bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2020.03.17.995795

Scientometric Trends for Coronaviruses and Other Emerging Viral Infections

Kagan, D.·Moran-Gilad, J.·Fire, M.
View original source ↗Export metadata ↓

Abstract

COVID-19 is the most rapidly expanding coronavirus outbreak in the past two decades. To provide a swift response to a novel outbreak, prior knowledge from similar outbreaks is essential. Here, we study the volume of research conducted on previous coronavirus outbreaks, specifically SARS and MERS, relative to other infectious diseases by analyzing over 35 million papers from the last 20 years. Our results demonstrate that previous coronavirus outbreaks have been understudied compared to other viruses. We also show that the research volume of emerging infectious diseases is very high after an outbreak and drops drastically upon the containment of the disease. This can yield inadequate research and limited investment in gaining a full understanding of novel coronavirus management and prevention. Independent of the outcome of the current COVID-19 outbreak, we believe that measures should be taken to encourage sustained research in the field.

Source connections

Explore related subjects

microbiologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Kagan, D., Moran-Gilad, J., Fire, M.. 2020-03-20. Scientometric Trends for Coronaviruses and Other Emerging Viral Infections. https://doi.org/10.1101/2020.03.17.995795

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

pTRIP, a novel integration plasmid for Listeria monocytogenes

In the past decades, several tools to genetically modify the human pathogen Listeria monocytogenes were developed. Here, we constructed a new integrative plasmid system for L. monocytogenes named pTRIP, for treB insertion plasmid. pTRIP is a vector which stably integrates into the treB locus of the wild type EGD-e. This locus encodes the sole trehalose-specific EIIB and EIIC component of a phosphotransferase system. Successful integration leads to the disruption of treB and thus, to an inability of the resulting L. monocytogenes strains to grow on trehalose as sole carbon source. Due to integration through double homologous recombination, it is the first integrative system which does not require antibiotic selection pressure. To assess functionality of the pTRIP system, prfA and its native promoter region were integrated into the treB locus of a {Delta}prfA strain. Complementation was confirmed in 78% of the isolated clones, indicating successful integration of prfA into the treB locus. We further constructed derivatives of pTRIP harboring the constitutive Pp60 (pTRIP1) and the inducible Prha (pTRIP2) promoter to further expand application possibilities. Microscopic analyses confirmed the functionality of both promoter constructs and showed dose-dependent induction for Prha. pTRIP is an efficient tool for stable gene expression as well as functional studies and expands genetic modification possibilities for L. monocytogenes.

microbiology↗
bioRxiv2026

Toxoplasma gondii GRA66 prevents premature egress driven by the host phospholipase RARRES3, independently of RNF213

Toxoplasma gondii replicates inside a host-derived parasitophorous vacuole (PV), and interferon-gamma (IFN{gamma}) induces host restriction factors that target this compartment. Previous CRISPR screens identified the dense granule protein GRA66 and the GRA57/GRA70/GRA71 complex as required for parasite fitness in IFN{gamma}-stimulated human cells, but the host pathways they oppose were unknown. Here, we show that GRA66, a PV membrane (PVM)-associated protein predicted to be an N-acylphosphatidylethanolamine (NAPE)-hydrolyzing phospholipase D, is required to prevent premature egress driven by the host phospholipase and acyltransferase RARRES3. Loss of GRA66 caused premature parasite egress, host cell death, and impaired replication in human cells. These phenotypes persisted in cells lacking RNF213, the E3 ubiquitin ligase that dominates IFN{gamma}-dependent Toxoplasma restriction in human cells, and{Delta} gra66 vacuoles recruited less RNF213 and ubiquitin than wild type, indicating an RNF213-independent mechanism rather than an exaggerated RNF213 response. Complementation with a catalytic-site mutant of the GRA66 zinc-binding motif failed to restore any of these phenotypes, indicating a requirement for its predicted enzymatic activity. Deleting RARRES3 rescued the premature egress of {Delta}gra66 and catalytic-mutant parasites but not of{Delta} gra70 parasites, whereas the replication defect persisted, revealing a second, RARRES3-independent consequence of GRA66 loss. RARRES3 was recruited to the PVM and intravacuolar network after IFN{gamma} stimulation, and structural modeling supported assignment of GRA66 to the NAPE-phospholipase D family with an intact di-zinc active site. These findings define a lipid-centered, RNF213-independent arm of human cell-autonomous immunity and identify the parasite effector required to withstand it.

microbiology↗
bioRxiv2026

Antibody evasion and receptor binding of SARS-CoV-2 RW.1.1

The continued evolution of SARS-CoV-2 is shaped by changes in antibody evasion and receptor engagement that influence viral fitness. RW.1.1, an emerging descendant of XFJ carrying five additional spike substitutions, has recently increased in frequency in North America. Here, we characterized the serum antibody evasion, monoclonal antibody sensitivity, and ACE2 receptor engagement of RW.1.1. Pseudovirus neutralization assays using sera from adults showed that RW.1.1 was not more resistant to serum neutralization than currently circulating variants, with neutralizing titers comparable to XFG, BA.3.2.2, and NB.1.8.1 in the tested cohort. Neutralization of RW.1.1 also did not differ significantly among adults, children, and infants and toddlers. Despite the absence of increased overall serum antibody resistance, monoclonal antibody neutralization assays revealed substantial resistance to several RBD class 1 antibodies and increased resistance to a subset of class 1/4 antibodies. Moreover, RW.1.1 exhibited reduced ACE2 receptor engagement compared with XFG, which itself has reduced receptor engagement relative to earlier JN.1 subvariants. Thus, RW.1.1 has continued to expand despite a further reduction in receptor engagement and without a substantial increase in overall serum antibody evasion. These findings suggest that the fitness of emerging SARS-CoV-2 variants may depend not only on the magnitude of antibody evasion but also on the specific components of the polyclonal antibody response that are evaded, highlighting the increasingly complex interplay between population immunity and receptor engagement in shaping SARS-CoV-2 evolution.

microbiology↗