Evidence in Kenya of Reassortment Between of Reassortment BetweenSeasonal Influenza A(H3N2) and Influenza A(H1N1)pdm09 to yield A(H3N2) Variants With the Matrix Gene Segment of A(H1N1)pdm09

Abstract

Influenza vaccines and antiviral drugs are the mainstay for preventing influenza and reducing the impact of influenza epidemics. Currently, there are two classes of antiviral drugs available for preventing and treating  the M gene. The neuraminidase inhibitors (NAI’s) interrupt the replication cycle by preventing virus release and allowing progeny virus to clump (Monto et al, 2002). The rapid emergence of adamantine drug resistant influenza A virus strains has limited these drugs’ clinical effectiveness.

The origin and evolution of antiviral drug resistance amongst influenza viruses can occur through different molecular mechanisms that also drive the evolution of the virus. The most crucial of these mechanisms result from the segmented nature of its genome. This permits the formation of new progeny viruses with novel combinations of segments through reassortment when two or more different virus subtypes infect a single cell, a phenomenon referred to as antigenic shift. This process is capable of introducing new genes in circulating viral populations that can drastically change the biological properties of the virus. Studies have shown that reassortment led to an increase in the frequency of amantadine-resistant seasonal influenza A(H1N1) viruses since the 2005-2006 season (Yang et al, 2011). This underscores the necessity to monitor genome dynamics in circulating influenza viruses because it is through such molecular surveillance that we are able to understand the evolution and mechanisms of the emergence and spread of antiviral resistance among influenza A viruses (Boni et al, 2010).

Thus, we set out to qualitatively analyze human influenza A(H3N2) viruses that circulated in Kenya in 2010, the period when influenza A(H3N2) and A(H1N1)pdm09 [previously referred to as swine flu] (WHO, 2011a) begun to co-circulate in the human population in the country, determine evidence of reassortment amongst the co-circulating subtypes and relate any such events to influenza antiviral resistance in the country. We applied the current laboratory testing protocol which involves routinely sequencing the HA, M and NA gene segments of the influenza viruses. These three gene segments were selected because they are the main antigens (NA & HA) and drug targets (M & NA) of the influenza A virus. Herein we provide evidence that indeed there was reassortment involving at least the M gene segment amongst cocirculating influenza A viruses in Kenya during this period.