CIDRAP: H5N2 Roundup & Detection In Environmental Air Samples

54 of Minnesota’s 84 Outbreaks Are Clustered in 3 Counties

 

# 10,030

 

Although migratory and wild birds are believed responsible for the delivery of HPAI H5 viruses to North America last fall and the subsequent spread of H5N8, H5N2, and H5N1 to at least 18 states, the clustering of infected farms (particularly in Minnesota and Iowa) has many wondering if there isn’t a second – as yet unidentified - mode of transmission at work.

 

While Minnesota has recorded 84 outbreaks across 21 counties, more than 1/3rd of those are from one county (Kandiyohi n=32), while the three county nexus of Stearns, Meeker & Kandiyohi account for nearly 65% of all of the cases.

Similarly, in hard hit Iowa, out of 44 farms infected across 12 counties, 2 counties (Buena Vista & Sioux) account for fully half their total.

 

In the past, human activities – the movement of personnel, or equipment, or poultry related items – has been viewed as the likely source of local `lateral’ transmission between farms, but so far epidemiological investigations have failed to find any solid evidence of such. 

Somehow, despite elaborate biosecurity measures, the virus continues to make its way into scores of farms.   And with the likely return of the virus next fall, figuring this out is a priority.

 

One idea, increasingly being considered, is the possibility that the virus is being dispersed – at least across short distances - `on the wind’.  Carried on dust particles from one farm to another (see last April’s Bird Flu’s Airborne `Division’ for a discussion of previous studies on this possibility).

 

Last night CIDRAP carried an update (including the news of 7 new farms presumed infected in Iowa), that contained the first tangible information on the possible airborne spread of H5N2 in Minnesota. 

 

Follow the link to read:

 

Signs of airborne H5N2 found; Iowa reports more outbreaks

Robert Roos | News Editor | CIDRAP News

May 08, 2015

Evidence of the H5N2 avian influenza virus has been found in air samples collected in and near infected Minnesota poultry barns, a researcher said today, supporting the suspicion that the virus may go airborne for short distances, while Iowa reported seven new H5 outbreaks involving 4 million chickens and an unknown number of turkeys.

In addition, Wisconsin authorities today reported finding H5N2 in an owl along Green Bay, while hard-hit Minnesota had its second day this week without any new poultry outbreaks.

Air sampling findings

Montse Torremorell, DVM, PhD, of the University of Minnesota said she and three colleagues did a pilot air sampling study at three Minnesota farms with infected poultry.

"Our results indicated that influenza genetic material can be detected in air samples collected inside and immediately outside of infected poultry facilities. We still don't know whether virus was viable or not, and those analyses are in progress," said Torremorell, who holds the Allen D. Leman Chair in swine health and productivity.

"So far we have shown that HPAI [highly pathogenic avian influenza] can be aerosolized from infected facilities," she added. "However, the implications of these findings in terms of understanding the transmission of HPAI between flocks needs further investigation." The study focused on a total of four poultry barns on the three farms.

Torremorell said the study was commissioned by the US Department of Agriculture's Animal and Plant Health Inspection Service (APHIS). The agency's National Veterinary Services Laboratories (NVSL) in Ames, Iowa, are testing the samples to see if they contain any viable virus particles.

(Continue . .. )

 

Humidity, ambient air temperatures, UV ray exposure levels . . . even the pH of whatever medium the virus clings to as it rides the air currents  . . . are all likely factors affecting the viability (and longevity) of avian flu viruses in the environment.  

 

While ideal conditions are likely to be short-lived - if you add the right amount of air movement and relatively closely clustered farms – you might have a legitimate route for lateral transmission. 

For earlier blogs on the viability of influenza viruses (avian and human) in the environment, you may wish to revisit:

 

NIH Study: Climate & Influenza Transmission

PLoS One: High Humidity Reduces Flu’s Infectivity

Influenza Virus Survival At Opposite Ends Of The Humidity Spectrum

Study: (H5N1): Effects Of Physico-Chemical Factors On Its Survival

EID Journal: The Stability Of The Ebola Virus On Surfaces & In Fluids

October 15th  Outside Nina Pham’s Apartment

 

# 9998

 

One of the critical issues that emerged during the Ebola epidemic in Western Africa is how little we actually knew about the stability and persistence of the virus in the environment, and how that might vary across different climates and settings. 

 

Variations in temperature, humidity, duration and strength of UV exposure, the types of fluids (including their pH), and the types of surfaces were all potentially mitigating factors. 

 

Last August, a CDC Interim Guidance and FAQ (see Interim Guidance for Environmental Infection Control in Hospitals for Ebola Virus) had this to say about the research to date:

 

6. How long does the Ebola virus persist in indoor environments?

Only one laboratory study has been reported, which was done under environmental conditions that favor virus persistence. This study found that under these ideal conditions, Ebola virus could remain active for up to six days.¹ In a follow-up study, Ebola virus was found, relative to other enveloped viruses, to be quite sensitive to inactivation by ultraviolet light and drying; yet subpopulations did persist in organic debris.²

In the only study to assess contamination of the patient care environment during an outbreak, conducted in an African hospital under "real-world conditions," Ebola virus was not detected by either nucleic acid amplification or culture in any of 33 samples collected from sites that were not visibly bloody. Virus was detected on a blood-stained glove and bloody intravenous insertion site by nucleic acid amplification, which may detect nonviable virus, but not by culture for live, infectious virus.³ Based upon these data and what is known regarding the environmental infection control of other enveloped RNA viruses, the expectation is that with consistent daily cleaning and disinfection practices in U.S. hospitals, the persistence of Ebola virus in the patient care environment would be short, with 24 hours³ considered a cautious upper limit.

 

That said, the CDC adopted some very strict guidance on dealing with potential environmental contamination from the Ebola virus, outlined in Interim Guidance for the U.S. Residence Decontamination for Ebola Virus Disease (Ebola) and Removal of Contaminated Waste  and CDC Interim Ebola Guidance: Mortuary Removal and Handling.

 

Last February, in EID Journal: Post Mortem Stability Of The Ebola Virus, we saw a study that found that viable Ebola virus could be isolated 7 days post-mortem in cynomolgus macaques, and that viral RNA continued to be detectable reliably for 3 weeks and sporadically for up to 10 weeks. 

 

The authors wrote, `. . .  viable virus can persist for >7 days on surfaces of bodies, confirming that transmission from deceased persons is possible for an extended period after death.’

