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David E. Krysztof

Researcher at American Red Cross

Publications -  36
Citations -  2109

David E. Krysztof is an academic researcher from American Red Cross. The author has contributed to research in topics: Hepatitis B virus & Virus. The author has an hindex of 18, co-authored 32 publications receiving 1870 citations. Previous affiliations of David E. Krysztof include National Institutes of Health.

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Enhancement of Zika virus pathogenesis by preexisting antiflavivirus immunity

TL;DR: Using convalescent plasma from DENV- and WNV-infected individuals, substantial enhancement of ZIKV infection in vitro was found that was mediated through immunoglobulin G engagement of Fcγ receptors, highlighting the need to exert great caution when designing flavivirus vaccines.
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Prevalence, incidence, and residual risk of human immunodeficiency virus and hepatitis C virus infections among United States blood donors since the introduction of nucleic acid testing

TL;DR: This study analyzes temporal trends of these two infections since NAT introduction into blood donation screening in the United States in 1999.
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Genetic Variation in OAS1 Is a Risk Factor for Initial Infection with West Nile Virus in Man

TL;DR: OAS1 SNP rs10774671 is identified as a host genetic risk factor for initial infection with WNV in humans and tested the effect of this SNP on viral replication in a novel ex vivo model of WNV infection in primary human lymphoid tissue.
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Dengue viremia in blood donors identified by RNA and detection of dengue transfusion transmission during the 2007 dengue outbreak in Puerto Rico

TL;DR: Blood donations were tested for dengue virus (DENV) RNA and recipients of RNA‐positive donations traced to assess transfusion transmission and no new cases were reported in Puerto Rico in 2007.
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CCR5 Deficiency Is a Risk Factor for Early Clinical Manifestations of West Nile Virus Infection but not for Viral Transmission

TL;DR: CCR5 deficiency is not a riskFactor for WNV infection per se, but it is a risk factor for both early and late clinical manifestations after infection, and CCR5 may function normally to limit disease due to WNV infections in humans.