The study aimed to analyze drug resistance and mutations and genetic evolution of influenza A and influenza B viruses during the 2013 and 2014 influenza season in Beijing, China. RNA was extracted from pharyngeal or nasal swabs of 28 patients, and determination of influenza genotypes was performed by using real-time reverse-transcription polymerase chain reaction. Influenza A virus samples were sequenced with the neuraminidase (NA) gene and M2 matrix protein gene to determine the NA inhibitor (NAI) resistance and amantadine resistance mutations, and influenza B virus samples were sequenced with the NA gene and hemagglutinin (HA) gene to analyze NAI resistance mutations. As a result, the enrolled subjects consisted of 19 patients with the A(H1N1)pdm09 subtype, four with A(H3N2) subtype and five with influenza B virus. All of the 23 samples with influenza A viruses harbored amantadine resistance mutation S31N in M2 matrix protein. V241I, a compensatory NAI resistance mutation, was detected in all of the 19 A(H1N1)pdm09 viruses. No other NAI resistance mutation was observed in both influenza A and B viruses. The NA gene of the five influenza B virus strains was classified as B-Victoria lineage, while the HA gene of five strains was classified as B-Yamagata lineage. In summary, all influenza A viruses from patients in Beijing in the 2013-2014 season were resistant to amantadine agent. Both influenza A and B viruses kept sensitive to NAIs. Lineage recombination was detected in influenza B virus strains and may impair the efficacy of influenza vaccination.