 

Today the same team of NIH researchers are back with another EID Dispatch, this time looking at the persistence of the Ebola virus in the environment.

Two of their most striking findings were;

1. That the Ebola virus lived longer on surfaces (stainless steel, plastic, or Tyvek) roughly twice as long in a climate controlled environment (temp 21°C, 40% RH) than it did in a  tropical environment (27°C, 80% relative humidity (RH)).
2. The Ebola virus remains viable in water for as long as 3 days at 27°C  or 6 days at 21°C

 

I’ve only excerpted part of the study, follow the link below to read it in its entirety.

 

Volume 21, Number 7—July 2015

Dispatch

Ebola Virus Stability on Surfaces and in Fluids in Simulated Outbreak Environments

Robert Fischer¹, Seth Judson¹, Kerri Miazgowicz, Trenton Bushmaker, Joseph Prescott, and Vincent J. Munster

Author affiliations: National Institutes of Health, Hamilton, Montana, USA

 

Abstract

We evaluated the stability of Ebola virus on surfaces and in fluids under simulated environmental conditions for the climate of West Africa and for climate-controlled hospitals. This virus remains viable for a longer duration on surfaces in hospital conditions than in African conditions and in liquid than in dried blood.

<SNIP>

We report stability of EBOV with a current outbreak strain from Guinea (Makona-WPGC07) (9) on 3 clinically relevant surfaces: stainless steel, plastic, and Tyvek (Dupont, Wilmington, DE, USA). We also determined the stability of EBOV in water, spiked human blood, and blood from infected nonhuman primates (NHPs). These experiments were conducted in 2 environmental conditions, 21°C, 40% RH, and 27°C, 80% RH, to simulate a climate-controlled hospital and the environment in West Africa, respectively.

Conclusions

We found that EBOV can persist on surfaces common in an ETU, highlighting the need for adherence to thorough disinfection and doffing protocols when exiting the ETUs and careful handling of medical waste. In addition, EBOV maintains viability for a longer duration in liquid than in dried blood. EBOV in blood of experimentally infected NHPs persists for a similar duration as EBOV in spiked human blood. A recent study showed that blood in the body cavity of an NHP contained viable EBOV for up to 7 days after death (13). We detected viable EBOV in drying blood for up to 5 days at both environmental conditions in human and NHP blood. Therefore, dried and liquid blood from an infected person in their home or ETU should be treated as potentially infectious. The finding that EBOV remains viable in water for as long as 3 (27°C) or 6 (21°C) days at the experimental concentration warrants further investigation into the persistence of the virus in aqueous environments, such as in wastewater or sewage canals. Viable EBOV has been isolated from urine (14) but not from human stool (8). Therefore, the potential for dissemination of EBOV through wastewater remains unknown.

This study is subject to several limitations. First, because standard volumes for samples were used, different volumes or matrices could influence the stability of EBOV under the tested conditions. Second, blood samples from the NHPs might have different immunologic or biochemical conditions, which can potentially influence virus stability. Third, the experimental conditions in the laboratory are sterile, but in disease-endemic areas and ETUs, bacteria or chemicals could influence EBOV viability.

Overall, we found that different environmental conditions, fluids, and surfaces influence the persistence of EBOV. These findings demonstrate that such factors are crucial in understanding transmission and improving safety practices.

CDC Interim Ebola Guidance: Environmental Infection Control In Hospitals

Credit CDC PHIL

 

 

# 8974

 

 

The CDC continues to roll out new interim guidance documents for health care professionals and facilities that at some point may be called upon to deal with an imported Ebola case in the United States.  As always, these are `works in progress’, and are subject to revision over time as more is learned about dealing with this virus.

 

Although laboratory experiments have shown that the Ebola virus can remain viable on solid surfaces for up to 6 days – at least under ideal environmental conditions -  very limited `real world’  field testing has suggested a far less hardy organism; one that is susceptible to degradation by sunlight, desiccation, and time. 

That said, the precise role of environmental transmission of Ebola is far from settled - and given its lethality and low infectious dose - guidance in these matters tends to err on the side of caution. Also included is a Frequently Asked Questions section (FAQ), which poses (and answers) several interesting questions, including:

 

• How should disposable materials (e.g., any single-use PPE, cleaning cloths, wipes, single-use microfiber cloths, linens, food service) and linens, privacy curtains, and other textiles be managed after their use in the patient room?

• Are wastes generated during delivery of care to Ebola virus-infected patients subject to select agent regulations?

I’ve only reproduced the main body of the guidance, so follow the link to read it, and the accompanying FAQ in its entirety.

 

Interim Guidance for Environmental Infection Control in Hospitals for Ebola Virus

 

On August 1, 2014, CDC released guidance titled, Infection Prevention and Control Recommendations for Hospitalized Patients with Known or Suspected Ebola Hemorrhagic Fever in U.S. Hospitals. Ebola viruses are transmitted through direct contact with blood or body fluids/substances (e.g., urine, feces, vomit) of an infected person with symptoms or through exposure to objects (such as needles) that have been contaminated with infected blood or body fluids. The role of the environment in transmission has not been established. Limited laboratory studies under favorable conditions indicate that Ebola virus can remain viable on solid surfaces, with concentrations falling slowly over several days.^{1, 2} In the only study to assess contamination of the patient care environment during an outbreak, virus was not detected in any of 33 samples collected from sites that were not visibly bloody. However, virus was detected on a blood-stained glove and bloody intravenous insertion site.³ There is no epidemiologic evidence of Ebola virus transmission via either the environment or fomites that could become contaminated during patient care (e.g., bed rails, door knobs, laundry). However, given the apparent low infectious dose, potential of high virus titers in the blood of ill patients, and disease severity, higher levels of precaution are warranted to reduce the potential risk posed by contaminated surfaces in the patient care environment.

