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Daniel Reyes
Center for Genome Sciences, United States Army Medical Research Institute of Infectious Diseases (USAMRIID), Fort Detrick, Frederick, MD 21702, USA

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Journal article
Published: 29 August 2020 in Viruses
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Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging human pathogen, endemic in areas of China, Japan, and the Korea (KOR). It is primarily transmitted through infected ticks and can cause a severe hemorrhagic fever disease with case fatality rates as high as 30%. Despite its high virulence and increasing prevalence, molecular and functional studies in situ are scarce due to the limited availability of high-titer SFTSV exposure stocks. During the course of field virologic surveillance in 2017, we detected SFTSV in ticks and in a symptomatic soldier in a KOR Army training area. SFTSV was isolated from the ticks producing a high-titer viral exposure stock. Through the use of advanced genomic tools, we present here a complete, in-depth characterization of this viral stock, including a comparison with both the virus in its arthropod source and in the human case, and an in vivo study of its pathogenicity. Thanks to this detailed characterization, this SFTSV viral exposure stock constitutes a quality biological tool for the study of this viral agent and for the development of medical countermeasures, fulfilling the requirements of the main regulatory agencies.

ACS Style

Unai Perez-Sautu; Se Gu; Katie Caviness; Dong Song; Yu-Jin Kim; Nicholas Paola; Daesang Lee; Terry Klein; Joseph Chitty; Elyse Nagle; Heung-Chul Kim; Sung-Tae Chong; Brett Beitzel; Daniel Reyes; Courtney Finch; Russ Byrum; Kurt Cooper; Janie Liang; Jens Kuhn; Xiankun Zeng; Kathleen Kuehl; Kayla Coffin; Jun Liu; Hong Oh; Woong Seog; Byung-Sub Choi; Mariano Sanchez-Lockhart; Gustavo Palacios; Seong Jeong. A Model for the Production of Regulatory Grade Viral Hemorrhagic Fever Exposure Stocks: From Field Surveillance to Advanced Characterization of SFTSV. Viruses 2020, 12, 958 .

AMA Style

Unai Perez-Sautu, Se Gu, Katie Caviness, Dong Song, Yu-Jin Kim, Nicholas Paola, Daesang Lee, Terry Klein, Joseph Chitty, Elyse Nagle, Heung-Chul Kim, Sung-Tae Chong, Brett Beitzel, Daniel Reyes, Courtney Finch, Russ Byrum, Kurt Cooper, Janie Liang, Jens Kuhn, Xiankun Zeng, Kathleen Kuehl, Kayla Coffin, Jun Liu, Hong Oh, Woong Seog, Byung-Sub Choi, Mariano Sanchez-Lockhart, Gustavo Palacios, Seong Jeong. A Model for the Production of Regulatory Grade Viral Hemorrhagic Fever Exposure Stocks: From Field Surveillance to Advanced Characterization of SFTSV. Viruses. 2020; 12 (9):958.

Chicago/Turabian Style

Unai Perez-Sautu; Se Gu; Katie Caviness; Dong Song; Yu-Jin Kim; Nicholas Paola; Daesang Lee; Terry Klein; Joseph Chitty; Elyse Nagle; Heung-Chul Kim; Sung-Tae Chong; Brett Beitzel; Daniel Reyes; Courtney Finch; Russ Byrum; Kurt Cooper; Janie Liang; Jens Kuhn; Xiankun Zeng; Kathleen Kuehl; Kayla Coffin; Jun Liu; Hong Oh; Woong Seog; Byung-Sub Choi; Mariano Sanchez-Lockhart; Gustavo Palacios; Seong Jeong. 2020. "A Model for the Production of Regulatory Grade Viral Hemorrhagic Fever Exposure Stocks: From Field Surveillance to Advanced Characterization of SFTSV." Viruses 12, no. 9: 958.

Journal article
Published: 15 September 2017 in Viruses
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Processing of unintegrated linear HIV-1 cDNA by the host DNA repair system results in its degradation and/or circularization. As a consequence, deficient viral cDNA integration generally leads to an increase in the levels of HIV-1 cDNA circles containing one or two long terminal repeats (LTRs). Intriguingly, impaired HIV-1 integration in LEDGF/p75-deficient cells does not result in a correspondent increase in viral cDNA circles. We postulate that increased degradation of unintegrated linear viral cDNA in cells lacking the lens epithelium-derived growth factor (LEDGF/p75) account for this inconsistency. To evaluate this hypothesis, we characterized the nucleotide sequence spanning 2-LTR junctions isolated from LEDGF/p75-deficient and control cells. LEDGF/p75 deficiency resulted in a significant increase in the frequency of 2-LTRs harboring large deletions. Of note, these deletions were dependent on the 3′ processing activity of integrase and were not originated by aberrant reverse transcription. Our findings suggest a novel role of LEDGF/p75 in protecting the unintegrated 3′ processed linear HIV-1 cDNA from exonucleolytic degradation.

ACS Style

Murilo T. D. Bueno; Daniel Reyes; Manuel Llano. LEDGF/p75 Deficiency Increases Deletions at the HIV-1 cDNA Ends. Viruses 2017, 9, 259 .

AMA Style

Murilo T. D. Bueno, Daniel Reyes, Manuel Llano. LEDGF/p75 Deficiency Increases Deletions at the HIV-1 cDNA Ends. Viruses. 2017; 9 (9):259.

Chicago/Turabian Style

Murilo T. D. Bueno; Daniel Reyes; Manuel Llano. 2017. "LEDGF/p75 Deficiency Increases Deletions at the HIV-1 cDNA Ends." Viruses 9, no. 9: 259.