Summary SARS-CoV-2 Spike protein is critical for virus infection via engagement of ACE2 1 , and is a major antibody target. Here we report chronic SARS-CoV-2 with reduced sensitivity to neutralising antibodies in an immune suppressed individual treated with convalescent plasma, generating whole genome ultradeep sequences over 23 time points spanning 101 days. Little change was observed in the overall viral population structure following two courses of remdesivir over the first 57 days. However, following convalescent plasma therapy we observed large, dynamic virus population shifts, with the emergence of a dominant viral strain bearing D796H in S2 and ΔH69/ΔV70 in the S1 N-terminal domain NTD of the Spike protein. As passively transferred serum antibodies diminished, viruses with the escape genotype diminished in frequency, before returning during a final, unsuccessful course of convalescent plasma. In vitro , the Spike escape double mutant bearing ΔH69/ΔV70 and D796H conferred modestly decreased sensitivity to convalescent plasma, whilst maintaining infectivity similar to wild type. D796H appeared to be the main contributor to decreased susceptibility but incurred an infectivity defect. The ΔH69/ΔV70 single mutant had two-fold higher infectivity compared to wild type, possibly compensating for the reduced infectivity of D796H. These data reveal strong selection on SARS-CoV-2 during convalescent plasma therapy associated with emergence of viral variants with evidence of reduced susceptibility to neutralising antibodies.

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This is a PDF file of a peer-reviewed paper that has been accepted for publication. Although unedited, the content has been subjected to preliminary formatting. Nature is providing this early version of the typeset paper as a service to our authors and readers. The text and figures will undergo copyediting and a proof review before the paper is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers apply.

An enzyme immunoassay was used for the rapid detection of herpes simplex virus type 1 (HSV-1). The test utilized specific antibodies to HSV-1 attached to a solid phase. A laboratory preparation of HSV-1 was detectable in amounts of greater than or equal to 50 50% tissue culture-infective doses by this method. Tests performed with clinical samples indicated a specificity of 95%. The sensitivity appeared to depend on the length of time the samples were stored. When samples were stored frozen for three to six months, the sensitivity was 46% of that of tissue culture isolations performed when the samples were first collected. The sensitivity was 89% in comparison with attempts at tissue culture reisolation with the same samples at the time of enzyme immunoassay. The immunoassay also detected HSV in seven of 10 positive samples that were stored frozen for no more than two weeks before testing.