In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

The isolation of neutralizing monoclonal antibodies (nmAbs) against the Zika virus (ZIKV) might lead to novel preventative strategies for infections in at-risk individuals, primarily pregnant women. Here we describe the characterization of human mAbs from the plasmablasts of an acutely infected patient. One of the 18 mAbs had the unusual feature of binding to and neutralizing ZIKV despite not appearing to have been diversified by affinity maturation. This mAb neutralized ZIKV (Neut 50~2 μg/ml) but did not react with any of the four dengue virus serotypes. Except for the expected junctional diversity created by the joining of the V-(D)-J genes, there was no deviation from immunoglobulin germline genes. This is a rare example of a human mAb with neutralizing activity in the absence of detectable somatic hypermutation. Importantly, binding of this mAb to ZIKV was specifically inhibited by human plasma from ZIKV-exposed individuals, suggesting that it may be of value in a diagnostic setting.
A human inferred germline antibody binds to an immunodominant epitope and neutralizes Zika virus

An oligonucleotide array (microarray) incorporating 13,000 elements representing selected strains of hepatitis A virus (HAV), human coxsackieviruses A and B (CVA and CVB), genogroups I and II of Norovirus (NV), and human rotavirus (RV) gene segments 3,4,10, and 11 was designed based on the principle of tiling. Each oligonucleotide was 29 bases long, starting at every 5 th base of every sequence, resulting in an overlap of 24 bases in two consecutive oligonucleotides. The applicability of the array for virus identification was examined using PCR amplified products from multiple HAV and CV strains. PCR products labeled with biotin were hybridized to the array, and the biotin was detected using a brief reaction with Cy3-labeled streptavidin, the array subjected to laser scanning, and the hybridization data plotted as fluorescence intensity against each oligonucleotide in the array. The combined signal intensities of all probes representing a particular strain of virus were calculated and plotted against all virus strains identified on a linear representation of the array. The profile of the total signal intensity identified the strain that is most likely represented in the amplified cDNA target. The results obtained with HAV and CV indicated that the hybridization profile thus generated can be used to identify closely related viral strains. This represents a significant improvement over current methods for virus identification using PCR amplification and amplicon sequencing.
A Microarray Based Approach for the Identification of Common Foodborne Viruses

word count: 359 20 Text word count: 4423 21 22 All rights reserved. No reuse allowed without permission. ABSTRACT 23 The 3¢-to-5¢ exoribonuclease in coronavirus (CoV) nonstructural protein 14 (nsp14-ExoN) 24 mediates RNA proofreading during genome replication. ExoN catalytic residues are arranged in 25 three motifs: I (DE), II (E), III (D). Alanine substitution of the motif I residues (AA-E-D, four 26 nucleotide substitutions) in murine hepatitis virus (MHV) and SARS-CoV yields viable mutants 27 with impaired replication and fitness, increased mutation rates, and attenuated virulence in vivo. 28 Despite these impairments, MHV-and SARS-CoV ExoN motif I AA mutants (ExoN-AA) have 29 not reverted at motif I in diverse in vitro and in vivo environments, suggesting that profound 30 fitness barriers prevent motif I reversion. To test this hypothesis, we engineered MHV-ExoN-AA 31 with 1, 2 or 3 nucleotide mutations along genetic pathways to AA-to-DE reversion. We show 32 that engineered intermediate revertants were viable but had no increased replication or 33 competitive fitness compared to MHV-ExoN-AA. In contrast, a low passage (P10) MHV-ExoN-34 AA showed increased replication and competitive fitness without reversion of ExoN-AA. 35 Finally, engineered reversion of ExoN-AA to ExoN-DE in the presence of ExoN-AA passage-36 adaptive mutations resulted in significant fitness loss. These results demonstrate that while 37 reversion is possible, at least one alternative adaptive pathway is more rapidly advantageous than 38 intermediate revertants and may alter the genetic background to render reversion detrimental to 39 fitness. Our results provide an evolutionary rationale for lack of ExoN-AA reversion, illuminate 40 potential multi-protein replicase interactions and coevolution, and support future studies aimed at 41 stabilizing attenuated CoV ExoN-AA mutants. 42 43 All rights reserved. No reuse allowed without permission. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/618249 doi: bioRxiv preprint Coronaviruses encode an exoribonuclease (ExoN) that is important for viral replication, fitness, 45 and virulence, yet coronaviruses with a defective ExoN (ExoN-AA) have not reverted under 46 diverse experimental conditions. In this study, we identify multiple impediments to MHV-ExoN-47 AA reversion. We show that ExoN-AA reversion is possible but evolutionarily unfavorable. 48 Instead, compensatory mutations outside of ExoN-AA motif I are more accessible and beneficial 49 than partial reversion. We also show that coevolution between replicase proteins over long-term 50 passage partially compensates for ExoN-AA motif I but renders the virus inhospitable to a 51 reverted ExoN. Our results reveal the evolutionary basis for the genetic stability of ExoN-52 inactivating mutations, illuminate complex functional and evolutionary relationships between 53 coronavirus replicase proteins, and identify potential mechanisms for stabilization of ExoN-AA 54 coronavirus mutants. 55 All rights reserved. No reuse allowed without permission.

Fitness barriers limit reversion of a proofreading-deficient coronavirus 1 2