Mia Kim Torchetti

Intercontinental Spread of Asian-Origin H5N8 to North America through Beringia by Migratory Birds

ABSTRACT Phylogenetic network analysis and understanding of waterfowl migration patterns suggest that the Eurasian H5N8 clade 2.3.4.4 avian influenza virus emerged in late 2013 in China, spread in early 2014 to South Korea and Japan, and reached Siberia and Beringia by summer 2014 via migratory birds. Three genetically distinct subgroups emerged and subsequently spread along different flyways during fall 2014 into Europe, North America, and East Asia, respectively. All three subgroups reappeared in Japan, a wintering site for waterfowl from Eurasia and parts of North America.

Novel Eurasian Highly Pathogenic Avian Influenza A H5 Viruses in Wild Birds, Washington, USA, 2014

Novel Eurasian lineage avian influenza A(H5N8) virus has spread rapidly and globally since January 2014. In December 2014, H5N8 and reassortant H5N2 viruses were detected in wild birds in Washington, USA, and subsequently in backyard birds. When they infect commercial poultry, these highly pathogenic viruses pose substantial trade issues.

Highly pathogenic avian influenza viruses and generation of novel reassortants,United States, 2014–2015

Asian highly pathogenic avian influenza A(H5N8) viruses spread into North America in 2014 during autumn bird migration. Complete genome sequencing and phylogenetic analysis of 32 H5 viruses identified novel H5N1, H5N2, and H5N8 viruses that emerged in late 2014 through reassortment with North American low-pathogenicity avian influenza viruses.

Novel H5 Clade 2.3.4.4 Reassortant (H5N1) Virus from a Green-Winged Teal in Washington, USA

ABSTRACT Eurasian (EA)-origin H5N8 clade 2.3.4.4 avian influenza viruses were first detected in North America during December 2014. Subsequent reassortment with North American (AM) low-pathogenic wild-bird-origin avian influenza has generated at least two reassortants, including an EA/AM H5N1 from an apparently healthy wild green-winged teal, suggesting continued ongoing reassortment.

Widespread detection of highly pathogenic H5 influenza viruses in wild birds from the Pacific Flyway of the United States.

A novel highly pathogenic avian influenza virus belonging to the H5 clade 2.3.4.4 variant viruses was detected in North America in late 2014. Motivated by the identification of these viruses in domestic poultry in Canada, an intensive study was initiated to conduct highly pathogenic avian influenza surveillance in wild birds in the Pacific Flyway of the United States. A total of 4,729 hunter-harvested wild birds were sampled and highly pathogenic avian influenza virus was detected in 1.3% (n = 63). Three H5 clade 2.3.4.4 subtypes were isolated from wild birds, H5N2, H5N8, and H5N1, representing the wholly Eurasian lineage H5N8 and two novel reassortant viruses. Testing of 150 additional wild birds during avian morbidity and mortality investigations in Washington yielded 10 (6.7%) additional highly pathogenic avian influenza isolates (H5N8 = 3 and H5N2 = 7). The geographically widespread detection of these viruses in apparently healthy wild waterfowl suggest that the H5 clade 2.3.4.4 variant viruses may behave similarly in this taxonomic group whereby many waterfowl species are susceptible to infection but do not demonstrate obvious clinical disease. Despite these findings in wild waterfowl, mortality has been documented for some wild bird species and losses in US domestic poultry during the first half of 2015 were unprecedented.

Changes in adaptation of H5N2 highly pathogenic avian influenza H5 clade 2.3.4.4 viruses in chickens and mallards.

H5N2 highly pathogenic avian influenza (HPAI) viruses caused a severe poultry outbreak in the United States (U.S.) during 2015. In order to examine changes in adaptation of this viral lineage, the infectivity, pathogenicity and transmission of poultry H5N2 viruses were investigated in chickens and mallards in comparison to the wild duck 2014 U.S. index H5N2 virus. The four poultry isolates examined had a lower mean bird infectious dose than the index virus but still transmitted poorly to direct contacts. In mallards, two of the H5N2 poultry isolates had similar high infectivity and transmissibility as the index H5N2 virus, the H5N8 U.S. index virus, and a 2005 H5N1 clade 2.2 virus. Mortality occurred with the H5N1 virus and, interestingly, with one of two poultry H5N2 isolates. Increased virus adaptation to chickens was observed with the poultry H5N2 viruses; however these viruses retained high adaptation to mallards but pathogenicity was differently affected.

Variation in protection of four divergent avian influenza virus vaccine seed strains against eight clade 2.2.1 and 2.2.1.1. Egyptian H5N1 high pathogenicity variants in poultry

Highly pathogenic (HP) H5N1 avian influenza virus (AIV) was introduced to Egyptian poultry in 2006 and has since become enzootic. Vaccination has been utilized as a control tool combined with other control methods, but for a variety of reasons, the disease has not been eradicated. In 2007, an antigenically divergent hemagglutinin subclade, 2.2.1.1, emerged from the original clade 2.2.1 viruses.

Reoccurrence of Avian Influenza A(H5N2) Virus Clade 2.3.4.4 in Wild Birds, Alaska, USA, 2016.

We report reoccurrence of highly pathogenic avian influenza A(H5N2) virus clade 2.3.4.4 in a wild mallard in Alaska, USA, in August 2016. Identification of this virus in a migratory species confirms low-frequency persistence in North America and the potential for re-dissemination of the virus during the 2016 fall migration.

Surveillance for highly pathogenic H5 avian influenza virus in synanthropic wildlife associated with poultry farms during an acute outbreak

In November 2014, a Eurasian strain H5N8 highly pathogenic avian influenza virus was detected in poultry in Canada. Introduced viruses were soon detected in the United States and within six months had spread to 21 states with more than 48 million poultry affected. In an effort to study potential mechanisms of spread of the Eurasian H5 virus, the United States Department of Agriculture coordinated several epidemiologic investigations at poultry farms. As part of those efforts, we sampled synanthropic birds and mammals at five infected and five uninfected poultry farms in northwest Iowa for exposure to avian influenza viruses. Across all farms, we collected 2,627 samples from 648 individual birds and mammals. House mice were the most common mammal species captured while house sparrows, European starlings, rock pigeons, swallows, and American robins were the most commonly captured birds. A single European starling was positive for Eurasian H5 viral RNA and seropositive for antibodies reactive to the Eurasian H5 virus. Two American robins were also seropositive. No mammal species showed evidence of infection. These results indicate synanthropic species merit further scrutiny to better understand potential biosecurity risks. We propose a set of management practices aimed at reducing wildlife incursions.

Investigation into the Airborne Dissemination of H5N2 Highly Pathogenic Avian Influenza Virus During the 2015 Spring Outbreaks in the Midwestern United States

SUMMARY We investigated the plausibility of aerosol transmission of H5N2 highly pathogenic avian influenza (HPAI) virus during the 2015 spring outbreaks that occurred in the U.S. midwest. Air samples were collected inside and outside of infected turkey and layer facilities. Samples were tested to assess HPAI virus concentration (RNA copies/m3 of air), virus viability, and virus distribution by particle size. HPAI virus RNA was detected inside and up to 1000 m from infected facilities. HPAI virus was isolated from air samples collected inside, immediately outside, up to 70 m from infected facilities, and in aerosol particles larger than 2.1 μm. Direct exposure to exhausted aerosols proved to be a significant source of environmental contamination. These findings demonstrate HPAI virus aerosolization from infected flocks, and that both the transport of infectious aerosolized particles and the deposition of particles on surfaces around infected premises represent a potential risk for the spread of HPAI.