Even so, when partial correlation and multiple linear regression was performed, only floor temperature demonstrates substantial unfavorable association with no. of influenza instances and was the strongest predictor amid all meteorological factors (Table 1). The real causal romantic relationship among ground temperature and influenza seasonality stays in concern. Although, these results propose that the influenza A and B seasonal action probably coincided with a combination of colder and rainier Malaysian Northeast Monsoon instead of the Southwest Monsoon. A significant unfavorable correlation among particulate subject (PM10) and influenza exercise was also identified in this review (Desk 1). Similar relationship was reported in Southern China [sixty two, sixty three], which postulated that reduced PM10 would outcome in higher ultraviolet radiation (UVR) that may reduce immune function. However, the function of UVR in growing host susceptibility to influenza continues to be controversial and demands more investigation. There was a big difference in the general prevalence in between influenza A and B viruses in the course of the study period of time. The number of influenza B circumstances was persistently reduce compared to influenza A cases every yr, and there is a time lag between their peak routines (Fig 1C). On the basis of a number of studies indicating reduced charges of nucleotide mutation and selection stress in influenza B viruses in contrast to influenza A viruses [39, sixty four], it is tempting to propose that they may play a part in the reduced prevalence of influenza B viruses. Although this kind of description continues to be speculative as prevalence reports could be influenced by sampling artifacts or the scale of surveillance. Whilst both influenza and B viruses continue to co-circulate, we also observed a slight increase of influenza B incidence when influenza A incidence decreased) (Fig 1C) The improve of influenza B incidence also coincided with shifts in the predominant influenza B lineage (from Victoria lineage in 2012 to Yamagata lineage in 2013) and clade (from Yam-two in 2013 to Yam-3 in 2014) (Fig 4). The mechanism on how the decrease of influenza A incidence might lead to a modify of influenza B lineage and clade requires even more investigation. Nonetheless, we hypothesize that the turnover of antigenically unique lineages from Victoria lineage in 2012 to Yamagata lineage in 2013 could be a result of immune alpha-Hederin 
variety because of to accumulated herd immunity in the human populace [39]. We propose that the much less dominant Yamagata lineage with distinct antigenicity may regain dominance when7214140 the predominating Victoria lineage has induced enough herd immunity in the hosts, possibly by way of restoration from an infection or vaccination.