As part of the care of patients who are persons under investigation, or with probable or confirmed Ebola virus infections, hospitals are recommended to:

• Be sure environmental services staff wear recommended personal protective equipment including, at a minimum, disposable gloves, gown (fluid resistant/ impermeable), eye protection (goggles or face shield), and facemask to protect against direct skin and mucous membrane exposure of cleaning chemicals, contamination, and splashes or spatters during environmental cleaning and disinfection activities. Additional barriers (e.g., leg covers, shoe covers) should be used as needed. If reusable heavy-duty gloves are used for cleaning and disinfecting, they should be disinfected and kept in the room or anteroom. Be sure staff are instructed in the proper use of personal protective equipment including safe removal to prevent contaminating themselves or others in the process, and that contaminated equipment is disposed of as regulated medical waste.
• Use a U.S. Environmental Protection Agency (EPA)-registered hospital disinfectant with a label claim for a non-enveloped virus (e.g., norovirus, rotavirus, adenovirus, poliovirus) to disinfect environmental surfaces in rooms of patients with suspected or confirmed Ebola virus infection. Although there are no products with specific label claims against the Ebola virus, enveloped viruses such as Ebola are susceptible to a broad range of hospital disinfectants used to disinfect hard, non-porous surfaces. In contrast, non-enveloped viruses are more resistant to disinfectants. As a precaution, selection of a disinfectant product with a higher potency than what is normally required for an enveloped virus is being recommended at this time. EPA-registered hospital disinfectants with label claims against non-enveloped viruses (e.g., norovirus, rotavirus, adenovirus, poliovirus) are broadly antiviral and capable of inactivating both enveloped and non-enveloped viruses.
• Avoid contamination of reusable porous surfaces that cannot be made single use. Use only a mattress and pillow with plastic or other covering that fluids cannot get through. Do not place patients with suspected or confirmed Ebola virus infection in carpeted rooms and remove all upholstered furniture and decorative curtains from patient rooms before use.
• To reduce exposure among staff to potentially contaminated textiles (cloth products) while laundering, discard all linens, non-fluid-impermeable pillows or mattresses, and textile privacy curtains as a regulated medical waste.

(Continue . . . )

WHO: Environmental Surveillance Detects WPV1 (Polio) In Brazil

Child receiving Polio Vaccine – CDC PHIL

 

# 8774

 

Although it may be not the most glamorous public health job at the World Cup in Brazil, the sampling of sewage for the poliovirus is an important part of the surveillance effort, since only 1 person in 100 who becomes infected actually develops the acute flaccid paralysis (AFP) we normally associate with the disease.

 

Everyone who is infected, however, sheds large quantities of the virus in their feces for weeks, making environmental sampling of sewage an efficient method of determining the presence of the virus in the community.

 

In January of 2013, you may recall, we saw a report (see Polio Virus Detected By Environmental Surveillance In Egypt) where this type of surveillance had detected Wild Poliovirus type 1 (WPV1) in sewage samples taken in Cairo, Egypt, and they closely matched those found in Pakistan.

 

Today, it has been announced that environmental surveillance has detected WPV1 in sewage samples taken from São Paulo, from an area where previous sampling has failed to produce positive results. This suggests a recent importation of the virus.  Genetic analysis shows this virus is a close match to strain recently detected in Equatorial Guinea.

 

There is no indication at this time that anyone has been infected in Brazil, and given the high level of local immunity due to regular immunization drives, the risks of forward transmission are considered low.

 

  This from the World Health Organization.

 

Detection of poliovirus in sewage, Brazil

Disease outbreak news
23 June 2014

On 18 June 2014, the National IHR Focal Point for Brazil reported the isolation of wild poliovirus type 1 (WPV1) from sewage samples collected in March 2014 at Viracopos International Airport, in Campinas municipality in the State of São Paulo, Brazil. Virus has been detected in the sewage only; sewage samples collected from the same site subsequent to the detection of WPV1 have been either negative or only positive for Sabin strains or non-polio enteroviruses; to date no case of paralytic polio has been reported. The isolate was detected through routine environmental surveillance testing of sewage water; there is no evidence of transmission of WPV1.

Genetic sequencing indicated a close match with a strain of WPV1 that was recently isolated from a case of polio in Equatorial Guinea. Additional epidemiological investigation is ongoing.

The Americas Region has been free of indigenous WPV transmission since 1991 and Brazil since 1989. There is no indigenous transmission of wild poliovirus reported in Brazil since 1989.

Brazil health authorities have enhanced their surveillance activity aimed to detect transmission of WPV1 and potential cases of paralytic polio as well as for any un-immunized persons. The vaccination coverage against polio in São Paulo State and Campinas municipality have been higher than 95% in the routine immunization program. The last national OPV campaign was conducted in June 2013. The campaign for this year is planned in November 2014 at the national level and the target group is children 6 months to less than 5 years of age with OPV.

Specimens collected through environmental surveillance at this and other sites in Brazil since 1994 have consistently tested negative for the presence of WPV.

Given the high levels of population immunity indicated by the high routine immunization coverage and implementation of periodic vaccination campaigns in the area — no evidence so far of WPV1 transmission and the response being implemented — the World Health Organization (WHO) assesses the risk of further international spread of this virus from Brazil as very low.

Given the ongoing WPV1 outbreak in Equatorial Guinea, low national routine immunization coverage, and the inconsistent quality of the initial outbreak response vaccination campaigns, WHO assesses the risk of additional exportation from Equatorial Guinea as high.

WHO note

Brazil was not re-infected with WPV; the country was exposed to a poliovirus importation.

The environmental surveillance system had the capacity to detect the poliovirus in sewage samples and the high immunity appears to have prevented transmission.

WHO travel recommendations

WHO’s International Travel and Health recommends that all travellers to and from polio-affected areas be fully vaccinated against polio. Brazil has detected a poliovirus importation event. Based on current evidence, the country is not considered polio-affected.

 

With hundreds of thousands of people flocking to Brazil for the World Cup from all corners of the world, one of public health concerns has revolved around what diseases might be imported into  (or exported from) Brazil during this month-long event. 

 

The sample being reported today was collected in March, long before the start of  FIFA World Cup, and is presumably not connected to that event.

 

Still, international travel carries with it the risk of acquiring or spreading infectious diseases, and so the WHO/PAHO have called for visitors to be vaccinated against a variety of diseases, including Polio (see The ECDC Risk Assessment On Brazil’s FIFA World Cup).

 

Vaccination coverage should include:

• all diseases included in the immunisation schedule of all EU Member States: poliomyelitis, diphtheria, tetanus, pertussis, measles, mumps and rubella;
• all diseases included in the immunisation schedule of some EU Member States: tuberculosis, pneumococcal disease, meningococcal disease, human papilloma virus (HPV) and chickenpox;
• diseases with an increased risk of acquisition for visitors to Brazil: hepatitis A, yellow fever, rabies, and typhoid fever; and
• one disease which could be re-introduced to Brazil: cholera.

