Overview of three influenza seasons in Georgia, 2014-2017

Abstract

Background: Influenza epidemiological and virologic data from Georgia are limited. We aimed to present Influenza Like Illness (ILI) and Severe Acute Respiratory Infection (SARI) surveillance data and characterize influenza viruses circulating in the country over three influenza seasons.

Methods: We analyzed sentinel site ILI and SARI data for the 2014-2017 seasons in Georgia. Patients' samples were screened by real-time RT-PCR and influenza viruses isolated were characterized antigenically by haemagglutination inhibition assay and genetically by sequencing of HA and NA genes.

Results: 32% (397/1248) of ILI and 29% (581/1997) of SARI patients tested were positive for influenza viruses. In 2014-2015 the median week of influenza detection was week 7/2015 with B/Yamagata lineage viruses dominating (79%); in 2015-2016-week 5/2016 was the median with A/H1N1pdm09 viruses prevailing (83%); and in 2016-2017 a bimodal distribution of influenza activity was observed-the first wave was caused by A/H3N2 (55%) with median week 51/2016 and the second by B/Victoria lineage viruses (45%) with median week 9/2017. For ILI, influenza virus detection was highest in children aged 5-14 years while for SARI patients most were aged >15 years and 27 (4.6%) of 581 SARI cases died during the three seasons. Persons aged 30-64 years had the highest risk of fatal outcome, notably those infected with A/H1N1pdm09 (OR 11.41, CI 3.94-33.04, p<0.001). A/H1N1pdm09 viruses analyzed by gene sequencing fell into genetic groups 6B and 6B.1; A/H3N2 viruses belonged to genetic subclades 3C.3b, 3C.3a, 3C.2a and 3C.2a1; B/Yamagata lineage viruses were of clade 3 and B/Victoria lineage viruses fell in clade1A.

Conclusion: In Georgia influenza virus activity occurred mainly from December through March in all seasons, with varying peak weeks and predominating viruses. Around one third of ILI/ SARI cases were associated with influenza caused by antigenically and genetically distinct influenza viruses over the course of the three seasons.

Fig 1. Distribution of influenza positive specimens by week during consecutive influenza seasons, 2014–2017, Georgia.

Numbers of influenza positive samples are displayed in vertical bars color-coded to show various types/subtypes of influenza viruses. The percentage of all samples collected each week that tested positive for influenza viruses is shown by the line.

Fig 2. Referral of ILI cases to outpatient clinic vs laboratory-confirmed influenza detections by week, 2014–2017, Georgia.

Vertical bars represent numbers of influenza positive samples among ILI cases each week over three consecutive seasons. The blue line shows weekly referrals of ILI cases to the outpatient clinic per 100 000 population.

Fig 3. Admission of SARI cases to hospitals vs laboratory-confirmed influenza detections by week, 2014–2017, Georgia.

Vertical bars show numbers of influenza positive specimens among SARI cases each week. The blue line represents percentages of influenza-positive cases among total SARI hospital admissions on a weekly basis.

Fig 4. HA gene phylogeny of influenza A/H1N1pdm09 viruses detected in Georgia during 2014–2015 and 2015–2016 seasons.

Vaccine viruses are indicated in red, viruses from Georgia for 2014–2015 and 2015–2016 seasons are shown in blue and pink respectively. Reference and vaccine viruses against which post-infection ferret antisera were raised for use in HI assays are in bold type. The scale bar represents nucleotide substitutions per site.

Fig 5. HA gene phylogeny of influenza A/H3N2 viruses detected in Georgia during three influenza seasons 2014–2017.

Vaccine viruses are indicated in red; 2014–2015, 2015–2016 and 2016–2017 viruses from Georgia in blue, pink and brown respectively. Reference and vaccine viruses against which post-infection ferret antisera were raised for use in HI assays are in bold type. The scale bar represents nucleotide substitutions per site.