Eurosurveillance: Emergence of A(H1N1)pdm09 Genogroup 6B In India, 2015

#10,971



In February of 2015, in India’s H1N1 Outbreak, we looked at the persistent media reports of unusually severe H1N1 flu activity on the Indian subcontinent, and the insistence by India’s National Institute of Virology (NIV) and their National Centre for Disease Control (NCDC) that there were No mutations in H1N1.

A few weeks later, in MIT: Genetic Changes In A 2014 Indian H1N1pdm09 Virus,  we saw analysis of at least one flu isolate collected in 2014 that researchers said contained  `amino acid changes linked to enhanced virulence and are potentially antigenically distinct from the current vaccine containing 2009 (Cal0709) H1N1 viral hemagglutinin.

The entire report/commentary – which emphasizes the need for more robust and timely influenza surveillance and sequencing data -  can be accessed at:  Influenza Surveillance: 2014–2015 H1N1 “Swine”-Derived Influenza Viruses from India.

Fast forward to today, and the ECDC's Eurosurveillance has done just that.  

They've published an analysis of sequencing data from H1N1pdm09 isolates gathered in India during the first half of 2015. One that not only finds the rapidly rising Genotype 6B present but provides evidence of additional mutations as well.


This study also references the MIT study mentioned above. I've only excerpted a small piece, so follow the link to read it in its entirety.

Rapid communication

Emergence of influenza A(H1N1)pdm09 genogroup 6B and drug resistant virus, India, January to May 2015

M Parida ¹ , PK Dash ¹ , JS Kumar ¹ , G Joshi ¹ , K Tandel ¹ , S Sharma ¹ , A Srivastava ¹ , A Agarwal ¹ , A Saha ¹ , S Saraswat ¹ , D Karothia ¹ , V Malviya ¹

+ Author affiliations

Received:11 December 2015; Accepted:04 February 2016

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To investigate the aetiology of the 2015 A(H1N1)pdm09 influenza outbreak in India, 1,083 nasopharyngeal swabs from suspect patients were screened for influenza A(H1N1)pdm09 in the state of Madhya Pradesh. Of 412 positive specimens, six were further characterised by phylogenetic analysis of haemagglutinin (HA) sequences revealing that they belonged to genogroup 6B. A new mutation (E164G) was observed in HA2 of two sequences. Neuraminidase genes in two of 12 isolates from fatal cases on prior oseltamivir treatment harboured the H275Y mutation.

An epidemic of influenza A(H1N1)pdm09, affecting over 39,000 persons and causing more than 2,500 deaths occurred in India in 2015 [1]. We show that genotype 6B strains forming two sub-lineages circulated during the outbreak.

Comparison of the sequences of six outbreak strains recovered in this work, to other published genotype 6B sequences, also reveals a unique combination of previously-reported mutations in the haemagglutinin (HA) gene. Two of the six sequences additionally display a E164G mutation in HA2, which has not been reported to date, moreover a N129D mutation in HA1 is observed for two sequences derived from patients with severe disease. Among strains analysed from 12 fatal cases on prior oseltamivir treatment, two harbour the H275Y mutation in the neuraminidase (NA) gene, which confers resistance to this antiviral.  

(Continue . . .)

The H275Y amino acid change, which confers resistance to Oseltamivir, has yet to take hold with the H1N1pdm09 virus, showing up in only 1%-2% of samples tested. That said, we have seen a few worrisome clusters of NAI resistant flu (see HERE & HERE), raising concerns that a resistant strain could evolve.


As mentioned previously, the A/H1N1pdm09 virus has remained remarkably stable since it first emerged as a pandemic strain in the spring of 2009.  But over time - and as all influenza A viruses do - the virus has picked up small genetic changes due to antigenic drift.

Most of these genetic changes go nowhere. They either offer no evolutionary advantage, or worse for the virus, they are detrimental to its survival.  

But occasionally - and through random chance -  a mutation (or set of mutations) provides the virus a biological advantage over its competitors; it infects its host more readily, transmits more easily, or replicates more efficiently.

The tendency is to become complacent with seasonal flu, and to worry only about the novel flu strains.  But the virulence of seasonal flu is not constant, and it is always possible for an old and familiar flu to learn new tricks. 

The changes observed in this study - and those recently reported by the Russians (see Week 5 Epi Report) - are intriguing and beg further investigation and study.  But it remains to be seen how much of an effect they will actually have on the virulence and future impact of the H1N1pdm09 virus.

 

Stay tuned.