MERS: A Focus On Fomites?

WHO team in Jeddah Investigation MERS - Credit @WHO

 

# 8555

This week a team from the World Health Organization is on the ground in Jeddah, where the largest concentration of MERS coronavirus cases has been reported to date. 

 

Although their investigation is on-going and it is too soon to reach any conclusions,  this morning WHO spokesperson Gregory Hartl suggested that fomites – inanimate objects and environmental surfaces –might be a significant player in the transmission of the MERS coronavirus.

 

 

While the role of fomites in the transmission of the virus has yet to be established (and indeed, its relevance may vary by location and/or cluster), it is probably worth taking a closer look at the environmental stability of the MERS virus, and how well it might be transmitted by contaminated surfaces or other inanimate media.

 

We have a pair of studies that address the survivability of the MERS virus outside of an animal host, and both suggest that – under the right environmental conditions – the virus remains viable for extended periods of time.

 

Three weeks ago, in EID Journal: Stability Of MERS-CoV In Milk, we saw a study where researchers inoculated various types of milk products (camel, goat, cow, etc.) and DMEM (a cell culture media) with MERS-CoV strain Jordan-N3/2012, stored multiple samples at 4°C or 22°C, and then tested their infectious disease titers at 0, 8, 24, 48, 72 hours post dilution. 

 

Their results?

 

At 0–72 hpd, virus titers decreased significantly only in goat milk (p = 0.0139, 1-tailed paired t test) and DMEM (p = 0.0311) but not in dromedary camel milk (p = 0.1414) or cow milk (p = 0.2895). Samples stored at 22°C showed a greater loss of infectivity than did samples stored at 4°C.

 

Making unpasteurized milk at least a plausible medium for carriage of the MERS virus or its transmission to humans. Unknown at this time is whether camels shed the virus in their milk, a project that Dr. Ian Lipkin’s group at Columbia University is reportedly going to tackle next.

 

Another study, going back to September of last year, appeared in the journal Eurosurveillance: Environmental Stability Of MERS-CoV.  Here researchers looked at the environmental stability of the MERS coronavirus, both on surfaces (fomites), and as an aerosol.

 

The researchers describe their experiments below (slightly reformatted for readability).

 

In this study, the stability of MERS-CoV (isolate HCoV-EMC/2012) was evaluated under three different environmental conditions:

• high temperature and low humidity, 30°C – 30% relative humidity (RH);
• high temperature and high humidity, 30°C – 80% RH
• and low temperature and low humidity, 20°C – 40% RH

to reflect a wide range of environmental conditions including an indoor environment (20°C – 40% RH).

The stability of MERS-CoV under the three tested environmental conditions was respectively compared with that of influenza A virus A/Mexico/4108/2009 (H1N1) originating from a human isolate obtained during the influenza A(H1N1)pdm09 pandemic in 2009 [9]. The stability of the two viruses in aerosols at 20°C with 40% or 70% RH was also assessed and compared.

 

The results?

 

• While the Influenza A virus became non-viable on steel and plastic surfaces in less than 4 hours for all testing environments, the MERS virus survived 48 hours in the 20°C – 40% RH environment. Survival of the coronavirus at 30°C – 30% RH was 24 hours, and 8 hours at 30°C – 80% RH.
• As an aerosol, the MERS virus remained very stable at 20°C – 40% RH, while its viability decreased  (89% – comparable to the Influenza A virus)  at 20°C – 70% RH.

 

The full study can be found at: Stability of Middle East respiratory syndrome coronavirus (MERS-CoV) under different environmental conditions by  N van Doremalen¹, T Bushmaker¹, V J Munster.

 

The bottom line, under favorable temperature and humidity conditions (such as you might find in an air conditioned hospital), the MERS virus survives quite well on surfaces, and in the air. This may help explain the high rate of nosocomial outbreaks we’ve seen in the Middle East.

 

While the route of infection with this virus has not been determined, this virus shows the kind of environmental hardiness that would be conducive for either fomite or droplet/aerosol  (contact) transmission.

 

When the WHO’s mission in Saudi Arabia is completed, and they’ve had time to look at the data they’ve collected, we should have a better idea of what is going on with this virus.

 

Stay tuned.

 

 

Eurosurveillance: Environmental Stability Of MERS-CoV

Coronavirus – Credit CDC PHIL

 

 

 

# 7793

 

Although viruses are generally pretty fragile, we know that under the right environmental conditions, some of them can retain their integrity and infectivity for hours, days, or even weeks outside of a host organism. Temperatures, UV exposure,  pH, humidity, and other factors can all effect how long a virus can remain viable in the environment.

We know, for instance, that temperature and humidity greatly affect the spread of influenza (see Influenza Virus Survival At Opposite Ends Of The Humidity Spectrum), which helps explain the seasonality of flu.

 

Today, Eurosurveillance Journal has published our first good look at the environmental stability of the MERS coronavirus, both on surfaces (fomites), and as an aerosol. The researchers describe their experiments thusly:

 

In this study, the stability of MERS-CoV (isolate HCoV-EMC/2012) was evaluated under three different environmental conditions: high temperature and low humidity, 30°C – 30% relative humidity (RH); high temperature and high humidity, 30°C – 80% RH and low temperature and low humidity, 20°C – 40% RH, to reflect a wide range of environmental conditions including an indoor environment (20°C – 40% RH). The stability of MERS-CoV under the three tested environmental conditions was respectively compared with that of influenza A virus A/Mexico/4108/2009 (H1N1) originating from a human isolate obtained during the influenza A(H1N1)pdm09 pandemic in 2009 [9]. The stability of the two viruses in aerosols at 20°C with 40% or 70% RH was also assessed and compared.

 

Their results are striking.  

 

• While the Influenza A virus became non-viable on steel and plastic surfaces in less than 4 hours for all testing environments, the MERS virus survived 48 hours in the 20°C – 40% RH environment. Survival of the coronavirus at 30°C – 30% RH was 24 hours, and 8 hours at 30°C – 80% RH.
• As an aerosol, the MERS virus remained very stable at 20°C – 40% RH, while its viability decreased  (89% – comparable to the Influenza A virus)  at 20°C – 70% RH.

 

The bottom line, under favorable temperature and humidity conditions (such as you might find in an air conditioned hospital), the MERS virus survives quite well on surfaces, and in the air. This may help explain the high rate of nosocomial outbreaks we’ve seen in the Middle East.

