Photo Credit – FAO
Although only a low pathogenic (LPAI) virus, and rarely reported to infect humans, the H9N2 virus nevertheless occupies a special place in the hierarchy of avian influenza viruses. Its internal genes routinely make up the backbone of many of the HPAI viruses that pose the greatest risks to both poultry, and human health.
While I don’t like to anthropomorphize viruses (they hate it when you do that), over the years I’ve begun to think of H9N2 as the Professor Moriarty of avian flu viruses.
Whenever something `bad’ happens with an avian flu strain – if you look deep enough – you’ll often find out H9N2 was involved. Of the three avian flu viruses we are currently watching with the most concern – H5N1, H7N9, and H5N6 – all share several important features (see Study: Sequence & Phylogenetic Analysis Of Emerging H9N2 influenza Viruses In China):
- They all first appeared in Mainland China
- They all have come about through viral reassortment in poultry
- And most telling of all, while their HA and NA genes may differ - they all carry the internal genes from the avian H9N2 virus
In the past, we’ve looked at the propensity of the H9N2 virus to reassort with other avian flu viruses (see PNAS: Reassortment Of H1N1 And H9N2 Avian viruses & PNAS: Reassortment Potential Of Avian H9N2) which have shown the H9N2 capable of producing `biologically fit’ and highly pathogenic reassortant viruses.
In a similar vein, in early 2014 The Lancet carried a report entitled Poultry carrying H9N2 act as incubators for novel human avian influenza viruses.
But risks from H9N2 go beyond facilitating the creation of viable reassorted subtypes. The H9N2 virus can infect humans (and other mammals) on its own - and while it generally produces a mild illness - we’ve only a handful of cases to evaluate.
Like many wide-ranging avian flu viruses, the H9N2 varies by locale. The virus you get in Bangladesh differs from the version you’ll find in China, or the Middle East. The Bangladeshi virus is a novel reassortant that has acquired some mammalian adaptations along the way, making this strain of particular interest to study.
Today we have a study that looks at the replication and transmission capacity of this H9N2 virus, that finds it can be carried by non-poultry avian (finches & parakeets) species, and while they rarely show signs of illness themselves, they can shed enough of the virus to spread it to poultry.
They also demonstrate the virus replicates well in human and swine tissues, confirming similar findings we looked at last year in PLoS Path: Genetics, Receptor Binding, and Transmissibility Of Avian H9N2.
The authors write that `Interspecies transmission of the Env/9306 strain remains a risk to mammals because of adaptation mutations’.
I’ve only excepted the Abstract and the closing remarks, so follow the link to read the study in its entirety.
Brian J. Lenny, Karthik Shanmuganatham, Stephanie Sonnberg, Mohammed M. Feeroz, S.M. Rabiul Alam, M. Kamrul Hasan, Lisa Jones-Engel, Pamela McKenzie, Scott Krauss, Robert G. Webster, and Jeremy C. Jones
Avian influenza A(H9N2) is an agricultural and public health threat. We characterized an H9N2 virus from a pet market in Bangladesh and demonstrated replication in samples from pet birds, swine tissues, human airway and ocular cells, and ferrets. Results implicated pet birds in the potential dissemination and zoonotic transmission of this virus.
Avian influenza A(H9N2) virus is endemic among poultry throughout Eurasia (1–3). In Bangladesh, subtype H9N2 viruses are unique reassortants, containing genes from highly pathogenic avian influenza A(H7N3) viruses. The H9N2 virus poses a substantial infection risk to poultry (2) and has infected pigs and humans (4,5). Its evolution is continually monitored by the World Health Organization (http://www.who.int/influenza/vaccines/virus/201502_zoonotic_vaccinevirusupdate.pdf?ua = 1).
Ongoing influenza surveillance in Bangladesh found H9N2 virus primarily in poultry (5,6); we also surveyed a pet market that sold avian pets (parrots, finches, pigeons) and poultry (quail, turkey, chickens) and obtained isolates from nonpoultry terrestrial birds (6). This mixture of birds and mammals, some for which little associated influenza pathogenesis data exists, provided a unique opportunity to study the ecology, host range, and transmission potential of H9N2 virus.
Live bird markets are crucial to zoonotic spread of avian influenza viruses (AIVs) (12). However, our data suggest transmission potential in pet markets and vendor sites other than poultry markets; these sites may house birds infected with AIVs and should be included in future surveillance.
Our results may also inform surveillance sample collection. Oropharyngeal samples were collected from pet birds; collecting environmental swabs alone may yield lower isolation rates or fail to detect this virus.
H9N2 virus replication in pet birds also has implications for viral spread. Poultry are a major source of dissemination, but our data show domesticated or pet birds can harbor H9N2. Pet trading can extend across international borders and greatly expand the range of AIVs, as when H9N2 virus was repeatedly imported into Japan in infected parakeets (13).
Finally, the unique influenza varieties among pet birds may provide more opportunities for H9N2 virus to gain novel genetic elements; this subtype has had remarkable levels of reassortment activity with influenza A(H7N9) and highly pathogenic avian influenza A(H5N1) viruses (14,15).
H9N2 virus will remain a threat in the foreseeable future. Efforts are needed to identify its presence in poultry and nonpoultry avian species. Phenotypic properties of these viruses, including replication ex vivo and in vivo, are a valuable supplement to existing genotypic data and further inform the risk for spread within avian and human populations.