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Parrington, H. M.

Publications and source records attributed to Parrington, H. M..

2 recordsLinked to original sources

Potently neutralizing human monoclonal antibodies against the zoonotic pararubulavirus Sosuga virus

Sosuga virus (SOSV) is a recently discovered paramyxovirus with a single known human case of disease. There has been little laboratory research on SOSV pathogenesis or immunity, and no approved therapeutics or vaccines are available. Here, we report the discovery of human monoclonal antibodies (mAbs) from the circulating memory B cells of the only known human case and survivor of SOSV infection. We isolated six mAbs recognizing the functional attachment protein (HN) and 18 mAbs against the fusion (F) protein. The anti-HN mAbs all target the globular head of the HN protein and can be organized into 4 competition-binding groups that exhibit epitope diversity. The anti-F mAbs can be divided into pre- or post-fusion conformation-specific categories and further into 8 competition-binding groups. Generally, pre-fusion conformation-specific anti-F mAbs showed higher potency in neutralization assays than did mAbs only recognizing the post-fusion conformation of F protein. Most of the anti-HN mAbs were more potently neutralizing than the anti-F mAbs, with mAbs in one of the HN competition-binding groups possessing ultra-potent (<1 ng/mL) half maximal inhibitory (IC50) virus neutralization values. These findings provide insight into the molecular basis for human antibody recognition of paramyxovirus surface proteins and the mechanisms of SOSV neutralization.

immunology↗

Group B rotavirus encodes a functional fusion-associated small transmembrane (FAST) protein

Rotavirus is an important cause of diarrheal disease in young mammals. Group A rotavirus (RVA) causes most human rotavirus diarrheal disease and primarily affects infants and young children. Group B rotavirus (RVB) has been associated with sporadic outbreaks of human adult diarrheal disease. RVA and RVB are predicted to encode mostly homologous proteins but differ significantly in the proteins encoded by the NSP1 gene. In the case of RVB, the NSP1 gene encodes two putative protein products of unknown function, NSP1-1 and NSP1-2. We demonstrate that human RVB NSP1-1 mediates syncytia formation in cultured human cells. Based on sequence alignment, NSP1-1 from groups B, G, and I contain features consistent with fusion-associated small transmembrane (FAST) proteins, which have previously been identified in other Reoviridae viruses. Like some other FAST proteins, RVB NSP1-1 is predicted to have an N-terminal myristoyl modification. Addition of an N-terminal FLAG peptide disrupts NSP1-1-mediated fusion, consistent with a role for this fatty-acid modification in NSP1-1 function. NSP1-1 from a human RVB mediates fusion of human cells but not hamster cells and, thus, may serve as a species tropism determinant. NSP1-1 also can enhance RVA replication in human cells, both in single-cycle infection studies and during a multi-cycle time course in the presence of fetal bovine serum, which inhibits rotavirus spread. These findings suggest potential yet untested roles for NSP1-1 in RVB species tropism, immune evasion, and pathogenesis.\n\nIMPORTANCEWhile group A rotavirus is commonly associated with diarrheal disease in young children, group B rotavirus has caused sporadic outbreaks of adult diarrheal disease. A major genetic difference between group A and B rotaviruses is the NSP1 gene, which encodes two proteins for group B rotavirus. We demonstrate that the smaller of these proteins, NSP1-1, can mediate fusion of cultured human cells. Comparison with viral proteins of similar function provides insight into NSP1-1 domain organization and fusion mechanism. Our findings are consistent with an important role for a fatty acid modification at the amino terminus of the protein in mediating its function. NSP1-1 from a human virus mediates fusion of human cells, but not hamster cells, and enhances rotavirus replication in culture. These findings suggest potential, but currently untested, roles for NSP1-1 in RVB species tropism, immune evasion, and pathogenesis.

microbiology↗