 

While the route of infection with this virus has not been determined, this virus shows the kind of environmental hardiness that would be conducive for either fomite or droplet/aerosol  (contact) transmission.

 

Here is a link to the  NIAID study (and excerpts).

 

Stability of Middle East respiratory syndrome coronavirus (MERS-CoV) under different environmental conditions

N van Doremalen¹, T Bushmaker¹, V J Munster ()¹

1. Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA

---

Citation style for this article: van Doremalen N, Bushmaker T, Munster VJ. Stability of Middle East respiratory syndrome coronavirus (MERS-CoV) under different environmental conditions. Euro Surveill. 2013;18(38):pii=20590. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20590
Date of submission: 10 September 2013

---

The stability of Middle East respiratory syndrome coronavirus (MERS-CoV) was determined at 20°C – 40% relative humidity (RH); 30°C – 30% RH and 30°C – 80% RH. MERS-CoV was more stable at low temperature/low humidity conditions and could still be recovered after 48 hours. During aerosolisation of MERS-CoV, no decrease in stability was observed at 20°C – 40% RH. These data suggest the potential of MERS-CoV to be transmitted via contact or fomite transmission due to prolonged environmental presence.

<BIG SNIP>

DISCUSSION (Excerpt)

Here we show that compared to A/Mexico/4108/2009 (H1N1) virus, MERS-CoV remains viable for a longer duration in the environment. After four hours no viable A/Mexico/4108/2009 (H1N1) virus was detected in comparison to 8, 24 or 48 hours for MERS-CoV depending on environmental conditions (Figure 1, panels A and D). MERS-CoV was very stable in aerosol form at 20°C – 40% RH. The decrease in viability at 20°C – 70% RH (89%) was comparable to that of A/Mexico/4108/2009 (H1N1) virus.

 

Severe acute respiratory syndrome coronavirus (SARS-CoV) has been reported to stay viable for up to five days at 22 to 25°C and 40 to 50% RH and increase in temperature and humidity resulted in a rapid loss of viability [19]. Although a comparison between different experimental studies should be approached cautiously, the relative stability of MERS-CoV at 20°C – 40% RH and the rapid decrease in virus viability at higher temperatures and higher humidity suggests that MERS-CoV and SARS-CoV share relatively similar stability characteristics.

 

Although the route of transmission for MERS-CoV is currently unknown, the spread of MERS-CoV between people in close contact settings suggest contact and fomite transmission routes are most likely involved [2,3,16]. Knowledge on the environmental stability of MERS-CoV does not provide direct insights in the route of transmission; yet it does provide us with a better understanding for the potential of aerosol, contact and fomite transmission. The prolonged survival of MERS-CoV compared to A/Mexico/4108/2009 (H1N1) virus on surfaces increases the likelihood of contact and fomite transmission. However, the decrease in viability observed at high temperature suggests that direct contact transmission, and not fomite transmission, in the Arabian Peninsula would be the most likely route of zoonotic and human-to-human transmission in outdoor settings.

 

The ability of MERS-CoV to remain viable in an airborne state suggests the potential for MERS-CoV to acquire the ability to be transmitted via aerosols. In the absence of therapeutic and prophylactic intervention strategies for MERS-CoV, a thorough understanding of the routes of transmission could be the most effective way to arrest the further spread of MERS-Co

EID Journal: Persistence Of H5N1 In Soil

 

Photo Credit – FAO

 

# 6478

 

The notion that the H5N1 `bird flu’ virus can persist in the environment – for hours or days (or perhaps even weeks) - is hardly new, yet very little is really known about how, and where, the virus resides outside of a living host.

 

As H5N1 is primarily a gastrointestinal malady in birds it is believed that the virus is commonly spread in the wild via shared feces-contaminated pond and lake waters (see Bogor: H5N1 Detected In Retention Pond).

 

But there appear to be other routes of transmission as well.

 

In June of 2010, we saw a study (see Birds Of A Feather . . . .) in PLoS One, suggesting that waterfowl may be spreading avian flu viruses because their preening oils bind the virus to their feathers.

 

Another study conducted by researchers at the  National Institute of Animal Health, Tsukuba, Ibaraki, Japan was reported in the August 2010 issue of Applied and Environmental Microbiology.

 

They determined that the H5N1 virus may persist on the dropped feathers from infected ducks and may therefore spread to the environment. 

 

Applied and Environmental Microbiology, August 2010, p. 5496-5499, Vol. 76, No. 16
0099-2240/10/$12.00+0     doi:10.1128/AEM.00563-10

Persistence of Avian Influenza Virus (H5N1) in Feathers Detached from Bodies of Infected Domestic Ducks

Yu Yamamoto, Kikuyasu Nakamura, Manabu Yamada, and Masaji Mase

 

The surprising part of this study is how long these feathers retained some degree of viral contamination at various temperatures.

 

At 4°C (39F) the virus was detectable for 160 days, while at the higher temperature 20°C (68F), the virus was detected for 15 days.

 

We saw another study from 2010, which appeared in Environmental Science and Technology, titled:

 

Environmental Persistence of a Highly Pathogenic Avian Influenza (H5N1) Virus

Joseph P. Wood, Young W. Choi, Daniel J. Chappie, James V. Rogers, and Jonatha

n Z. Kaye

DOI: 10.1021/es1016153

Copyright © 2010 American Chemical Society

 

Researchers conducted tests on four inanimate materials (glass, wood, galvanized metal, and top soil) to determine how long – and under what environmental conditions – the virus could survive.

 

They adjusted factors such as  temperature, relative humidity, and simulated sunlight and checked the samples over a period of 13 days. The virus was most persistent at lower temperatures, and on surfaces such as glass and steel.

 

Their conclusion?: under the right conditions, the virus could be expected to persist beyond 13 days.

 

 

Earlier this year we looked at a study published in the journal Influenza and Other Respiratory Viruses that examined environmental samples taken in Cambodia between April 2007 and February 2010 during several bird flu outbreaks (see Environment: a potential source of animal and human infection with influenza A (H5N1) virus  Gutiérrez, Buchy et al.)

Out of 246 samples taken around farms with outbreaks, 19% of dust, mud and soil samples showed contamination from the H5N1 virus.

