I posted this on the CE flu site the other day, and thought that this might be helpful for discussion here…
From the same presentation I referenced the other day. It seems that the life span of influenza is much, much longer with dry humidity than high humidity.
According to the attached graph, this is the following data I have gleaned.
At a room temperatures of 27 - 29 C (80.6 - 84.2), the life span of influenza (as it relates to infecting mice) goes from 100% to 0% at the following humidities
Relative humidity 23% - It never drops to zero, and as a matter of fact, when the room is disturbed by a fan, at it’s lowest point, 22 hours later, at 24 hours, it goes up.
Relative humidity 48% - It drops to zero at 6 hours after introduction.
Relative humidity 89% - It drops to zero at 1 hour after introduction.
The implications of the graph, if accurate, are very clear. Influenza virii are more “spreadable” the lower the humidity. Therefore, during seasons where the humidity is low (either environmentally or artificially due to indoor heating), the relative infectivity of any flu laden individual (R0) becomes higher than if that same individual, with the same flu, was out and about during periods of high humidity.
Thus, Ro may not be an absolute function of any one virus’ genetic code, but may indeed have a high environmental component.
It may therefore mean, that one of the best means of reducing the risk of spread is to install humidifiers in all public facilities.
To reiterate. Flu is a winter disease because of low humidity and therefore increased infectivity of the sick, not because of some african swallow carrying coconuts.
www.publichealth.pitt.edu/supercourse/SupercoursePPT/21011-22001/21431.ppt
slide number 29? (Sorry, I do not know how to attach pictures here.)
and the discussion that followed…
http://www.curevents.com/vb/showthread.php?t=61783
the research seems to back up this premise
2004 study from Tokyo implying the same thing…
The dynamics of influenza viruses in relation to one meteorological factor, absolute humidity, was investigated. The number of influenza patients, absolute humidity, and isolation of influenza viruses were compared between Odate City the north and Akita City in central Akita Prefecture from 2001 to 2002. The results were as follows: 1) In both Odate and Akita cities, Influenza A (H1N1 and H3N2) and Influenza B (Victoria and Yamagata) viruses were isolated when absolute humidity ranged between 2.7 and 8.8 g/m3. 2) In Akita City in 2002, the influenza viruses were isolated in May (weeks 20 and 22), and the absolute humidity was below 9 g/m3, suggesting that the influenza season lasted until May in this year. 3) A correlation between absolute humidity and isolation of influenza viruses was observed, and the influenza prevalence may occur below 9 g/m3 of absolute humidity. 4) In Odate and Akita cities, the absolute humidity of 10 g/m3, a level at which 5% of influenza viruses can survive after six hours, was observed from January to June and October to December. 5) Influenza prevalence show differential occurrence by time and place. Therefore, further research is required to clarify the absolute humidity related to influenza prevalence
the CDC has in their emerging infectious disease publications this month, a very good article, basically saying, amoung other things, we’re screwed.
. In experiments that used homogeneous aerosolized influenza virus suspensions (mean diameter 6 ¦Ìm), virus infectivity (assessed by in vitro culture) at a fixed relative humidity undergoes an exponential decay; this decay is characterized by very low death rate constants, provided that the relative humidity was in the low range of 15%¨C40% (15,16). These results are consistent with those of an older study (admittedly performed in a more rudimentary manner) in which infectious influenza viruses in an aerosol could be demonstrated for up to 24 h by using infection in mice as a detection method, provided that the relative humidity was 17%−24% (17). In all these studies, the decay of virus infectivity increased rapidly at relative humidity >40%. The increased survival of influenza virus in aerosols at low relative humidity has been suggested as a factor that accounts for the seasonality of influenza (15,16). The sharply increased decay of infectivity at high humidity has also been observed for other enveloped viruses (e.g., measles virus); in contrast, exactly the opposite relationship has been shown for some nonenveloped viruses (e.g., poliovirus) (11,15,16).
Abstract
In theory, influenza viruses can be transmitted through aerosols, large droplets, or direct contact with secretions (or fomites). These 3 modes are not mutually exclusive. Published findings that support the occurrence of aerosol transmission were reviewed to assess the importance of this mode of transmission. Published evidence indicates that aerosol transmission of influenza can be an important mode of transmission, which has obvious implications for pandemic influenza planning and in particular for recommendations about the use of N95 respirators as part of personal protective equipment.
