash your hands and stay 3 (or if you prefer 6 feet away)with surgical masks offering some protection against direct hits. BUT if the virus survives in the air for extended periods you can be infected by virus first sneezed or coughed by a person distant in time and/or space from you. And surgical masks won't help you much because air follows the path of least resistance (around the edges of the mask.) If we knew which temperature and humidity combinations caused airborne transmission, could we alter the indoor environment during influenza surges so that airborne transmission was not supported, decrease our exposure time to certain outdoor temperature and humidity combinations, and/or wear protective masks when we could not? But figuring out which temperature and humidity combinations need to be avoided is not easy. Remember it is the environmental conditions at the time of exposure, not at the onset of infection or time of diagnosis that matters.I think this is the type of topic that would benefit from a wiki discussion. It is too complex for soundbites and requires the expertise of multiple disciplines. I have copied and pasted below a number of references and abstracts for those interested in learning more.
You may or may not be aware that MIT offers a LOT of high quality undergrad and grad level courses online and for free (not interactive from what I can tell tho)
I thought these might be of interest.
7.340 Nano-life: An Introduction to Virus Structure and Assembly
This course features a complete bibliography of readings and sample student assignments in the assignments section.
Watson and Crick noted that the size of a viral genome was insufficient to encode a protein large enough to encapsidate it and reasoned, therefore that a virus shell must be composed of multiple, but identical subunits. Today, high resolution structures of virus capsids reveal the basis of this genetic economy as a highly symmetrical structure, much like a geodesic dome composed of protein subunits. Crystallographic structures and cryo-electron microscopy reconstructions combined with molecular data are beginning to reveal how these nano-structures are built. Topics covered in the course will include basic principles of virus structure and symmetry, capsid assembly, strategies for enclosing nucleic acid, proteins involved in entry and exit, and the life cycles of well understood pathogens such as HIV, influenza, polio, and Herpes. A review of cutting edge structural methods is also covered.
Is there anything known whether migrating birds picked up the Mexican flu?
The 1918 flu was mild in the spring, mutated in the summer, and was extremely deadly in the fall and winter.
Although the 2009 Mexican flu appears to be mild, the mutation rate of the flu is so uniquely high that within a short time, with just some minor mutations, a similar deadly 1918 pandemic could easily occur as well.
Out of each 1 million virus particles which burst out of an infected human cell, 99% are so mutated that they can not infect other cells anymore.
That leaves, however, 10.000 closely related, but slightly mutated virus particles, which either attack other cells or are coughed out. If these
mutations occur at the right place, the virus can either become milder or more deadly.
This is the reason why pandemics appear to come in
waves or appear to be more deadly in some (remote) communities.
Other, (major) mutations occur when two different flu strains are combined in a single cell, as is very likely when migrating birds pick up multiple strains of the avian flu virus.
I would like to know if migrating birds picked up the Mexican flu? And I would like to know if there are any labs testing this virus on birds to check if they can carry it?
Currently data is sketchy coming out of Mexico, where public health and hospital officials seem to be struggling to keep up with the logistical difficulties of the current epidemic. As of now, they report 1995 hospitalizations for pneumonia like symptoms, though it is unknown how many of these are cases of swine flu. Of these 149 have died, with 20 of those being confirmed cases of swine flu. Abroad the picture is much rosier, with 69 suspected/confirmed cases and no fatalities. (source: http://www.nzherald.co.nz/worl...
Comparing the rates of suspected illness vs. suspected death, we can perform a statistical test (Chi-squared) to determine if there is indeed a difference. The chi-square test is significant (p=.023) indicating that the rate of suspected deaths is lower outside of Mexico.
This difference could be due to more rigorous surveillance outside Mexico, or due to the fact that not all cases outside Mexico were hospitalized. To alleviate this concern, let's look only at laboratory confirmed cases.
According to WHO :
27 April 2009 -- The current situation regarding the outbreak of swine influenza A(H1N1) is evolving rapidly. As of 27 April 2009, the United States Government has reported 40 laboratory confirmed human cases of swine influenza A(H1N1), with no deaths. Mexico has reported 26 confirmed human cases of infection with the same virus, including seven deaths. Canada has reported six cases, with no deaths, while Spain has reported one case, with no deaths.
Testing significance here we get an even more significant difference with a p-value of .0003. Given the high statistical significance of this result, it is very unlikely that the rates of mortality are the same.