 

Admittedly, just because RT-PRC testing was able to detect a virus in a sample doesn’t necessarily mean that the virus is viable.  But it does give us an idea of the environment spread of the virus.

 

All of which brings us to a letter, again from  Ramona A. Gutiérrez and Philippe Buchy of the Institut Pasteur in Cambodia, that appears in September’s edition of the CDC’s EID journal.

 

Volume 18, Number 9—September 2012

Letter

Contaminated Soil and Transmission of Influenza Virus (H5N1)

To the Editor: Highly pathogenic avian influenza (HPAI) virus (H5N1) has been responsible for 603 confirmed human cases worldwide, including 356 that resulted in death, and for >7,000 epizootic outbreaks (1,2). Direct contact between hosts is the main mechanism of transmission for avian influenza viruses, but the possible role of the environment as a source of HPAI virus (H5N1) infection has been rarely studied, particularly in the context of countries where the virus is enzootic or epizootic (3–7). To determine if contaminated soil contributes to the transmission cycle of HPAI virus (H5N1), we used experimental and simulated field conditions to assess possible transmission in chickens.

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Essentially, these researchers took 3 types of soil, described as:

 

(1) sandy topsoil collected from around rice fields in Phnom Penh Province, Cambodia;

2) building sand purchased from a local building company; and

3) soil-based compost purchased from a local tree nursery

. . . and inoculated samples with low to high doses of the H5N1 virus. They then introduced these soil samples to the bottom of cages where chickens were housed, and then tested the chickens for infection over the next several days.

You can read the entire letter for more details on their methods and materials. The results are summarized in the chart below:

 

Essentially, sandy topsoil collected from rice fields proved to be a poor environment for transmitting the H5N1 virus, while soil-based compost proved highly effective. 

 

The authors believe that the highly acidic nature of the sandy topsoil may work to inactivate viral particles.

 

Since one of the methods used to control and contain an avian flu outbreak is environmental decontamination, knowing which types of soil are unlikely to harbor and transmit the virus can save time, and reduce the use of harsh (and often scarce) chemicals in the environment.

 

Interestingly, the authors also found evidence to suggest that exposure to moderately contaminated soil may help poultry to develop a protective immune response to the virus.

 

H5N1 is not the only viral contender to spark the next pandemic, but due to its apparent high lethality, it is the one we tend to concentrate on the most.  

 

Fortunately the virus remains adapted primarily to avian physiology – not human - and must mutate further if it is to become an imminent public health threat. 

 

But with 20+ clades of the virus now circulating, and numerous opportunities to expose and infect other hosts (human, swine, mammal, and avian), the concern is this virus may one day succeed.

H5N1: Hiding In Plain Sight

 

 

Photo Credit – FAO

# 6164

 

A pair of related stories this morning that reinforce the notion that in some places the H5N1 virus may be hiding in the environment, or alternatively, in healthy looking chickens.

 

Neither of which are exactly new ideas, but thus far evidence for both scenarios has been less than overwhelming.

 

First, as study out of Cambodia (h/t Tetano on FluTrackers) that was published on Feb. 17th by the journal Influenza and Other Respiratory Viruses.

 

In this study, environmental samples were collected following outbreaks of bird flu in Cambodia between April 2007 and February 2010.

 

 

Environment: a potential source of animal and human infection with influenza A (H5N1) virus

Srey V. Horm, Ramona A. Gutiérrez, San Sorn, Philippe Buchy

Article first published online: 17 FEB 2012

DOI: 10.1111/j.1750-2659.2012.00338.x

ABTRACT (excerpt)

Results Of a total of 246 samples, 46 (19%) tested positive for H5N1 by qRT-PCRs. Viral RNA was frequently detected in dust, mud and soil samples from the farms’ environment (respectively, 46%, 31% and 15%).

Samples collected from ponds gave a lower proportion of positive samples (6%) as compared to those collected from the farms (24%). In only one sample, infectious virus particles were successfully isolated.

Conclusion During H5N1 virus outbreaks, numerous environmental samples surrounding outbreak areas are contaminated by the virus and may act as potential sources for human and/or animal contamination.

 

It should be noted that given the sensitivity of modern RT-PRC testing, the ability to detect a virus in the environment doesn’t always tell us if it is viable.  That is . . .  whether it remains capable of infecting a host.

 

This report reinforces similar research over the past few years that have expressed similar concerns.

 

During the summer of 2010, in a blog called Of Ducks, And Feathers, And H5N1 we looked at a study that determined that the H5N1 virus may persist on the dropped feathers from infected ducks and that they may spread the virus to the environment.

 

The surprising part of this study is how long these feathers retained some degree of viral contamination at various temperatures.

 

At 4°C (39F) the virus was detectable for 160 days, while at the higher temperature 20°C (68F), the virus was detected for 15 days.

 

The following month, in a study that appeared in Environmental Science and Technology titled:

 

Environmental Persistence of a Highly Pathogenic Avian Influenza (H5N1) Virus

Joseph P. Wood, Young W. Choi, Daniel J. Chappie, James V. Rogers, and Jonatha

n Z. Kaye

DOI: 10.1021/es1016153

Copyright © 2010 American Chemical Society

 

Researchers conducted tests on four inanimate materials (glass, wood, galvanized metal, and top soil) to determine how long – and under what environmental conditions – the virus could survive.

 

They adjusted factors such as  temperature, relative humidity, and simulated sunlight and checked the samples over a period of 13 days.

 

The virus was most persistent at lower temperatures, and on surfaces such as glass and steel. Their conclusion?: at these conditions, the virus would be expected to persist appreciably beyond 13 days.

 

And in November of 2010, we saw an EID Journal study that surveyed LBMs (Live Bird Markets) in Indonesia, and found traces of the H5N1 virus in nearly half of the environmental samples tested (see EID Journal: Indonesian Bird Markets Tested For H5N1).

 

 

Next stop, comments published today in the Indonesian newspaper TEMPO  (h/t Commonground) from Professor C.A. Nidom, of the Institute of Tropical Disease, Airlangga University. 

He repeats a warning that he (and others) have given before; that ineffective or improperly dispensed poultry vaccines can mask H5N1 infection in poultry, allowing people to be exposed via `healthy looking’ chickens.

 

 

Wednesday, February 22, 2012 | 10:43 pm

Can Bird Flu Virus Found in Poultry Healthy

TEMPO.CO, Jakarta - Head of Avian Influenza, Zoonosis Research Center University of Airlangga, CA Nidom, said that the bird flu virus (H5N1) can be found in healthy birds. Under these conditions because the vaccine is given to poultry.

