Avian Flu Diary: Sci Repts: Surprising Co-subsistence of LPAI & HPAI Viruses In Poultry

#14,112

It certainly isn't news that poultry - or any susceptible host, for that matter - can be co-infected with more than one type of influenza virus. Were that not true, viral reassortment would be impossible, and influenza pandemics far less common.

We've a study today, however, which describes an unexpectedly diverse array of viruses (H5, H7 & H9) discovered to be co-circulating in Bangladesh's poultry, which appears to broaden the amount of avian flu genetic material that may be available for reassortment.

I say `appears' because the authors are calling for `. . . . confirmation of these results by targeted surveillance in the area of origin of the investigated samples.'

Not only were 5 subtypes detected (HPAI H5N1, H5N2, H7N1, H7N2 and LPAI H9N2), they found 8 different genotypes as well. Including some containing genetic material from much older, and presumed extinct, clades.

This is a very lengthy, and detailed report, so I've only posted a few excerpts. Follow the link to read its surprising findings.

Co-subsistence of avian influenza virus subtypes of low and high pathogenicity in Bangladesh: Challenges for diagnosis, risk assessment and control

Rokshana Parvin, Jahan Ara Begum,Emadadul Haque Chowdhury, Mohammed Rafiqul Islam, Martin Beer & Timm Harder

Scientific Reports 9, Article number: 8306 (2019)

Abstract

Endemic co-circulation of potentially zoonotic avian influenza viruses (AIV) of subtypes H5N1 and H9N2 (G1 lineage) in poultry in Bangladesh accelerated diversifying evolution. Two clinical samples from poultry obtained in 2016 yielded five different subtypes (highly pathogenic [HP] H5N1, HP H5N2, HP H7N1, HP H7N2, H9N2) and eight genotypes of AIV by plaque purification.

H5 sequences grouped with clade 2.3.2.1a viruses while N1 was related to an older, preceding clade, 2.2.2. The internal genome segments of the plaque-purified viruses originated from clade 2.2.2 of H5N1 or from G1/H9N2 viruses.H9 and N2 segments clustered with contemporary H9N2 strains.

In addition, HP H7 sequences were detected for the first time in samples and linked to Pakistani HP H7N3 viruses of 2003.

The unexpected findings of mixtures of reassorted HP H5N1 and G1-like H9N2 viruses, which carry genome segments of older clades in association with the detection of HP H7 HA segments calls for confirmation of these results by targeted surveillance in the area of origin of the investigated samples.

Hidden niches and obscured transmission pathways may exist that retain or re-introduce genome segments of older viruses or reassortants thereof which causes additional challenges for diagnosis, risk assessment and disease control.

(SNIP)

In depth molecular analyses revealed that the rescued H5N1 and H5N2 viruses derived their HA H5 segment from clade 2.3.2.1a viruses of the years 2012–2014 (HA, Fig. 2, H5), while the N1 segment along with six internal genes most likely originated from clade 2.2.2/H5N1 (Fig. 2, N1). However, the H5N1 viruses of this clade became apparently extinct from Bangladesh after 2011^14,15.

Continued circulation of genome segments of that clade therefore was unexpected and currently stands as a solitary but important finding.

As such, the possibility of undetected circulating clade 2.2.2 HPAI viruses or gene segments thereof in other reassortant subtypes must be considered. Chicken and duck samples (C1/2016 and D1/2016) obtained in the Mymensingh district in late 2016 and treated similarly in our labs proved to contain each a single AIV strain which carried contemporary 2.3.2.1a HA and NA genome segments (Fig. 2, H5).

Even more surprising was the finding of an HPAI H7 virus having an HA gene similar to that of HPAI Pak/H7N3 viruses that had caused outbreaks in Pakistan during 2000–2003²⁴, but which had not been detected at that or any time in Bangladesh. Although subtype H7 viruses have been detected in backyard and free ranging ducks in Bangladesh, they were of low pathogenicity and their HA segment was of a Eurasian wild bird lineage unrelated to the HP H7 Pakistan viruses^7,25 (Fig. 2, H7).

(SNIP)

The much unexpected findings of mixtures of reassorted HP H5N1 and G1-like H9N2 viruses which carry genome segments of older gs/GD clades and the detection of HP H7 HA segments previously not reported from Bangladesh, calls for confirmation of these results by targeted surveillance in the area of origin of the investigated samples.

Virus strains or reassorted gene segments thereof believed to be extinct may yet still reside in small regional pockets or populations.

In general, our findings emphasize the need of a broader and deeper analysis of (AI) viral populations in clinical samples and corresponding viral isolates originating from AI outbreaks. While next-generation sequencing techniques provide ultimate tools for this approach, available multiplexed or arrayed RT-qPCR applications allow for a rapid screening at more sensible costs and of higher sample numbers.

(Continue . . . .)

Influenza viruses evolve via two well established routes; Antigenic drift & Antigenic Shift (reassortment).

Antigenic drift causes small, incremental changes in the virus over time. Drift is the standard evolutionary process of influenza viruses, and often come about due to replication errors that are common with single-strand RNA viruses (see NIAID Video: Antigenic Drift).
Shift occurs when one virus swap out chunks of their genetic code with gene segments from another virus. This is known as reassortment. While far less common than drift, shift can produce abrupt, dramatic, and sometimes pandemic inducing changes to the virus (see NIAID Video: How Influenza Pandemics Occur).

In either case, most mutations and/or reassortments are evolutionary failures.

They die out quickly because they are not as biologically `fit’ as the parental virus they must compete with. Only rarely does a mutation convey enough of an evolutionary advantage to allow it to become `fixed' in a host, and potentially transmitted onward.

And while these mutations enable influenza viruses to evade host immunity and avoid extinction, they are random, chance events. It is only through an absolutely astronomical number of rolls of the genetic dice that influenza viruses eventually stumble upon a more advantageous genome sequence.