Background: The genus Norovirus comprises large genetic diversity, and new GII.4 variants emerge every 2-3 years. It is unknown in which host these new variants originate. Here we study whether prolonged shedders within the immunocompromised population could be a reservoir for newly emerging strains. Methods: Sixty-five fecal samples from 16 immunocompromised patients were retrospectively selected. Isolated viral RNA was enriched by hybridization with a custom norovirus whole-genome RNA bait set and deep sequenced on the Illumina MiSeq platform. Results: Patients shed virus for average 352 days (range, 76-716 days). Phylogenetic analysis showed distinct GII.4 variants in 3 of 13 patients (23%). The viral mutation rates were variable between patients but did not differ between various immune status groups. All within-host GII.4 viral populations showed amino acid changes at blocking epitopes over time, and the majority of VP1 amino acid mutations were located at the capsid surface. Conclusions: This study found viruses in immunocompromised hosts that are genetically distinct from viruses circulating in the general population, and these patients therefore may contain a reservoir for newly emerging strains. Future studies need to determine whether these new strains are of risk to other immunocompromised patients and the general population.
Background: The genus Norovirus comprises large genetic diversity, and new GII.4 variants emerge every 2-3 years. It is unknown in which host these new variants originate. Here we study whether prolonged shedders within the immunocompromised population could be a reservoir for newly emerging strains. Methods: Sixty-five fecal samples from 16 immunocompromised patients were retrospectively selected. Isolated viral RNA was enriched by hybridization with a custom norovirus whole-genome RNA bait set and deep sequenced on the Illumina MiSeq platform. Results:Patients shed virus for average 352 days (range, 76-716 days). Phylogenetic analysis showed distinct GII.4 variants in 3 of 13 patients (23%). The viral mutation rates were variable between patients but did not differ between various immune status groups. All within-host GII.4 viral populations showed amino acid changes at blocking epitopes over time, and the majority of VP1 amino acid mutations were located at the capsid surface. Conclusions: This study found viruses in immunocompromised hosts that are genetically distinct from viruses circulating in the general population, and these patients therefore may contain a reservoir for newly emerging strains. Future studies need to determine whether these new strains are of risk to other immunocompromised patients and the general population.
Authors: Susana Guix; Cristina Fuentes; Rosa M Pintó; Albert Blanco; Aurora Sabrià; Eduard Anfruns-Estrada; Virginia Rodríguez Garrido; Manuel Alonso; Rosa Bartolomé; Thais Cornejo; Tomàs Pumarola; Albert Bosch Journal: Emerg Infect Dis Date: 2020-01 Impact factor: 6.883
Authors: Forrest C Walker; Ebrahim Hassan; Stefan T Peterson; Rachel Rodgers; Lawrence A Schriefer; Cassandra E Thompson; Yuhao Li; Gowri Kalugotla; Carla Blum-Johnston; Dylan Lawrence; Broc T McCune; Vincent R Graziano; Larissa Lushniak; Sanghyun Lee; Alexa N Roth; Stephanie M Karst; Timothy J Nice; Jonathan J Miner; Craig B Wilen; Megan T Baldridge Journal: PLoS Pathog Date: 2021-03-11 Impact factor: 6.823
Authors: Amy Davis; Valerie Cortez; Marco Grodzki; Ronald Dallas; Jose Ferrolino; Pamela Freiden; Gabriela Maron; Hana Hakim; Randall T Hayden; Li Tang; Adam Huys; Abimbola O Kolawole; Christiane E Wobus; Melissa K Jones; Stephanie M Karst; Stacey Schultz-Cherry Journal: Viruses Date: 2020-06-05 Impact factor: 5.048
Authors: Lisa C Lindesmith; Paul D Brewer-Jensen; Michael L Mallory; Boyd Yount; Matthew H Collins; Kari Debbink; Rachel L Graham; Ralph S Baric Journal: J Virol Date: 2019-01-04 Impact factor: 5.103