Why this is the case is unknown, and I wouldn't trust myself speculate on any medical reason. That said, there could very well be bias in the case reports. In Mexico, 27% of confirmed cases are mortalities. This is far above what would be expected from a new pandemic influenza. The 1918 flu had an overall mortality somewhere in the range of 2.5%. This leads one to believe that Mexico is testing their mortalities more rigorously than those who recover, possibly leading to an inflated mortality to recovery ratio. Similarly, in the suspected case data, Mexico is only reporting hospitalization rates, whereas the rest of the world is reporting all suspected cases. This could also lead to inflated numbers.
The bottom line is that, given the numbers we have now, the mortality rate in Mexico is much higher than abroad; however, there are several biases in reporting which could explain the higher numbers. This bears watching as new, more reliable, data comes in.
In 2004, NASA scientists started looking forward to a new solar minimum. In 2005, it began. At this time most scientists expected the new solar cycle 24 to begin in late 2006 or early 2007 with a following ramp up in solar activity.
According to Wikipedia, the Dalton Minimum was a period of low solar activity stretching from 1790 to 1830.
Like other long period solar minimums such as the Maunder Minimum and the Sporer Minimum, it resulted in crop failures, lower than average global temperatures, and little ice age conditions in the Northern Hemisphere.
If the sun is entering a new period of very low activity it would presage a 30 year or more drop in global temperatures.
Some scientists are already beginning to speculate that just this sort of thing may be occurring now.
Perhaps the lateness of cycle 24 might even be the start of another Little Ice Age."
This diary is for the science discussed at the BirdFlu2008 Conference held in Oxford between the 10th and 11th of September 2008.
I went to the conference and exhibition in Oxford with SusanC. She will have more coherent opinions of the conference than mine, but here's my beginners eye view. The notes I will relate are not a complete picture of the conference for three reasons 1) Some of it we already know well and/or have discussed it before or 2) Some of it was too far beyond my understanding to offer any sensible comment. 3) I can't guarantee that my grasp of what was reported is accurate for which I apologise to the fine scientists at the conference.
The conference was small (about 130) but attended by many of the stars of the flu world. It was a wonderful if challenging opportunity to be there. My thanks to Susan for giving me the opportunity :-)
Since UK did not stockpile respirators (or only in a very limited quantity) to protect public workers in case of a pandemic influenza, what would all the healthcare workers, first responders, etc... be wearing during a pandemic?
This report from the Health & Safety Laboratories establishes the very limited protection offered by surgical masks against the influenza virus...
Please feel free to share this information with whoever you know that will be given a surgical mask during a pandemic. Employees deserve to know at what level they will be (un)protected...
From your local bus route to international air travel, infectious diseases can spread across the globe in a matter of hours. In this video podcast episode filmed at the Koshland Science Museum in Washington, D.C., Stephen Eubank from the Virginia Bioinformatics Institute of Virginia Tech and Daniel Lucey from Georgetown University discuss the role of transportation in the spread of disease and examine the effectiveness of various measures to curb transmission.
Stephen Eubank, Ph.D., is a project director at the Network Dynamics and Simulation Science Laboratory at the Virginia Bioinformatics Institute of Virginia Tech. His research focuses on modeling and simulating the spread of disease and regional transportation, and the analysis of complex systems.
Daniel Lucey, M.D., M.P.H., is an adjunct professor in the Department of Microbiology and Immunology at Georgetown University, where he is co-director of the master of science program in biohazardous threat agents and emerging infectious diseases. In recent years, his teaching focus has been on SARS, avian flu, and the threat of pandemic human influenza.
The WHO and the CDC have created a model of how a pandemic starts; their model shows a more or less steady progression from no pandemic risk to a full blown pandemic, and has various stages which recognize the 'milestones' in the progression of influenza toward a pandemic.
Most governmental and non-governmental organizations have incorporated this model into their preparedness plans, as have many individuals and families. It is reasonable to see why they would do this apart from the (erroneous) idea that the WHO must know what they are doing- it's reassuring to think that this is a more or less orderly linear progression, and that the evolution toward a pandemic can be tracked and predicted. But is that really how it works?
My question is, "Is this model valid? Is that how disease epidemics, especially influenza, really start?"
The recent publication of a study (which confirms what many observers thought about H2H transmission) of the Karo cluster last year has some disturbing implications which challenge the WHO/CDC model.
Free download of new prepublication pdf of a 200+ page Institute of Medicine report titled Preparing for an Influenza Pandemic: Personal Protective Equipment for Healthcare Workers is available from the National Academy Press at: http://books.nap.edu...
In the process of fulfilling this task, the urgency that a potential pandemic caused by the H5N1 virus instills in planners lies not in its imminence, but in the enormous amount of work required to prepare the whole world.
We, indeed the whole of humanity, will not have a future unless we do everything in our power to protect the young. We must not fail.