Friday, November 24, 2017

Eurosurveillance: Detection Of Amantadine Sensitive H3N2 During 2017 Flu Season

2006 CDC HAN On Amantadine
















#12,918


Twelve years ago Amantadine was the preferred influenza antiviral.  It was cheap, plentiful, and worked reasonably well as both a treatment, and a preventative. 

But by late 2005 Amantadine began to lose its effectiveness against the H3N2 seasonal flu virus and some strains of the H5N1 bird flu. In January of 2006 the CDC issued a warning (see above) to doctors not to rely on Amantadine or Rimantadine to treat influenza.
Tamiflu (Oseltamivir), while far more expensive, became the new treatment standard.  
But within a couple of years seasonal H1N1 began to show growing resistance to Tamiflu as well (although H3N2 remained sensitive).  By the spring of 2009, - in the space of just about a year – seasonal H1N1 had gone from almost 100% sensitive to the drug to nearly 100% resistant.
It seemed as if antiviral crisis was inevitable, when in a Deus Ex Machina moment a new swine-origin H1N1 virus - that happened to be sensitive to Tamiflu - swooped in as a pandemic strain in the spring of 2009, supplanting the older resistant H1N1 virus. 
Both incidents showed that antivirals - much like antibiotics - can lose effectiveness over time, as pathogens evolve and resistant strains emerge. 

While Amantadine resistance has appeared permanently `fixed' in both seasonal and most novel flu viruses tested over the past decade, there may be a glimmer of hope in a report published yesterday in the Eurosurveillance Journal that finds an unexpected jump in amantadine sensitive H3N2 viruses in Australia during their recent flu season.
The number of Australian amantadine sensitive samples was small (n=15), but exceeded the combined number reported globally between 2011-2016.
Amantadine sensitive isolates were detected during July, August and September in four states in Australia (Victoria: n = 10; New South Wales: n = 2; Queensland: n = 2; Northern Territory: n = 1) along with one reported from New Zealand.  At its peak, in August, 8.7% of samples tested (10 of 115) showed sensitivity to Amantadine. 
 So far surveillance has not picked up any similar changes in H1N1 viruses.
While none of this is enough to make Amantadine useful for treating influenza again, it is a remarkable turn of events, and we'll be keen to see if this trend continues during during this winter's Northern Hemisphere flu season.

Follow the link to read the full report in its entirety.

Rapid communication Open Access

Detection of adamantae-sensitive influenza A(H3N2) viruses in Australia, 2017: a cause for hope? 


Aeron Hurt1,2, Naomi Komadina1, Yi-Mo Deng1, Matthew Kaye1, Sheena Sullivan1,3, Kanta Subbarao1,2, Ian Barr1,2

Amantadine and rimantadine are compounds of the adamantane class of antivirals which act on influenza A viruses by binding to the M2 ion channel, preventing uncoating of the virus during replication. Treatment of influenza A virus infection with these drugs within 48 hours of symptom onset reduces illness by ca 24 hours, and when given prophylactically, the drugs can prevent ca 60% of influenza cases [1]. 


However, effectiveness of both drugs is lost when viruses acquire an amino acid substitution at one of five critical residues of the M2 protein i.e. positions 26, 27, 30, 31 and 34 [2]. The occurrence of adamantane-resistant influenza A viruses was rare among circulating influenza viruses [3] until 2000, when an increasing proportion of viruses from Asia, particularly China, contained the serine (S) to asparagine (N) substitution at residue 31 (S31N) of the M2 protein [4]. 

By the end of the 2005/06 influenza season, over 90% of circulating A(H3N2) viruses in North America and other parts of the northern hemisphere, such as Asia, contained the S31N substitution even though the vast majority of resistant viruses were from patients who had not been treated with adamantanes [5]. After more than 7 years of almost complete dominance of adamantane-resistant A(H3N2) influenza viruses globally, we describe the detection in Australia of increased numbers of adamantane-sensitive viruses during the 2017 influenza season.

