Replacement of neuraminidase inhibitor‐susceptible influenza A(H1N1) with resistant phenotype in 2008 and circulation of susceptible influenza A and B viruses during 2009‐2013, South Africa

BACKGROUND: Data on the susceptibility of influenza viruses from South Africa to neuraminidase inhibitors (NAIs) are scarce, and no extensive analysis was done. OBJECTIVES: We aimed to determine oseltamivir and zanamivir susceptibility of influenza A and B virus neuraminidases (NAs), 2007‐2013, Sout...

Descripción completa

Detalles Bibliográficos
Autores principales: Treurnicht, Florette K., Buys, Amelia, Tempia, Stefano, Seleka, Mpho, Cohen, Adam L., Walaza, Sibongile, Glass, Allison J., Rossouw, Inéz, McAnerney, Johanna, Blumberg, Lucille, Cohen, Cheryl, Venter, Marietjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Original Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304311/
https://www.ncbi.nlm.nih.gov/pubmed/30218485
http://dx.doi.org/10.1111/irv.12611
Descripción
Sumario:BACKGROUND: Data on the susceptibility of influenza viruses from South Africa to neuraminidase inhibitors (NAIs) are scarce, and no extensive analysis was done. OBJECTIVES: We aimed to determine oseltamivir and zanamivir susceptibility of influenza A and B virus neuraminidases (NAs), 2007‐2013, South Africa. PATIENTS/METHODS: We enrolled participants through national influenza‐like illness surveillance, 2007‐2013. Influenza diagnosis was by virus isolation and quantitative polymerase chain reaction (qPCR). Drug susceptibility was determined by chemiluminescence‐based NA‐STAR/NA‐XTD assay. Sanger sequencing was used to determine molecular markers of NAI resistance. RESULTS: Forty percent (6341/15 985) of participants were positive for influenza viruses using virus isolation (2007‐2009) and qPCR (2009‐2013) methods. A total of 1236/6341 (19.5%) virus isolates were generated of which 307/1236 (25%) were tested for drug susceptibility. During 2007‐2008, the median 50% inhibitory concentration (IC(50)) of oseltamivir for seasonal influenza A(H1N1) increased from of 0.08 nmol/L (range 0.01‐3.60) in 2007 to 73 nmol/L (range 1.56‐305 nmol/L) in 2008. Influenza A isolates from 2009 to 2013 were susceptible to oseltamivir [A(H3N2) median IC(50) = 0.05 nmol/L (range 0.01‐0.08); A(H1N1)pdm09 = 0.11 nmol/L (range 0.01‐0.78)] and zanamivir [A(H3N2) median IC(50) = 0.56 nmol/L (range 0.47‐0.66); A(H1N1)pdm09 = 0.35 nmol/L (range 0.27‐0.533)]. Influenza B viruses were susceptible to both NAIs. NAI resistance‐associated substitutions H275Y, E119V, and R150K (N1 numbering) were not detected in influenza A viruses that circulated in 2009‐2013. CONCLUSIONS: We confirm replacement of NAI susceptible by resistant phenotype influenza A(H1N1) in 2008. Influenza A and B viruses (2009‐2013) remained susceptible to NAIs; therefore, these drugs are useful for treating influenza‐infected patients.

Ejemplares similares