He said the bird flu in poultry vaccine made antibodies to poultry so that the birds will stay healthy and not die even if hit by bird flu virus. As a result, signs of the virus has already infected, but not seen. So that public awareness is less because they think that their birds have in a healthy state.

"Our research states that avian flu has been vaccinated birds can still carry the virus even look healthy," he said by telephone on Wednesday, February 22, 2012.

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If this sounds familiar, you may recall that Dr. Nidom has previously warned on using poultry vaccines to control Indonesia’s bird flu problem (see Indonesia: Debate Over Poultry Vaccination), as opposed to culling.

 

Similar warnings were expressed in early 2009 from Zhong Nanshan, a hero of the SARS outbreak and a highly respected respiratory disease specialist in China, who warned that vaccinated poultry can still become infected with the H5N1 virus.

 

Chinese expert issues new bird flu warning

www.chinaview.cn  2009-02-06 17:59:50

GUANGZHOU, Feb. 6 (Xinhua) -- A leading Chinese expert on respiratory diseases has warned the public to be aware that poultry can be infected with the bird flu virus but show no symptoms.

 

"Special attention should be paid to such animals, including those that have been vaccinated," said Zhong Nanshan.

 

"The existing vaccines can only reduce the amount of virus, rather than totally inactivating it," he said.

(Continue . . . )

 

The OIE (World Organization For Animal Health) has been aware of the potential of vaccines to hide infection for many years, warning that vaccination of poultry cannot be considered a long-term solution to combating the avian flu virus.

 

In Avian influenza and vaccination: what is the scientific recommendation?, the OIE reiterates their strong recommendation that humane culling be employed to control avian influenza, and advising that vaccines should only be used as a temporary measure.

While the OIE concedes that some nations may require the use of vaccines for `several years', they strongly urge that countries move away from that program and towards the more conventional culling policy.

They call this shift away from vaccines an `Exit Strategy’, something which China, Indonesia, Vietnam, and have shown no move towards.

 

And the big news now out of Vietnam over the past year has been the failure of their poultry vaccine against the emerging 2.3.2.1 clade of the virus which is now widely circulating in the north.

 

In August 2011 the FAO issued a statement on this 2.3.2.1 clade (see FAO Warns On Bird Flu) that is not covered by currently available poultry vaccines.

 

Despite the growing concerns over asymptomatic poultry carrying the H5N1 virus, and evidence of environmental contamination by the virus, the limited number of human cases we have seen to date indicate that the virus still has a hard time infecting humans.

 

It is adapted to avian physiology – not human - and must mutate further if it is to become an imminent public health threat.

 

But with 20+ clades of the virus now circulating, and numerous opportunities to expose and infect other hosts (human, swine, mammal, and avian), the virus may one day succeed.

 

 

Which is why the world remains in pre-pandemic phase III on the H5N1 virus, and we watch its progress intently.

EID Journal: Indonesian Bird Markets Tested For H5N1

 

 

# 5065

 

 

Timing, they say, is everything.

 

And so it is fitting that on a day when we learn of an H5N1 positive Hong Kong resident - who reportedly visited live bird markets on the mainland  - we get this survey of H5N1 environmental contamination at LBMs (Live Bird Markets) in Indonesia.

 

The `big news’ here is that traces of the H5N1 virus were detected (using real-time reverse transcription–PCR and virus isolation) in nearly half (47%) of the 83 markets tested.

 

You should know, however, that RT-PCR testing can detect non-viable virus particles. And so just because the virus was detected, that doesn’t necessarily mean the virus was capable of infecting a new host.

 

Virus isolation, while less well suited for testing environment samples, only detects viable viral contamination.

 

As you might expect, the percentage of positives by virus isolation was considerably lower than that returned by RT-PCR.

 

Of the 280 positive samples by RT-PCR, only  13 (4.6%) were positive by virus isolation (Probably a low-ball number, given the sensitivity of the test).

 

These numbers do give us an idea of just how prevalent H5N1 is in domestic poultry in Indonesia, and argue compellingly for better sanitation procedures in live markets.

 

I suppose the solace we can take from all this is that – despite numerous contaminated live bird markets in Indonesia - we haven’t seen a huge number of human infections. 

 

Given the amount of human contact with infected birds and contaminated environments, this strongly suggests that the virus remains poorly adapted to human physiology and difficult to contract.

 

This study is published ahead of print in today’s EID Journal.

 

 

Volume 16, Number 12–December 2010

Research

Environmental Sampling for Avian Influenza Virus A (H5N1) in Live-Bird Markets, Indonesia

Indriani R, Samaan G, Gultom A, Loth L, Indryani S, Adjid R, et al. Environmental sampling for avian influenza virus A (H5N1) in live-bird markets, Indonesia. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1889.htm

DOI: 10.3201/eid1612.100402

Abstract

To identify environmental sites commonly contaminated by avian influenza virus A (H5N1) in live-bird markets in Indonesia, we investigated 83 markets in 3 provinces in Indonesia.

 

At each market, samples were collected from up to 27 poultry-related sites to assess the extent of contamination. Samples were tested by using real-time reverse transcription–PCR and virus isolation. A questionnaire was used to ascertain types of birds in the market, general infrastructure, and work practices.

 

Thirty-nine (47%) markets showed contamination with avian influenza virus in >1 of the sites sampled. Risk factors were slaughtering birds in the market and being located in West Java province.

 

Protective factors included daily removal of waste and zoning that segregated poultry-related work flow areas. These results can aid in the design of evidence-based programs concerning environmental sanitation, food safety, and surveillance to reduce the risk for avian influenza virus A (H5N1) transmission in live-bird markets.

 

Follow the link to read details about the methods of sample collecting,testing and the results. 

Study: H5N1 - A Very Persistent Virus

 

# 4893

 

 

The `conventional wisdom’ is that human influenza viruses are pretty fragile, and are unlikely to survive in the environment (outside of a host) for more than a few hours.

 

In fact, the CDC’s  Fact Sheet on Preventing Seasonal Flu gives the following advice:

 

How long can human influenza viruses remain viable on inanimate items (such as books and doorknobs)?

Studies have shown that human influenza viruses generally can survive on surfaces for between 2 and 8 hours.