(SNIP)

The Australian 2017 influenza season was dominated by high levels of A(H3N2) influenza virus activity. During this season, 15 adamantane-sensitive A(H3N2) viruses encoding M2 S31 were detected in Australia (Table 2), which exceeded the cumulative total of 11 adamantane-sensitive influenza A viruses detected globally between 2011 and 2016 (Table 1). In contrast, the frequency of adamantane-resistance in circulating A(H1N1)pdm09 viruses has remained unchanged at > 99.9% both in Australia and worldwide.


(SNIP)

Discussion and conclusion

Adamantane-resistance was first detected in persons infected with influenza virus who were treated with adamantanes in the late 1980s, in closed settings, such as nursing homes [10,11], as well as community settings [12]. In the latter, there was apparent transmission of drug-resistant strains, when rimantadine was used for treatment or post-exposure prophylaxis in families [12]. Adamantane-resistant viruses were also detected in nursing home patients without exposure to these drugs [13], demonstrating that adamantane-resistant variants may be able to spread in the community. Up to 45% of children treated with rimantadine have been reported to shed resistant viruses [14].
In addition to widespread adamantane-resistance among A(H3N2) influenza viruses circulating globally, seasonal influenza A(H1N1) viruses also developed adamantane-resistance between 2005 and 2008 [15,16], and the A(H1N1)pdm09 virus that emerged and caused the influenza pandemic in 2009 was also adamantane-resistant. As consequence of these developments, adamantanes are no longer recommended for treatment of influenza [5].

The spread of M2 N31 viruses in the early 2000s was thought to be due to linkage to advantageous substitutions elsewhere in the virus, in a process referred to as genetic ‘hitch-hiking’, and not related to adamantane-induced selection pressure [17]. Even though the A(H3N2) virus has continued to undergo substantial antigenic and genetic evolution over the last decade, the M2 N31 residue has remained almost completely fixed, suggesting that during that time it contributed to viral fitness.
However, the recent detection of M2 S31 and D31 viruses in Australia suggests that the importance of the M2 N31 residue in viral fitness may no longer be as strong as it was. We encourage surveillance laboratories, where possible, to conduct M2 sequencing of A(H3N2) viruses during the upcoming 2017/18 northern hemisphere influenza season to see if the M2 S31 or D31 viruses begin to circulate in greater numbers globally.

In the seminal publication by Bright et al. on the emergence of the S31N variant in the early 2000s [4], the authors stated that ‘further genetic and antigenic evolution of influenza A(H3N2) viruses resulting in the disappearance of the S31N mutation and reversion back to the drug sensitive phenotype should not be excluded’.
It may be that the M2 S31 viruses detected in Australasia in 2017 could be the progenitors for a reversion back to more widely circulating adamantane-sensitive A(H3N2) viruses, some 12 years after the resistant strain emerged and then dominated globally. If this were the case, it would revive the option of using adamantanes to treat A(H3N2) virus infections and improve the opportunities for using these drugs in combination with other antivirals [18].
         (Continue . . . )



Nature Sci Rpts: H5N6 Viruses Exhibit Varying Pathogenicity & Transmissibility In Mammals

