Steven Bradfute

Dr. Steven Bradfute

orcid

Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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4 May 2023 in eLife
Verified
Journal Article
Open access
BCBenjamin Chen
Benjamin Chen
BJBoris Julg
Boris Julg
SMSindhu Mohandas
Sindhu Mohandas
Steven BradfuteSteven Bradfute
Steven Bradfute
RFRecover Mechanistic Pathways Task Force
Recover Mechanistic Pathways Task Force
The COVID-19 global pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has infected hundreds of millions of individuals. Following COVID-19 infection, a subset can develop a wide range of chronic symptoms affecting diverse organ systems referred to as post-acute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID. A National Institutes of Health-sponsored initiative, RECOVER: Researching COVID to Enhance Recovery, has sought to understand the basis of long COVID in a large cohort. Given the range of symptoms that occur in long COVID, the mechanisms that may underlie these diverse symptoms may also be diverse. In this review, we focus on the emerging literature supporting the role(s) that viral persistence or reactivation of viruses may play in PASC. Persistence of SARS-CoV-2 RNA or antigens is reported in some organs, yet the mechanism by which they do so and how they may be associated with pathogenic immune responses is unclear. Understanding the mechanisms of persistence of RNA, antigen or other reactivated viruses and how they may relate to specific inflammatory responses that drive symptoms of PASC may provide a rationale for treatment.

4 September 2020 in Archives of Virology
Verified
Journal Article
Closed access
PDF file
Jens H. KuhnJens H. Kuhn
Jens H. Kuhn
SAScott Adkins
Scott Adkins
DADaniela Alioto
Daniela Alioto
SASergey Alkhovsky
Sergey Alkhovsky
GAGaya Amarasinghe
Gaya Amarasinghe
XZXueping Zhou
Xueping Zhou

25 August 2023 in Journal of General Virology
Verified
Journal Article
Open access
Jens H. KuhnJens H. Kuhn
Jens H. Kuhn
JAJunya Abe
Junya Abe
SAScott Adkins
Scott Adkins
SASergey Alkhovsky
Sergey Alkhovsky
TATatjana Avsic-Zupanc
Tatjana Avsic-Zupanc
AØArnfinn Lodden Økland
Arnfinn Lodden Økland
In April 2023, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. The phylum was expanded by one new family, 14 new genera, and 140 new species. Two genera and 538 species were renamed. One species was moved, and four were abolished. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV.

28 November 2022 in Archives of Virology
Verified
Journal Article
Open access
PDF file
Jens H. KuhnJens H. Kuhn
Jens H. Kuhn
SAScott Adkins
Scott Adkins
SASergey Alkhovsky
Sergey Alkhovsky
TATatjana Avsic-Zupanc
Tatjana Avsic-Zupanc
MAMaría Angeles Ayllón
María Angeles Ayllón
AØArnfinn Lodden Økland
Arnfinn Lodden Økland
In March 2022, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. The phylum was expanded by two new families (bunyaviral Discoviridae and Tulasviridae), 41 new genera, and 98 new species. Three hundred forty-nine species were renamed and/or moved. The accidentally misspelled names of seven species were corrected. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV.

31 August 2021 in Archives of Virology
Verified
Journal Article
Closed access
PDF file
Jens H. KuhnJens H. Kuhn
Jens H. Kuhn
SAScott Adkins
Scott Adkins
BABernard Agwanda
Bernard Agwanda
RKRim Al Kubrusli
Rim Al Kubrusli
SASergey Alkhovsky
Sergey Alkhovsky
XZXueping Zhou
Xueping Zhou

7 September 2012 in Viruses
Verified
Journal Article
Open access
PDF file
Steven BradfuteSteven Bradfute
Steven Bradfute
KWKelly L. Warfield
Kelly L. Warfield
MBMike Bray
Mike Bray
The filoviruses marburg- and ebolaviruses can cause severe hemorrhagic fever (HF) in humans and nonhuman primates. Because many cases have occurred in geographical areas lacking a medical research infrastructure, most studies of the pathogenesis of filoviral HF, and all efforts to develop drugs and vaccines, have been carried out in biocontainment laboratories in non-endemic countries, using nonhuman primates (NHPs), guinea pigs and mice as animal models. NHPs appear to closely mirror filoviral HF in humans (based on limited clinical data), but only small numbers may be used in carefully regulated experiments; much research is therefore done in rodents. Because of their availability in large numbers and the existence of a wealth of reagents for biochemical and immunological testing, mice have become the preferred small animal model for filovirus research. Since the first experiments following the initial 1967 marburgvirus outbreak, wild-type or mouse-adapted viruses have been tested in immunocompetent or immunodeficient mice. In this paper, we review how these types of studies have been used to investigate the pathogenesis of filoviral disease, identify immune responses to infection and evaluate antiviral drugs and vaccines. We also discuss the strengths and weaknesses of murine models for filovirus research, and identify important questions for further study.