Ruth Elliott

1.3k total citations
16 papers, 960 citations indexed

About

Ruth Elliott is a scholar working on Infectious Diseases, Animal Science and Zoology and Immunology. According to data from OpenAlex, Ruth Elliott has authored 16 papers receiving a total of 960 indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Infectious Diseases, 9 papers in Animal Science and Zoology and 8 papers in Immunology. Recurrent topics in Ruth Elliott's work include Animal Virus Infections Studies (9 papers), interferon and immune responses (8 papers) and SARS-CoV-2 and COVID-19 Research (6 papers). Ruth Elliott is often cited by papers focused on Animal Virus Infections Studies (9 papers), interferon and immune responses (8 papers) and SARS-CoV-2 and COVID-19 Research (6 papers). Ruth Elliott collaborates with scholars based in United States, Netherlands and Germany. Ruth Elliott's co-authors include Susan R. Weiss, Robert H. Silverman, Babal K. Jha, Ling Zhao, Kristine M. Rose, Zachary B. Zalinger, Ashley Y. Wu, Yize Li, John Ziebuhr and Alexander E. Gorbalenya and has published in prestigious journals such as Proceedings of the National Academy of Sciences, PLoS ONE and Journal of Virology.

In The Last Decade

Ruth Elliott

16 papers receiving 950 citations

Peers

Countries citing papers authored by Ruth Elliott

Since Specialization

Citations

This map shows the geographic impact of Ruth Elliott's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Ruth Elliott with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ruth Elliott more than expected).

Fields of papers citing papers by Ruth Elliott

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ruth Elliott. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Ruth Elliott. The network helps show where Ruth Elliott may publish in the future.

Co-authorship network of co-authors of Ruth Elliott

This figure shows the co-authorship network connecting the top 25 collaborators of Ruth Elliott. A scholar is included among the top collaborators of Ruth Elliott based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Ruth Elliott. Ruth Elliott is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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16 of 16 papers shown

#	Title	Journal	Authors	Indexed citations
1	A novel mechanism of RNase L inhibition: Theiler's virus L* protein prevents 2-5A from binding to RNase L	PLoS Pathogens	Babal K. Jha, Ruth Elliott et al.	28
2	Murine Hepatitis Virus nsp14 Exoribonuclease Activity Is Required for Resistance to Innate Immunity	Journal of Virology	James Brett Case, Yize Li et al.	49
3	Role of the inflammasome-related cytokines Il-1 and Il-18 during infection with murine coronavirus	Journal of NeuroVirology	Zachary B. Zalinger, Ruth Elliott et al.	47
4	Lineage A Betacoronavirus NS2 Proteins and the Homologous Torovirus Berne pp1a Carboxy-Terminal Domain Are Phosphodiesterases That Antagonize Activation of RNase L	Journal of Virology	Stephen A. Goldstein, Rong Zhang et al.	24
5	Activation of RNase L by Murine Coronavirus in Myeloid Cells Is Dependent on BasalOasGene Expression and Independent of Virus-Induced Interferon	Journal of Virology	Zachary B. Zalinger, Yize Li et al.	34
6	Middle East Respiratory Syndrome Coronavirus NS4b Protein Inhibits Host RNase L Activation	mBio	Babal K. Jha, Boyd L. Yount et al.	112
7	MDA5 Is Critical to Host Defense during Infection with Murine Coronavirus	Journal of Virology	Zachary B. Zalinger, Ruth Elliott et al.	65
8	Evaluation of SSYA10-001 as a Replication Inhibitor of Severe Acute Respiratory Syndrome, Mouse Hepatitis, and Middle East Respiratory Syndrome Coronaviruses	Antimicrobial Agents and Chemotherapy	Adeyemi O. Adedeji, Kamalendra Singh et al.	94
9	Murine AKAP7 Has a 2′,5′-Phosphodiesterase Domain That Can Complement an Inactive Murine Coronavirus ns2 Gene	mBio	Elona Gusho, Rong Zhang et al.	32
10	Analysis of the Host Transcriptome from Demyelinating Spinal Cord of Murine Coronavirus-Infected Mice	PLoS ONE	Ruth Elliott, Fan Li et al.	23
11	Homologous 2′,5′-phosphodiesterases from disparate RNA viruses antagonize antiviral innate immunity	Proceedings of the National Academy of Sciences	Rong Zhang, Babal K. Jha et al.	98
12	Cell-Type-Specific Activation of the Oligoadenylate Synthetase–RNase L Pathway by a Murine Coronavirus	Journal of Virology	Ling Zhao, Ashley Y. Wu et al.	47
13	Antagonism of the Interferon-Induced OAS-RNase L Pathway by Murine Coronavirus ns2 Protein Is Required for Virus Replication and Liver Pathology	Cell Host & Microbe	Ling Zhao, Babal K. Jha et al.	207
14	Cell-Type-Specific Type I Interferon Antagonism Influences Organ Tropism of Murine Coronavirus	Journal of Virology	Ling Zhao, Kristine M. Rose et al.	58
15	Murine Coronavirus Delays Expression of a Subset of Interferon-Stimulated Genes	Journal of Virology	Kristine M. Rose, Ruth Elliott et al.	37
16	Structural and molecular virology	ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam)	Ruth Elliott, John McLauchlan et al.	5

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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