Horizontal Transmission Results - Credit Sci Rpts














#12,917

One of the recurring themes in this blog is that while we talk about avian H5N6 (or H5N8, H5N1, or H7N9) as if they were single entities - in truth, each of these subtypes contains multiple (sometimes dozens of) genotypes - and within each of these genotypes can be numerous minor variants.
Novel flu viruses continually reassort, evolve, and reinvent themselves in the wild.  Which is why - over the past 14 years - the WHO has been forced to select three dozen different H5N1 candidate vaccine viruses (CVVs) just to keep up.
Avian viruses can be remarkably promiscuous, capable of churning out new genotypes - and occasionally new subtypes - with remarkable speed.  While many of these new iterations will fade into oblivion - unable to compete against more biological `fit' variants - the roster of viruses in circulation continues to expand. 
This diversity helps to explain how H5N1 has caused major outbreaks in humans in places like Egypt and Indonesia, yet India  - where the virus has also been rife - has never reported a human infection (see Differences In Virulence Between Closely Related H5N1 Strains).
The avian H5N6 virus, which emerged in the spring of 2014, has caused at least 18 human infections in China, with roughly 60% mortality. Yet, despite hundreds of outbreaks across South Korea, Japan, Taiwan, Vietnam, and the Philippines over the past year, none of those places have reported a human case. 
Additionally, China - which saw a surge of human infections in late 2015 and through most of 2016 - has gone nearly a year (until last week) without reporting a new case, despite numerous H5N6 outbreaks in poultry.
While the very good news to all of this is that not all HPAI H5 avian viruses are equally dangerous, the bad news is there are a great many variants of each subtype evolving in the wild, providing many more opportunities for a pandemic strain to emerge.

Today the Journal Nature has a fascinating (open access) report that compares three genetically similar, but behaviorally different, H5N6 viruses collected in Hubei Province, China. 
  • One of the variants (CK918) produced only minor physical effects on inoculated lab mice, and zero mortality, while two others (DK01 and CK165) produced rapid weight loss, and a high mortality rate. 
  •  In transmission testing (using guinea pigs) CK918 and DK01 did not appear to transmit via direct contact or aerosol route, but CK165 transmitted to 2 out of 3 guinea pigs via direct contact (but not aerosol).
While not nearly as dramatic of a finding as last month's announced ferret-to-ferret airborne transmission of avian H7N9 (see Cell Host & Microbe: HPAI H7N9 Lethality & Transmission In Ferrets), this nevertheless demonstrates a significant step towards mammalian adaptation of this particular H5N6 variant.

I've only posted some excerpts, so follow the link to read it in its entirety.

Avian Influenza H5N6 Viruses Exhibit Differing Pathogenicities and Transmissibilities in Mammals

Zongzheng Zhao, Zhendong Guo, Chunmao Zhang, Lina Liu, Ligong Chen, Cheng Zhang, Zhongyi Wang, Yingying Fu, Jianming Li, Huabin Shao, Qingping Luo, Jun Qian & Linna Liu

Scientific Reports 7, Article number: 16280 (2017)
doi:10.1038/s41598-017-16139-1
 
Received: 31 August 2017
Accepted: 08 November 2017
Published online:  24 November 2017

Abstract


Since 2013, highly pathogenic avian influenza H5N6 viruses have emerged in poultry and caused sporadic infections in humans, increasing global concerns regarding their potential as human pandemic threats. Here, we characterized the receptor-binding specificities, pathogenicities and transmissibilities of three H5N6 viruses isolated from poultry in China. 


The surface genes hemagglutinin (HA) and neuraminidase (NA) were closely related to the human-originating strain A/Changsha/1/2014 (H5N6). Phylogenetic analyses showed that the HA genes were clustered in the 2.3.4.4 clade, and the NA genes were derived from H6N6 viruses.
These H5N6 viruses bound both α-2,3-linked and α-2,6-linked sialic acid receptors, but they exhibited different pathogenicities in mice. 

In addition, one virus was fully infective and transmissible by direct contact in guinea pigs. These results highlight the importance of monitoring the continual adaptation of H5N6 viruses in poultry due to their potential threat to human health

