Regional and widespread outbreaks were reported in the Republic of Korea and Japan in January. Low-level activity was reported in Europe from September to November but increased during December and January in many countries. In northern Africa, activity increased in January with widespread outbreaks reported in Algeria. Sporadic and localised A(H3N2) activity was also reported in Oceania, central (Cameroon) and southern Africa and a number of countries in South America. Influenza B virus activity increased in North America from November with regional outbreaks reported by Mexico and the United States of America

and was predominant in Mexico. In Europe, widespread outbreaks were reported in many countries in January. In Asia activity was generally low. Localised and sporadic B activity Stem Cells inhibitor was also reported by a number of countries in Africa, Oceania and South America. Influenza activity maps (maximum level of activity shown) for the period August 2012–January 2013 along with graphs showing the number of influenza viruses detected, typed and subtyped by the GISRS laboratories from 2010 to 2013 are presented in Fig. 1. At the time of the VCM, data collected from the GISRS laboratory network showed

that, of the influenza viruses collected from September 2012 to February 2013, SB203580 in vivo approximately 92,298 (77%) were type A and 27,695 (23%) type B; of the type A viruses 14,306 (15.5%) were A(H1N1)pdm09, 47,213 (51.2%) were A(H3N2) and 30,779 (33.3%) were not subtyped. For the Consultation, WHO CCs performed detailed antigenic analyses on 3147 influenza viruses (Table 1). Viruses were collected from September 2012 to the beginning of February 2013 and recovered from either clinical specimens or virus isolates provided by NICs and other laboratories within and outside GISRS. Antigenic characterisation was carried out predominantly by haemagglutination inhibition (HI) assays using viruses isolated and propagated in either mammalian

tissue culture cells (most frequently Madin-Darby canine kidney cells not (MDCK) or MDCK-SIAT-1 cells, the latter engineered to express increased levels of α-2,6 sialyl transferase [2]) or in embryonated hens’ eggs. HI assays using turkey or guinea pig red blood cells (RBC) were performed to compare the reactivity of cultured viruses with post-infection ferret antisera raised against egg- or cell-propagated reference viruses [3]. A subset of viruses also underwent genetic characterisation. Genetic analyses were focused on the sequencing of the haemagglutinin (HA) and neuraminidase (NA) genes, with matrix (M) gene or full genome sequencing performed on a smaller subset of viruses.