[GENETIC CHARACTERISTICS OF INFLUENZA A/H3N2 AND B VIRUSES THAT HAD CIRCULATED IN RUSSIA IN 2013 - 2015].

AIM: Establish genetic characteristics, carry out phylogenetic analysis and determination of molecular markers of resistance to etiotropic preparations against influenza A/H3N2 and B viruses that had circulated in Russia in 2013 - 2015. MATERIALS AND METHODS: 80 biological samples containing influenza A/H3N2 virus RNA and 31 samples containing influenza B virus RNA were studied. Sequencing of PCR fragments was carried out inABI-3 100 PRIZMTM GeneticAnalyzer (AppliedBiosystems, USA) and using MiSeq (Illumina, USA). Data treatment and analysis was carried out using CLC v.3.6.5., DNASTAR and BioNumerics v.6.5. programs. RESULTS: In 2013 -2014 A/Texas/50/2012-like-clade 3C.3 influenza A/H3N2 viruses dominated, 10% belonged to subclade 3C.2a and 10% - to 3C.3b. Most of the viruses (8 1%) of 2014 - 2015 were of 3C.2a clade, the portion of viruses belonging to 3C.3b and 3C.3a was 9 and 10%. Yamagata-like viruses predominated among the studied influenza B viruses, only 1 virus of 2014 - 2015 belonged to Victoria lineage, 1 reassortant of Yamagata and Victoria lineages was detected. Rimantadine- resistance mutationS3 lN(M2 protein) was detected in all the influenza A/H3N2 viruses. Mutations determining resistance to oseltamivir (NA gene) were not detected in influenza A/H3N2 and B viruses. CONCLUSION: Increase of influenza morbidity in 2014 - 2015 was determined by the emergence of influenza A/H3N2 and B viruses, antigenically distinct from those that had circulated previously and those included into the vaccine, thus resulting in the WHO decision to change A/ H3N2 and B components of the 2015 - 2016 vaccine: Simultaneous circulation of 2 lineages of influenza B virus and emergence of their reassortants gives evidence on the necessity of use of quadrivalent vaccines, containing both lineages.

[ADENOVIRUSES IN THE ETIOLOGICAL STRUCTURE OF ACUTE RESPIRATORY VIRAL INFECTION IN MOSCOW IN 2004 - 2014].

AIM: Study prevalence of adenovirus species and serotypes that had caused acute respiratory viral infection (ARVI) in Moscow in 2004 - 2014. MATERIALS AND METHODS: Material from respiratory tract of 4731 patients with ARVI and 663 conditionally healthy children and adults was used. ARVI causative agents were detected by PCR with real-time detection using AmpliSens reagent kits (CRIE, Moscow). Membership of adenoviruses to a certain serotype was determined by sequencing of hexon gene segment. Adenoviruses that had caused ARD in servicemen in 2010 - 2014 were also studied. RESULTS: ARVI causative agents were detected in 64.6% ill children and 58% of adults. Respiratory-syncytial and rhinoviruses prevailed in children, influenza A virus--in adults. Adenoviruses were detected in 6.9% of ill children and 2.9% of adults during the whole year, with a rise in October-December. B and C species occurred at an equal frequency, E species was found less often. Serotypes 3 and 2 prevailed in 34% and 21% of cases of adenovirus mono-infection, respectively, serotypes 7, 6 and 4 occurred less often. 4 out of 5 outbreaks of adenovirus infection in servicemen were caused by serotype 7. Adenoviruses were absent in the group of healthy adults, in conditionally healthy children were detected in 0.4% of cases and were attributed to serotypes 1 and 2. CONCLUSION: Etiological structure of ARVI was studied for the last decade. Adenovirus infection ranked 5th in children and 7th in adults. 9 serotypes of 3 species of respiratory adenoviruses were identified. Varying prevalence of species and serotypes depending in season, clinical diagnosis and patient age was demonstrated.