Allison S. Thomas

1.1k total citations · 1 hit paper
16 papers, 409 citations indexed

About

Allison S. Thomas is a scholar working on Virology, Infectious Diseases and Immunology. According to data from OpenAlex, Allison S. Thomas has authored 16 papers receiving a total of 409 indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Virology, 9 papers in Infectious Diseases and 6 papers in Immunology. Recurrent topics in Allison S. Thomas's work include HIV Research and Treatment (12 papers), HIV/AIDS Research and Interventions (6 papers) and Immune Cell Function and Interaction (5 papers). Allison S. Thomas is often cited by papers focused on HIV Research and Treatment (12 papers), HIV/AIDS Research and Interventions (6 papers) and Immune Cell Function and Interaction (5 papers). Allison S. Thomas collaborates with scholars based in United States, Germany and Switzerland. Allison S. Thomas's co-authors include R. Brad Jones, Szu-Han Huang, Colin Kovacs, Erika Benko, Sara Karandish, Ya‐Chi Ho, Adam A. Capoferri, Alyssa R. Martin, Mihaela Pertea and Haiping Hao and has published in prestigious journals such as Physical Review Letters, Journal of Virology and Cell Host & Microbe.

In The Last Decade

Allison S. Thomas

16 papers receiving 406 citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

Defective HIV-1 Proviruses Are Expressed and Can Be Recognized by Cytotoxic T Lymphocytes, which Shape the Proviral Landscape

2017 254 citations Ross A. Pollack, R. Brad Jones et al. Cell Host & Microbe profile →

Peers

Allison S. Thomas

VIROL

IMMUN

EPIDE

AMPO

Hanna‐Mari Baldauf Germany

María Inés Figueroa Argentina

Jessica M. Conway United States

Shabir Lakhi United States

Christopher Gu United States

Michael F. Powers United States

Vlad Novitsky United States

Saleha Omarjee South Africa

Joachim Büch Germany

Daniel P. Leaman United States

Hanna‐Mari Baldauf Germany

Allison S. Thomas

67 ×0.2

VIROL

89 ×0.4

93 ×0.6

IMMUN

38 ×0.5

EPIDE

115 ×2.7

AMPO

Citations per year, relative to Allison S. Thomas Allison S. Thomas (= 1×) peers Hanna‐Mari Baldauf

Countries citing papers authored by Allison S. Thomas

Since Specialization

Citations

This map shows the geographic impact of Allison S. Thomas'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 Allison S. Thomas with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Allison S. Thomas more than expected).

Fields of papers citing papers by Allison S. Thomas

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Allison S. Thomas. 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 Allison S. Thomas. The network helps show where Allison S. Thomas may publish in the future.

Co-authorship network of co-authors of Allison S. Thomas

This figure shows the co-authorship network connecting the top 25 collaborators of Allison S. Thomas. A scholar is included among the top collaborators of Allison S. Thomas 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 Allison S. Thomas. Allison S. Thomas 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

Ward, Adam R., Allison S. Thomas, Szu-Han Huang, et al.. (2022). No evidence that circulating HIV-specific immune responses contribute to persistent inflammation and immune activation in persons on long-term ART. AIDS. 36(12). 1617–1628. 3 indexed citations

Thomas, Allison S., et al.. (2022). Antibody-dependent cellular cytotoxicity responses and susceptibility influence HIV-1 mother-to-child transmission. JCI Insight. 7(9). 7 indexed citations

Kumar, Amit, Elena Giorgi, Joshua Eudailey, et al.. (2022). Vertical HIV-1 Transmission in the Setting of Maternal Broad and Potent Antibody Responses. Journal of Virology. 96(11). e0023122–e0023122. 4 indexed citations

Iwanaga, Kanako, et al.. (2022). Psychometric Validation of the Brief-COPE Scale in a Sample of Individuals with Multiple Sclerosis: A Brief Report. Rehabilitation Counseling Bulletin. 67(4). 295–301. 1 indexed citations

Thomas, Allison S., Wenqing Jiang, Alexander C. Ewing, et al.. (2021). Pre-existing infant antibody-dependent cellular cytotoxicity associates with reduced HIV-1 acquisition and lower morbidity. Cell Reports Medicine. 2(10). 100412–100412. 16 indexed citations

Thomas, Allison S., Wenqing Jiang, Alexander C. Ewing, et al.. (2021). Pre-Existing Infant Antibody-Dependent Cellular Cytotoxicity Associates with Reduced HIV-1 Acquisition and Lower Morbidity. SSRN Electronic Journal. 2 indexed citations

Thomas, Allison S., et al.. (2020). A new cell line for assessing HIV-1 antibody dependent cellular cytotoxicity against a broad range of variants. Journal of Immunological Methods. 480. 112766–112766. 3 indexed citations

Macatangay, Bernard, Rajesh T. Gandhi, R. Brad Jones, et al.. (2019). T cells with high PD-1 expression are associated with lower HIV-specific immune responses despite long-term antiretroviral therapy. AIDS. 34(1). 15–24. 22 indexed citations

Thomas, Allison S., et al.. (2018). Neutralization and beyond: Antibodies and HIV-1 acquisition.. PubMed. 15. 73–86. 2 indexed citations

10.

Thomas, Allison S., Kimberley Jones, Rajesh T. Gandhi, et al.. (2017). T-cell responses targeting HIV Nef uniquely correlate with infected cell frequencies after long-term antiretroviral therapy. PLoS Pathogens. 13(9). e1006629–e1006629. 33 indexed citations

11.

Pollack, Ross A., R. Brad Jones, Mihaela Pertea, et al.. (2017). Defective HIV-1 Proviruses Are Expressed and Can Be Recognized by Cytotoxic T Lymphocytes, which Shape the Proviral Landscape. Cell Host & Microbe. 21(4). 494–506.e4. 254 indexed citations breakdown →

12.

Raposo, Rui André Saraiva, Miguel de Mulder Rougvie, Dominic Paquin‐Proulx, et al.. (2017). IFITM1 targets HIV-1 latently infected cells for antibody-dependent cytolysis. JCI Insight. 2(1). e85811–e85811. 9 indexed citations

13.

Huang, Szu-Han, Allison S. Thomas, Sara Karandish, et al.. (2017). CTLs Eliminate Defective HIV Proviruses Without Impacting Infectious Latent Reservoirs. 1 indexed citations

14.

Sangouard, Nicolas, Nicolas Gisin, Hartmut Herrmann, et al.. (2010). Purification of Single-Photon Entanglement. Physical Review Letters. 104(18). 180504–180504. 41 indexed citations

15.

Martin, Anthony, Laurent Labonté, Allison S. Thomas, et al.. (2010). Polarization entangled photon-pair source based on a type-II PPLN waveguide emitting at a telecom wavelength. 1. 1–4. 4 indexed citations

16.

Marsh, Jon W., et al.. (1992). A restaurant-associated outbreak of E. coli O157 infection. 14(1). 78–83. 7 indexed citations

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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