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#11,533
We've a report in the CDC's EID Journal that confirms earlier reports that it is clade 2.3.2.1c of the H5N1 virus that reemerged in West Africa in 2014, and not a resurgence of the the clade 2.2 virus that circulated there in the second half of the last decade.
In April of 2015, in EID Journal: H5N1 In Nigerian Poultry – 2015, we saw the first reports that it was clade 2.3.2.1c that had returned after a 7 year absence.While we often talk about H5N1 as if it were single entity, in truth it now encompasses a large family of viruses (see chart above) with varying degrees of infectivity and pathogenicity (see Differences In Virulence Between Closely Related H5N1 Strains).
These clades are constantly evolving, and reassorting, and so new incarnations of H5N1 are continually appearing.
Some are destined to fade away, while others being more biologically `fit’ are able to successfully compete, and thrive. Many of the older clades shown in the chart at the top of this post no longer circulate, having been supplanted by newer, more competitive variants.
Since clades are based on the HA gene of the flu virus, we can see several different subtypes (H5N1, H5N8, H5N2) fall into the same clade.
Last summer, in a blog on The International Spread Of H5N1 Clade 2.3.2.1c, I wrote on 2.3.2.1c's recent appearances around the globe:
Over the past two years, the H5N1 virus and its progeny have seen a striking renaissance, with recently emerged clades and their reassorted subtypes (H5N8, H5N2, H5N3, H5N6) spreading with renewed vigor around the globe. Nations that have not seen outbreaks in poultry, or wild birds, since the last decade are now reporting sporadic HPAI H5 once again.
Even more impressively, last fall HPAI H5 has made it to North America for the first time. H5 is clearly on the move again, and helping to drive this revived expansion are two relatively new clades; 2.3.2.1c and 2.3.4.4.
- Clade 2.3.4.4 includes subtypes A(H5N1), A(H5N2), A(H5N6) and A(H5N8), HPAI viruses that have spread rapidly in China over the past couple of years, and some have migrated to Europe and North America.
- Clade 2.3.2.1c has been showing up in Vietnam, China, India, Bulgaria, and Indonesia for several years, and was recently detected in Western Africa This clade was isolated from a nurse who returned to Alberta, Canada from a trip to China (see Alberta Canada Reports Fatal (Imported) H5N1 Infection) in late 2013, and similar to one that killed a captive tiger in Jiangsu Province in 2013.
Clade 2.3.2.1c also made headlines in 2015 when more than 100 birds at the Sanmenxia Reservoir Area of China died as the result of infection with a novel reassortment of the H5N1 virus possessing a Clade 2.3.2.1c HA gene and a H9N2-derived PB2 gene (see Novel H5N1 Reassortment Detected In Migratory Birds - China).
Clade 2.3.2.1c also gets our attention because it has been linked to unusual neurological symptomology in human - and feline - infections. In the study the above mentioned blog was based on, the authors wrote:
It should be noted that meningoencephalitis was also observed in the fatal human case with Alberta2014, an unusual outcome for infections with H5N1 HPAIV in humans20.
Neurological symptoms were also noted in the non-surviving tiger infected with Tiger2013, with the heart, liver, spleen, lung, kidney, aquae pericardii, and cerebrospinal fluid all positive for H5N1 virus as detected by real-time RT-PCR21.
This suggests that the novel Sanmenxia Clade 2.3.2.1c-like H5N1 viruses possesses tropism for the nervous system in several mammal species, and could pose a significant threat to humans if these viruses develop the ability to bind human-type receptors more effectively.
Which brings us to today's report, which finds two genetically distinct strains of clade 2.3.2.1c virus circulating in West Africa, suggesting more than one introduction of the virus - probably in 2014.
Genetically Different Highly Pathogenic Avian Influenza A(H5N1) Viruses in West Africa, 2015
Luca Tassoni, Alice Fusaro, Adelaide Milani, Philippe Lemey, Joseph Adongo Awuni, Victoria Bernice Sedor, Otilia Dogbey, Abraham Nii Okai Commey, Clement Meseko, Tony Joannis, Germaine L. Minoungou, Lassina Ouattara, Abdoul Malick Haido, Diarra Cisse-Aman, Emmanuel Couacy-Hymann, Gwenaelle Dauphin, Giovanni Cattoli, and Isabella Monne
Abstract
To trace the evolution of highly pathogenic influenza A(H5N1) virus in West Africa, we sequenced genomes of 43 viruses collected during 2015 from poultry and wild birds in 5 countries. We found 2 co-circulating genetic groups within clade 2.3.2.1c. Mutations that may increase adaptation to mammals raise concern over possible risk for humans.
In December 2014, a strain of highly pathogenic avian influenza (HPAI) A(H5N1) virus responsible for deaths among poultry was detected in southwestern Nigeria, specifically in a live bird market in Lagos State (1). Since then, other outbreaks have occurred in Nigeria, and the HPAI A(H5N1) virus has also been officially reported in Burkina Faso (February 2015) and Niger, Ghana, and Côte d’Ivoire (April 2015), to date causing the death of ≈1.6 million birds (2).
Previous HPAI A(H5N1) epidemics in West Africa occurred in 2006–2008 and involved exclusively viruses of clade 2.2 (3). So far, a full-genome characterization is publicly available for only 1 HPAI A(H5N1) virus, collected in Nigeria in early 2015 (4) and classified as clade 2.3.2.1c. To our knowledge, this clade has not been previously detected in Africa. Since 2009, this clade has been widely circulating in domestic and wild birds in several countries in Asia (5); in 2010, it was reported in Europe (6) and in 2014, in the Middle East (7). In 2015, clade 2.3.2.1c was detected in rooks, chickens, and dalmatian pelicans in Russia, Bulgaria, and Romania, respectively (8). To trace the evolution of HPAI A(H5N1) virus in West Africa, we examined the genetic characteristics of 43 such viruses collected during January–August 2015 in all affected countries in West Africa.
(SNIP)
Of note, all the viruses from West Africa display the same genetic constellation of a strain (A/Alberta/01/2014) isolated from a human, a Canada resident who had returned from China. These viruses contain mutations that have been described as being associated with an enhanced binding affinity for α2,6 sialic acid or with increased virulence in mammals.
As during the 2006–2008 HPAI A(H5N1) epidemics, West Africa countries are again facing devastating economic and social consequences from these infections. It is imperative for regional and international organizations to join forces in generating and making available detailed genetic and epidemiologic information that can be used to better trace the spread and evolution in West Africa of influenza A(H5N1) virus and to provide input for informed decisions on control measures and resource allocation.
Dr. Tassoni is a biotechnologist at the Istituto Zooprofilattico Sperimentale delle Venezie. His primary research interests include studying the molecular phylogeny and the evolutionary dynamics of viruses.