Introduction

Since the first human H5N6 virus infection was reported in China1, H5N6 viruses have caused sporadic infections in humans; at least 17 human infections have been reported in China. The emergence of human H5N6 influenza virus infection has raised global concerns regarding potential threats to human health.
The first H5N6 virus was detected in mallards in North America in 19752. In the past, H5N6 viruses exhibited low pathogenicity and had little impact on the poultry industry and human health, including in Germany in 19843 and in Sweden in 20024. However, the recently emerged Asian H5N6 strain showed high pathogenicity, and a series of poultry outbreaks resulting from H5N6 recently occurred in China, Laos, Vietnam, Korea, and Japan5,6,7,8,9,10.
H5N6 initially arose from the reassortment of H5N1 and H6N6. The second reassortment may have occurred between H5N6 and ZJ-HJ/07-like H9N2 viruses11, which are similar to H7N912 and H10N8 viruses13. In 2015, the third reassortment was generated by a deletion in the NA protein at residues 59–69, resulting in novel H5N6 viruses that were more likely to cross species barriers to infect humans14.
Currently, H5N6 has replaced H5N1 as the dominant avian influenza virus subtype in poultry in southern China. Furthermore, H5N6 was also detected in migratory waterfowl prior to the first human case15,16. Migratory waterfowl, which transverse long distances, played a major role in the geographical spread of H5N6. Chickens and ducks functioned as “vessels” to deliver H5N6 from avian species to humans14,17, and H5N6 continued to evolve to adapt to mammals.
We recently isolated three H5N6 viruses from domestic ducks and chickens in Hubei province, China. However, the zoonotic capabilities and pathogenicities of H5N6 viruses in poultry remained unknown. In the present study, we used phylogenetic analysis and evaluated the receptor-binding properties, pathogenicities and transmissibilities of H5N6 viruses. These studies expand our understanding of the pathogenicity and transmissibility of H5N6 viruses and will aid in influenza pandemic preparedness efforts.
(SNIP)


Discussion

In this study, we found that the three H5N6 viruses exhibited different pathogenicities and transmissibilities in mammals. Each of the three H5N6 viruses acquired varying degrees of binding affinity for human-like receptors, and CK165 could transmit between guinea pigs by direct contact but not via aerosol.

(SNIP)

In summary, three avian influenza H5N6 viruses exhibited varying degrees of affinity for human-type (α-2,6) receptors, replicated well in a mouse model, and one was capable of transmitting in guinea pigs by direct contact. Notably, H5N6 viruses have maintained their adaptation for mammals, and human isolates have been found to reassort with H9N2 viruses. Therefore, H5N6 viruses may become the next potential candidates for global dissemination.
         (Continue . . . .) 

For some more recent blogs on the evolution of avian H5N6, you may wish to revisit:

Study: Experimental Infection Of Dogs With HPAI H5N1 & HPAI H5N6
Virology: Five Distinct Reassortants of HPAI H5N6 In Japan - Winter 2016–2017

Arch. Of Virology: Novel Reassortant H5N6 Isolated From Cats - Eastern China
Emerg. Microbes & Inf.: Human Infections With A Novel Reassortant H5N6

OIE Notification: LPAI H5N2 In Germany















#12,916


Yesterday the OIE announced that they had been notified of a small outbreak of LPAI (low path) H5N2 on a farm in the Lower Saxony region of Germany.  LPAI viruses are commonly found in wild and migratory birds, and occasionally jump to poultry, where they generally produce mild symptoms. 
The concern is -  when LPAI H5 and H7 poultry outbreaks are not quickly controlled -  they have the potential to mutate into highly pathogenic strains. 
Over the summer, in Arch. Of VIrology: Rapid Virulence Shift Of An LPAI H5N2 Virus During A Single Passage In Mice, we looked at a lab experiment which showed somewhat surprisingly that LPAI H5N2 viruses could - through host adaptation - acquired enhanced pathogenicity after just one passage through mice.

For these reasons, all H5 and H7 outbreaks - regardless of pathogenicity - are reportable to the OIE, and immediate containment and eradication are required.


http://www.oie.int/wahis_2/public/wahid.php/Reviewreport/Review?page_refer=MapFullEventReport&reportid=25284&newlang=en

Wednesday, November 22, 2017

South Korea: MAFRA Confirms LPAI H7N7, Testing More H5 Samples


















#12,915


Not unexpectedly, results from yesterday's report of H7N7 detected in wild bird feces has come back as less worrisome low path avian influenza (LPAI).  Low path H7N7 was detected in this general region last September, as well.

