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The influenza virus is one of the most critical viruses in epidemiology. The 2009 pandemic was caused by a reassortment of the human–avian–swine virus with eight RNA segments responsible for all virus proteins. Segment 7 codifies for matrix proteins M1 and M2. These proteins exhibited low mutation rate because the matrix is fundamental for virion encapsidation and ion channel formation. However, hemagglutinin (HA) segment 4 is one of the most important segments for virulence and hence, is more studied. Brazil had many influenza virus infection cases just before 2009 and from 2011 to 2015, particularly in the Rio Grande do Sul (RS) State. Two hundred samples obtained during the pandemic were used for amplification and sequencing of the viral genome; a total of 19 M and 17 HA amplified segments were sequenced. Sequencing of the M fragment showed that RS has a virus origin different from that in Eastern Asia, Western Europe, USA, and Central America (Mexico and Nicaragua). All the sequences showed amantadine resistance (S31N) and one was out of the phylogenetic tree (Brazil/RS-3335/2009) due to high mutation rate. RS-3335 was the only sample obtained from a patient who died. Many migratory birds that flock to RS are from Europe, Asia, and USA, which could explain this rate of mutation. Insertions and deletions were found in the M1 protein in these samples. The HA sequences showed worldwide spread and less diversity than the M sequences in this study. The most divergent sample was Brazil/RS-3093/2009 that showed mutations in the sialic acid ligation site.

Correlation between virologic profile and clinical features of patients infected by influenza virus provides important information for epidemiological control and clinical management of future disease outbreaks. Samples from patients in Southern Brazil, from June to December 2009, were examined and the viral load was correlated with epidemiological data. All samples were analyzed by qRT-PCR for detection of the 2009-pandemic Influenza A (H1N1). Relative viral loads were assessed based on the 2(-ΔCT) method and epidemiological data were obtained for each patient, following ethical policies. A total of 933 samples were positive for pH1N1 (2009) influenza; 172 were positive for seasonal influenza A; 13 were undetermined; 1992 samples were negative for influenza A. Combined molecular and epidemiological data were available for 38 seasonal and 198 pandemic samples. The median viral load was higher in pandemic than in seasonal influenza samples; in patients infected with pH1N1 (2009), viral load associated positively with chills, myalgia and rhinorrhea, and negatively with dyspnea, but no association was observed with other symptoms, nor with clinical conditions such as pregnancy, smoking, immunodepression and co-morbidities. Regarding patients infected with seasonal influenza, viral loads did not show statistically significant association with any of the symptoms. This is the first study in Brazil that examines epidemiological and molecular data from the 2009 influenza pandemic. The results may serve as a basis for developing strategies to control human-to-human infection and viral dissemination, and for implementing effective measures and public health policies against future novel disease outbreaks.