 

Of course . . . there are exceptions.  Certain environmental conditions that promote longer survival.

 

In 2008 we saw a study from the Central Laboratory of Virology in Geneva, Switzerland showing that seasonal influenza viruses could survive on Swiss banknotes (when encapsulated in mucus) for up to 17 days.

Survival of influenza virus on banknotes.

Thomas Y, Vogel G, Wunderli W, Suter P, Witschi M, Koch D, Tapparel C, Kaiser L.

 

Abstract (Excerpt)

Influenza A viruses tested by cell culture survived up to 3 days when they were inoculated at high concentrations. The same inoculum in the presence of respiratory mucus showed a striking increase in survival time (up to 17 days).

 

Similarly, B/Hong Kong/335/2001 virus was still infectious after 1 day when it was mixed with respiratory mucus. When nasopharyngeal secretions of naturally infected children were used, influenza virus survived for at least 48 h in one-third of the cases.

 

Temperature, humidity, sunlight (UV rays) and the type of environment (hard surface, porous material, water, etc) all play a role in how long a virus might survive outside of a living host.

 

As you might imagine, given the difficulty that countries like Indonesia, Egypt, and Vietnam have had in eradicating the H5N1 virus, research in its ability to survive in the environment is of great interest.

 

Last month (see Of Ducks, And Feathers, And H5N1) we saw a study that determined that the H5N1 virus may persist on the dropped feathers from infected ducks and that they may spread the virus to the environment.  You can follow the link below to read the abstract.

 

Applied and Environmental Microbiology, August 2010, p. 5496-5499, Vol. 76, No. 16
0099-2240/10/$12.00+0     doi:10.1128/AEM.00563-10

Persistence of Avian Influenza Virus (H5N1) in Feathers Detached from Bodies of Infected Domestic Ducks

Yu Yamamoto, Kikuyasu Nakamura, Manabu Yamada, and Masaji Mase

 

The surprising part of this study is how long these feathers retained some degree of viral contamination at various temperatures.

 

At 4°C (39F) the virus was detectable for 160 days, while at the higher temperature 20°C (68F), the virus was detected for 15 days.

 

Today, a new study that appears in Environmental Science and Technology titled:

 

Environmental Persistence of a Highly Pathogenic Avian Influenza (H5N1) Virus

Joseph P. Wood, Young W. Choi, Daniel J. Chappie, James V. Rogers, and Jonathan Z. Kaye

DOI: 10.1021/es1016153

Publication Date (Web): September 3, 2010

Copyright © 2010 American Chemical Society

 

Here researchers conducted tests on four inanimate materials (glass, wood, galvanized metal, and top soil) to determine how long – and under what environmental conditions – the virus could survive.

They adjusted factors such as  temperature, relative humidity, and simulated sunlight and checked the samples over a period of 13 days.

 

The virus was most persistent at lower temperatures, and on surfaces such as glass and steel. Their conclusion?:  at these conditions, the virus would be expected to persist appreciably beyond 13 days.

 

For some more on this story, the Emerging Health Threats Forum  (h/t Carol@SC on the Flu Wiki) has on this study, and another on the effects of humidity on influenza viruses at:

 

 

Friday 10 September 2010

Long-lived bird flu stays on surfaces

Virus can remain infectious for up to two weeks at low temperatures

 

The second study:

 

Modeling the airborne survival of influenza virus in a residential setting: the impacts of home humidification

Theodore A Myatt , Matthew H Kaufman , Joseph G Allen , David L Macintosh , M PATRICIA Fabian  and James J McDevitt

 

Environmental Health 2010, 9:55doi:10.1186/1476-069X-9-55

 

Suggests that the use of portable humidifiers might lower the survival of aerosolized influenza viruses by raising humidity indoors.

 

Amazingly, even in 2010, there is still much to learn about the basics of influenza viruses and how they adapt and survive in our environment.

Absolute Humidity And Flu Transmission

 

 

 

# 4176

 

 

Figuring out why influenza is (primarily) a winter disease has been a goal for scientists for many years.  There are a number of theories out there, but the science – while not non-existent – has been a bit sparse.

 

Over the years we’ve touched on this subject a number of times. 

 

In October of 2007, a study appeared in  PLoS Pathogens  entitled  Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature  by Anice C. Lowen, Samira Mubareka, John Steel,  and Peter Palese.  I covered this story in a blog called Cold And Dry Statistics.

 

Using a guinea pig as a model host, they showed that airborne spread of the  influenza virus was at least partially dependent upon both ambient relative humidity and temperature.

 

The link was significant, but not overwhelming.

 

A little more than a year later, a study appeared in PNAS (Proceedings Of the National Academy of Sciences) that took another look at the data and found an even stronger correlation between the AH (Absolute Humidity) and the survival, and transmission of the virus.,  entitled:

 

Absolute humidity modulates influenza survival, transmission, and seasonality

Jeffrey Shaman, Melvin Kohn

 

I wrote about that study last February in It's Not So Much The Heat, It's The Humidity.

 

Today Jeffrey Shaman from Oregon State University, returns with the aid of 4 other researchers, to correlate the incidence and spread of influenza in the human population with the levels of absolute humidity.

 

This admittedly math and statistics heavy paper appears in:

 

PLoS Currents: Influenza

A moderated collection for rapid and open sharing of useful new scientific data, analyses, and ideas.

 

 

I’ve just posted the abstract (slightly reformatted for readability).  The entire article is freely available at the link below.

 

 

Absolute Humidity and the Seasonal Onset of Influenza in the Continental US

By Jeffrey Shaman, Virginia Pitzer, Cecile Viboud, Marc Lipsitch et al (5 authors)

Much of the observed wintertime increase of mortality in temperate regions is attributed to seasonal influenza. A recent re-analysis of laboratory experiments indicates that absolute humidity strongly modulates the airborne survival and transmission of the influenza virus.

 

Here we extend these findings to the human population level, showing that the onset of increased wintertime influenza-related mortality in the United States is associated with anomalously low absolute humidity levels during the prior weeks. We then use an epidemiological model, in which observed absolute humidity conditions temper influenza transmission rates, to successfully simulate the seasonal cycle of observed influenza-related mortality.

 

The model results indicate that direct modulation of influenza transmissibility by absolute humidity alone is sufficient to produce this observed seasonality. These findings provide epidemiological support for the hypothesis that absolute humidity drives seasonal variations of influenza transmission in temperate regions.

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