INFLUENZA – MICROBIOLOGY, IMMUNOLOGY AND EPIDEMIOLOGY FOR THE PHYSICIAN CONTEMPLATING IMMUNIZATION
This review of influenza microbiology, immunology and spread is garnished with epidemiological data of the past 10 seasons, in order to enable physicians an informed navigation through the arguments for their own vaccination. The reasons for antigenic mismatch, including the role of vaccine production technology are discussed. A tabulated comparison of circulating and vaccine type viruses over the past 10 seasons is layed out. The proportion of A subtypes and B types (lineages) in each season, antigenic match and average protectiveness of the influenza vaccine is extracted from the data available at The Centers of Disease Control and Prevention in the USA and the The Institute of Public Health of Croatia. A growing proportion of influenza cases are due to the second B virus. Tetravalent vaccines including 2 A subtypes and 2 B types are increasingly recommended. Indirect data from the 2009 H1N1 pandemic disclosed that immunity against a specific influenza A subtype can hold significantly longer than a single season. Broader but less specific long lasting immunity may be conferred by heterosubtypic antigens contained within the influenza virus acquired by natural infection. The current seasonal influenza is expected to be caused by 4 viruses: A/Michigan, A/Singapore, B/Colorado and B/Phuket (the latter is included only in the 4-valent vaccines). Of these, A/Michigan is a drifted 2009 pandemic virus (A/California/07/2009) and A/Singapore and B/Colorado are new strains. B/Phuket could be found in the trivalent 2015-16 vaccine, and in the tetravalent 2016-17 and 2017-18 vaccines. Individuals who did not get vaccinated since the 2014-15 season, should offer themselves a tetravalent vaccine, while those who received a trivalent vaccine for the season 2015-16 or a tetravalent one for the 2016-17 and 2017-18 seasons should be well off with a trivalent vaccine.