Abstract
The first outbreak of influenza A(H3N2) occurred in 1968 and caused the third flu pandemic of the 20th century. It has affected multiple countries over time. The best strategy to reduce the burden of influenza is through vaccination whose efficacy varies with respect to the circulating strains. This study was performed to better understand the molecular evolution of influenza A(H3N2) and assess vaccine efficacy in Cameroon. Complete sequences of three gene segments were obtained from 2014 to 2016 influenza seasons in Cameroon. Hemagglutinin (HA), Neuraminidase (NA) and matrix (M) genes of 35 A(H3N2) virus strains were amplified and sequenced. Predicted vaccine efficacy was measured using the Pepitope model. Phylogenetic analysis of the HA gene showed that all Cameroonian strains had evolved away from the 3C.1-A/Texas/50/2012-like clade. Globally, 2014 virus strains clustered with the 2015–2016 vaccine strain, 3C.3a-A/Switzerland/9715293/2013, whereas 2015 and 2016 virus strains clustered with the 2016–2017 vaccine strain, 3C.2a-A/HongKong/4801/2014. In order to determine the genotypic drug susceptibility to neuraminidase inhibitors and amantadine, the NA and M2 protein coding sequences were analyzed. There was no strain with characteristic mutation for resistance to neuraminidase inhibitors, per contra; all strains possessed the substitution S31N, peculiar of resistance to adamantanes. There was drift in influenza A(H3N2) dominant epitopes B (2014 and 2015) to epitopes A (2016) with a theoretical efficiency in vaccine ranging from low to moderate. The presence of several antigenic site mutations among H3N2 virus strains between 2014–2016 influenza seasons in Cameroon confirms the progressing evolution of circulating H3N2 strains.
Highlights
Influenza A virus is a major cause of acute respiratory disease in humans and is responsible for approximately 250,000–500,000 deaths annually worldwide [1]
Nucleotide and amino acid sequences for the 3 selected genes were compared within the Cameroon virus strains and with the WHO vaccine strains, WHO reference strains and available sequences of other African virus strains
Virus strains from 2014 clustered with the 2015–2016 vaccine strain (3C.3a-A/Switzerland/9715293/2013) while virus strains from 2015 and 2016 clustered with the 2016–2017 vaccine strain (3C.2a-A/HongKong/4801/ 2014) except for one isolate (A/Cameroon/15V-8790/2015) which clustered with the reference strain, 3C.3a-A/Switzerland/9715293/2013
Summary
Influenza A virus is a major cause of acute respiratory disease in humans and is responsible for approximately 250,000–500,000 deaths annually worldwide [1]. Pandemic influenza A virus infection resulted in significant morbidity and mortality in 1918 (H1N1), 1957 (H2N2), 1968 (H3N2), and 2009 (H1N1) [2, 3]. The primary target of host neutralizing antibodies is the HA glycoprotein where it inhibits binding to the sialic acid receptors present in the respiratory tract [9]. Non-recognition of some strains by neutralizing antibodies present in the host is the consequence of mutations at these sites [11]. Continuous build-up of mutations at these antigenic sites is the basis for the evolutionary dynamics observed in the influenza virus resulting in antigenic drift [12]. Viruses in clade 3 are the dominant group, which has diversified further into three major subclades designated 3A, 3B, and 3C, with subclade 3C containing several distinguishable genetic groups [13, 14]
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