In contrast, the situation with a pandemic strain of influenza A (H5) would become only too clear because no one would have any degree of immunity against such a virus, vaccines would not be available for months, and these viruses would likely be highly virulent. Even though efficient human-to-human transmission of the A (H5N1) virus has not yet been observed (by any mode), transmission of influenza A (H5N1) by aerosols from geese to quails has been demonstrated in the laboratory (33). Thus, even in the current incarnation of A (H5N1), infection by the virus can generate aerosols that are infectious for highly susceptible hosts. As far as we know, 1 of the main blocks to efficient human-to-human transmission of influenza A (H5N1) is the virus’s current preference for specific sialic acid receptors. The current strains still prefer ¦Á-2,3¨Clinked sialic acids, which is typical of avian influenza viruses, whereas human influenza viruses bind preferentially to ¦Á-2,6¨Clinked sialic acids (34¨C36). In all likelihood, 1 of the mutations required for influenza A (H5N1) to give rise to a pandemic strain would be to change its receptor affinity to favor the ¦Á-2,6¨Clinked sialic acids. For the influenza A (H1N1) pandemic strain of 1918, this change required only 1 or 2 amino acid substitutions (36). Once a highly transmissible strain of influenza A (H5) has arisen, it will likely spread in part by aerosols, like other human influenza viruses.
Currently, several pandemic plans differ considerably in their recommendations for infection control precautions and PPE. The current version of the Canadian pandemic plan recommends surgical masks only, disregarding data that support the aerosol transmission of influenza (4). The US pandemic plans (5) and the British plans, from both the National Health Service and the Health Protection Agency acknowledge the contribution of aerosols in influenza but curiously recommend surgical masks for routine care; the use of N95 respirators is reserved for protection during “aerosolizing procedures” (5,40). These recommendations fail to recognize that infectious aerosols will also be generated by coughing and sneezing. The Australian Management Plan for Pandemic Influenza (June 2005) recommends N95 respirators for healthcare workers and in France, the Plan gouvernemental de pr¨¦vention et de lutte recommends FFP2 respirators (equivalent to N95 respirators) Given the scientific evidence that supports the occurrence of aerosol transmission of influenza, carefully reexamining current recommendations for PPE equipment would appear necessary.
Thank you for posting all that information. The only problem is that in Indonesia, Thailand, etc. there are high humidity levels. The question is if and when it goes H2H, will the same hold true of H5N1 vs seasonal flu viruses?
Ah, LauraB. Indonesia proves the point. Maybe the reason TS has NOT HTF is justly because of the humidity levels. Remember, R-nought is the measure of clustering. Higher humidity therefore, the harder it is for H5N1 to spread. Where would we be today if the Indonesian strain happened in a place of low humidity? Maybe “the grace of god” is that the indo clusters petered out due to the humidity.
from the lack of comment, I assume that the inverse relationship between humidity and influenza infectivity is common knowledge at the fluwikie and everyone here has humidifiers in their prep kit and hospitals, schools, and businesses are working on ways to integrate humidifiers into their infrastructure.
My point is that there is a qualitative and substantive difference between active and passive methodologies to reduce the severity of any pandemic.
Passive - Get pneumo vax, prepurchase medicines, store food, water. Purchase material to survive the storm. Monitor news to identify start of pandemic, etc.
Active - create doable vaccine production plans (distributed small lot / Non GMP / local production), Encourage others to prep, create and implement plans to sustain infrastructure, create and implement plans to reduce infection (SIP, PPE, UV sterilization,and humidity control), etc.
So you have to ask yourself. Are you an active player? Or are you a passive player?
I read over and over here that the passives are frustrated with the actives (especially when the actives aren’t even putting into place some passive plan).
Me? I’m about ready to cross over into the active side. Wish me luck.
excuse me but are you pablo escobar from Asian Times?
Good point Pablo. If that is the reason Asia hasn’t exploded yet, then I guess we should very worried about more recent cases in Egypt - not exactly a tropical rain forest there. And yes, we have discussed the humidity/flu link before.