Pohang wild bird feces inspection results, according to the chronicles off room jeobyeongwonseong AI confirmed 

Added     2017-11-22 17:00:00

Agriculture, Forestry, Animal Husbandry and Food (Minister: gimyoungrok) last 11.14 days Gyeongbuk Pohang (Hyeongsan River) wild birds mange known as the inspection results, jeobyeongwonseong AI (H7N7 type) of the Agriculture, Forestry and Livestock Quarantine Office for feces to the final diagnosis November 22 collected from depending said that the Defense costs were set off in the area.

In the west of the country, in Gyeonggi Hwaseong - which sits just 30 miles south and west of the nation's capital Seoul - environmental samples have tested positive for avian H5, and further testing is ongoing to determine the subtype and pathogenicity. 

Hwaseong, Gyeonggi-type H5 AI virus detected in wild birds feces press release (11.22, deployment) 

Added     2017-11-22 18:35:00

Gyeonggi Hwaseong (Tuesday defended) Bird detection type H5 AI virus in feces - AI biosecurity measures in accordance with the emergency action plan (SOP) - Agriculture, Forestry, Animal Husbandry and Food (Minister: gimyoungrok) are wild collected from 11.20 days, Gyeonggi Hwaseong (Tuesday defended) Agriculture, Forestry and Livestock quarantine office for bird feces intermediate test results AI H5-type virus has been detected * 11.22 days announced that the preventative measures taken in accordance with the AI ​​urgent action guidelines (SOP).


Set to 'wild birds current surveillance area "** for detecting the center point of a radius 10km area was to be subjected to movement control and disinfection with respect to poultry and birds bred in the area for 21 days, as well as, poultry farms and migratory doraeji, Small Stream AI enhanced biosecurity and its municipalities, etc., for the mobilization of Defense announced that a vehicle such as broadband bangjegi take biosecurity measures, including disinfection carried out every day. * N-type and highly pathogenic whether check is scheduled to take 3 to 6 ** Hwaseong Gyeonggi Chemistry advocate one AI detected center point within 10km poultry breeding farms (154 farms, about 1,569 shallow water) with respect to surveillance (clinical examination or inspection)  


Meanwhile the number of dead birds that have tested positive for HPAI H5N6 in Japan has risen to 7 (out of 9 tested) - all collected from Shimane Prefecture - according to the latest chart posted on Japan's Ministry of Environment website. 

Shimane Prefecture - Credit Wikipedia


EID Journal: Human Clusters Of H7N9 In China, 2013 - 2017

Credit WHO

















#12,914


Last September, in J. Infect. Diseases: Human Clusters Of H7N9 In China - March 2013 to June 2015, we looked at an analysis of suspected and probable human-to-human transmission of H7N9 during its first three epidemic waves in China.
That study described 21 H7N9 clusters (involving 22 contacts) from the first three waves, and found that at least 12 infections were likely the result of human-to-human transmission, another 4 were considered `possible', while 6 were determined to be unlikely.
But, as I pointed out at the time, the H7N9 virus has undergone a great many changes over the past couple of years.  A new LPAI Yangtze River Delta lineage of H7N9 has emerged, and become the dominant strain - while perhaps more ominously - an HPAI virus emerged in Guangdong Province and has quickly spread to other provinces.

Early reports (see Eurosurveillance: Epidemiology of Human HPAI H7N9 Infection - Guangdong Province) have suggested this recently emerged HPAI version might pose a greater threat to human health than the two LPAI lineages, but until recently, we've had little data to go on.

Over the past month or so, the research floodgates have opened, and we've seen:
Cell Host & Microbe: HPAI H7N9 Lethality & Transmission In Ferrets
Cell Research: Another Cautionary H7N9 Study Out Of China
J. Virology: Emergence & Adaptation Of HPAI H7N9 In Birds and Humans
EID Journal: H7N9 Viruses Co-circulating In Chickens In Southern China, 2016–2017

All of these studies suggest that HPAI H7N9 has acquired important mammalian adaptations that may increase both its virulence, and its transmissibility, and together they may enhance its pandemic potential.

