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Rothman, R.

Publications and source records attributed to Rothman, R..

2 recordsLinked to original sources
bioRxiv2020

Identification of H3N2 NA and PB1-F2 genetic variants and their association with disease symptoms in the 2014-15 influenza season

The 2014-15 influenza season saw the emergence of an H3N2 antigenic drift variant that formed the 3C.2a HA clade. Whole viral genomes were sequenced from nasopharyngeal swabs of 94 patients with confirmed influenza A virus infection and primary human nasal epithelial cell cultures used to efficiently isolate H3N2 viruses. The isolates were classified by HA clade and the presence of a new set of co-selected mutations in NA (a glycosylation site, NAg+) and PB1-F2 (H75P). The NA and PB1-F2 mutations were present in a subset of clade 3C.2a viruses (NAg+F2P) which dominated during the subsequent influenza seasons. In human nasal epithelial cell cultures, a virus with the novel NAg+F2P genotype replicated less well compared to a virus with the parental genotype. Retrospective analyses of clinical data showed that NAg+F2P genotype viruses were associated with increased cough and shortness of breath in infected patients.

microbiology↗
bioRxiv2020

Human Influenza A Virus H1N1pdm Full-length Genome Sequencing in USA and Taiwan in 2015-16 Flu Season and Disease Correlation

During the 2015-16 winter, the US experienced a relatively mild influenza season compared to Taiwan which had a higher number of total and severe cases. While H1N1pdm viruses dominated global surveillance efforts that season, the global distribution of genetic variants and their contributions to disease severity have not been investigated. Samples collected from influenza A positive patients by the Johns Hopkins Center of Excellence for Influenza Research and Surveillance (JH-CEIRS) active surveillance in the emergency rooms in Baltimore, Maryland, USA and northern Taiwan between November 2015 and April 2016, were processed for influenza A virus whole genome sequencing. In Baltimore, the majority of the viruses were the H1N1pdm clade 6B.1 and no H1N1pdm clade 6B.2 viruses were detected. In northern Taiwan, more than half of the H1N1pdm viruses were clade 6B.1 and 38% were clade 6B.2, consistent with the global observation that most 6B.2 viruses circulated in Asia and not North America. Whole virus genome sequence analysis identified two genetic subgroups present in each of the 6B.1 and 6B.2 clades and one 6B.1 intraclade reassortant virus. Clinical data showed 6B.2 patients had more disease symptoms including higher crude and inverse probability weighted odds of pneumonia than 6B.1 patients, suggesting 6B.2 circulation may contribute to the severe flu season in Taiwan. Local surveillance efforts linking H1N1pdm virus sequences to patient clinical and demographic data improve our understanding of influenza circulation and disease potential.

microbiology↗