While all very concerning, particularly on top of seeing a record number of human H7N9 infections during the 5th epidemic wave (see chart at top of blog), we haven't (yet) seen any signs of increased human-to-human transmission in the field. 
At least, not based on the limited real-time reporting provided by the Chinese government, the quality of which seriously declined in the spring of 2015 (see H7N9: No News Is . . . . Curious).
After slow rolling the release of dozens of cases last December, in January the momentum of the 5th wave was so great the Chinese government began releasing weekly updates  (see HK CHP: China Reports An Additional 83 H7N9 Cases For December), albeit with only limited epidemiological details.  
The good news is that studies coming out of China - while delayed by many months - often do an excellent job filling in those blanks.
Yesterday the EID Journal published a new study which examines human clusters from all 5 epidemic waves (through mid-summer 2017), and while the number of clusters has nearly doubled (n=40) over the past two waves, they did not find any signs of increased or more efficient H-2-H transmission.

I've posted some excerpts, but you'll want to follow the link to read it in its entirety. 

Volume 24, Number 2—February 2018
Dispatch


Clusters of Human Infection and Human-to-Human Transmission of Avian Influenza A(H7N9) Virus, 2013–2017

Lei Zhou1, Enfu Chen1, Changjun Bao1, Nijuan Xiang1, Jiabing Wu, Shengen Wu, Jian Shi, Xianjun Wang, Yaxu Zheng, Yi Zhang, Ruiqi Ren, Carolyn M. Greene, Fiona Havers, A. Danielle Iuliano, Ying Song, Chao Li, Tao Chen, Yali Wang, Dan Li, Daxin Ni, Yanping Zhang, Zijian Feng, Timothy M. Uyeki, and Qun LiComments to Author

Abstract

To detect changes in human-to-human transmission of influenza A(H7N9) virus, we analyzed characteristics of 40 clusters of case-patients during 5 epidemics in China in 2013–2017. Similarities in number and size of clusters and proportion of clusters with probable human-to-human transmission across all epidemics suggest no change in human-to-human transmission risk.

Since December 2016, the number of human infections with avian influenza A(H7N9) virus in China has increased markedly (1,2), prompting concerns of pandemic influenza. Early signals of greater human-to-human transmissibility might be increased number and size of clusters of epidemiologically linked human infections and clusters of case-patients who are not blood relatives or increased numbers of case-patients with mild illness (3). 


To elucidate whether the increase in humans infections during the fifth epidemic (2016–2017) in China was associated with increased human-to-human transmissibility of A(H7N9) virus, we compared the characteristics of clusters of A(H7N9) case-patients during the fifth epidemic with those of clusters of case-patients identified from the previous 4 epidemics (2013–2016).


(SNIP)

Conclusions

Despite the surge in human infections with A(H7N9) virus during the fifth epidemic in China, the similarity in numbers and sizes of clusters and proportions of clusters with probable human-to-human transmission during 2013–2017 suggest no change in human-to-human A(H7N9) virus transmission risk over time.
These findings suggest that the increase in human infections during the fifth epidemic probably reflects an increase in sporadic poultry-to-human A(H7N9) virus transmission over a wide geographic area in China (1).
Although we restricted the assessment of human-to-human A/(H7N9) virus transmission in probable clusters to secondary case-patients without identified poultry exposure, we may have overestimated human-to-human transmission in clusters if not all poultry exposures were identified and reported. We could have underestimated human-to-human transmission by excluding infections in possible clusters with exposures to both poultry and symptomatic case-patients. Only symptomatic close contacts of index case-patients were tested, possibly underestimating the size of clusters of patients with asymptomatic infections (4). 

Clusters of probable limited human-to-human A(H7N9) virus infections, including in healthcare settings, underscore the value of adhering to recommended infection prevention and control measures to prevent nosocomial A(H7N9) virus transmission (5-8). Ongoing assessment of the epidemiology of human infections with avian influenza A(H7N9) virus to identify any increase in human-to-human transmission will inform pandemic risk assessment, preparedness, and response (9).

Dr. Zhou is deputy chief of the Branch for Emerging Infectious Diseases, Public Health Emergency Center, China CDC. Her research interests are prevention and control of emerging infectious diseases and pandemic influenza preparedness and response.
The fact that we are not waist deep in an H7N9 pandemic right now is pretty good evidence that the virus is not quite ready for prime time, but it is (at least temporarily) reassuring that Chinese researchers have not been able to detect any signs of increased transmissibility between humans.

That said, the virus that returns this winter may have gained additional mutations over its `summer vacation', and we'll be watching closely for any changes in its behavior.

Tuesday, November 21, 2017

South Korea: MAFRA Testing Environmental H7N7 For Pathogenicity


















#12,913

In late September South Korea announced they would increase their surveillance and containment procedures for the expected return of avian flu this fall and winter.  Since then we've seen a growing number of reports of both LPAI H5 and H7 viruses in wild birds, or their feces, and more recently, HPAI H5N6 in wild birds and poultry. 

There are two broad categories of avian influenza; LPAI (Low Pathogenic Avian Influenza) and HPAI (Highly Pathogenic Avian Influenza).
  • LPAI viruses are quite common in wild birds, cause little illness, and only rarely death. They are not considered to be a serious health to public health. The concern is (particularly with H5 & H7 strains) that LPAI viruses have the potential to mutate into HPAI strains.
  • HPAI viruses are more dangerous, can produce high morbidity and mortality in wild birds and poultry, and can sometimes infect humans with serious result. The type of bird flu scientists have been watching closely for the past decade has been HPAI H5 (and to a lesser extent HPAI H7s & H9s).
While HPAI H5N6 is currently considered South Korea's greatest threat, the possibility of seeing new reassortant (H5 or H7) viruses is always present, and so all findings must be fully examined.

Nearly two months ago, we saw South Korean H7N7 Indentified As LPAI from samples retrieved from Yeongcheon.Today, we learn that MAFRA is testing new samples taken from Pohang, roughly 25 miles further east. 

While likely to be LPAI, given the rapid reassortment potential for avian influenza viruses, no one in South Korea can afford to take the results for granted. 
Gyeongsangbuk-do Pohang wild bird H7N7 AI virus type detected in the feces (11.21, deployment) 
Added     2017-11-21 20:49:00

Gyeongsangbuk-do Pohang (Hyeongsan River) wild bird H7N7 type AI virus detected in the feces - AI biosecurity measures in accordance with the emergency action plan (SOP) - Agriculture, Forestry, Animal Husbandry and Food (Minister: gimyoungrok) is a wild bird feces collected from 11.14 days Gyeongbuk Pohang (Hyeongsan River) Agriculture, Forestry and Livestock quarantine office intermediate tests AI H7N7 type virus is detected - 11.21 days against the AI ​​urgent action in accordance with the instructions (SOP) announced that take preventative measures.
Set to 'wild birds current surveillance area "** for detecting the center point of a radius 10km area was to be subjected to movement control and disinfection with respect to poultry and birds bred in the area for 21 days, as well as, poultry farms and migratory doraeji, Small Stream AI enhanced biosecurity and its municipalities for such vehicles is to mobilize the Defense wide Area bangjegi announced that total take biosecurity measures, including disinfection carried out every day. * Check whether the highly pathogenic 11.22 days ** will Gyeongsangbuk-gu, Pohang Yeonil AI detection point with respect to the forecasting center within 10km poultry breeding farms (about 285 farmers, 150 Tianshui) (clinical examination or inspection) carried out