Aleksandar Radonic

Dr. Aleksandar Radonic


Research Focus & Metrics

Academic Career Length

28Years (1999-Present)

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

Representative Publications

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1 January 2004 in Biochemical and Biophysical Research Communications
Verified
Journal Article
Closed access
ARAleksandar Radonic
Aleksandar Radonic
STStefanie Thulke
Stefanie Thulke
Ian MackayIan Mackay
Ian Mackay
OLOlfert Landt
Olfert Landt
WSWolfgang Siegert
Wolfgang Siegert
ANAndreas Nitsche
Andreas Nitsche

30 December 2014 in EMBO Molecular Medicine
Verified
Journal Article
Open access
PDF file
ASAlmudena Marí Saéz
Almudena Marí Saéz
SWSabrina Weiss
Sabrina Weiss
KNKathrin Nowak
Kathrin Nowak
VLVincent Lapeyre
Vincent Lapeyre
FZFee Zimmermann
Fee Zimmermann
FLFabian H. Leendertz
Fabian H. Leendertz
The severe Ebola virus disease epidemic occurring in West Africa stems from a single zoonotic transmission event to a 2‐year‐old boy in Meliandou, Guinea. We investigated the zoonotic origins of the epidemic using wildlife surveys, interviews, and molecular analyses of bat and environmental samples. We found no evidence for a concurrent outbreak in larger wildlife. Exposure to fruit bats is common in the region, but the index case may have been infected by playing in a hollow tree housing a colony of insectivorous free‐tailed bats ( Mops condylurus ). Bats in this family have previously been discussed as potential sources for Ebola virus outbreaks, and experimental data have shown that this species can survive experimental infection. These analyses expand the range of possible Ebola virus sources to include insectivorous bats and reiterate the importance of broader sampling efforts for understanding Ebola virus ecology.

7 October 2005 in Journal of Molecular Medicine
Verified
Journal Article
Open access
PDF file
FOFalk Ohl
Falk Ohl
MJMonika Jung
Monika Jung
CXChuanliang Xu
Chuanliang Xu
CSCarsten Stephan
Carsten Stephan
ARAnja Rabien
Anja Rabien
KJKlaus Jung
Klaus Jung
Using quantitative reverse transcription–polymerase chain reaction (RT-PCR), reference genes are utilized as endogenous controls for relative quantification of target genes in gene profiling studies. The suitability of housekeeping genes for that purpose in prostate cancer tissue has not been sufficiently investigated so far. The objective of this study was to select from a panel of 16 potential candidate reference genes the most stable genes for gene normalization. Expression of mRNA encoding ACTB, ALAS1, ALB, B2M, G6PD, GAPD, HMBS, HPRT1, K-ALPHA-1, POLR2A, PPIA, RPL13A, SDHA, TBP, UBC, and YWHAZ was examined in matched, microdissected malignant and nonmalignant tissue specimens obtained from 17 nontreated prostate carcinomas after radical prostatectomy by real-time RT-PCR. The genes studied displayed a wide expression range with cycle threshold values between 16 and 37. The expression was not different between samples from pT2 and pT3 tumors or between samples with Gleason scores 0.05). ACTB, RPL13A, and HMBS showed significant differences (P<0.02 at least) in expressions between malignant and nonmalignant pairs. All other genes did not differ between the matched pairs, and the software programs geNorm and NormFinder were used to ascertain the most suitable reference genes from these candidates. HPRT1, ALAS1, and K-ALPHA-1 were calculated by both programs to be the most stable genes covering a broad range of expression. The expression of the target gene RECK normalized with HRPT1 alone and with the normalization factors generated by the combination of these three reference genes as well as with the unstable genes ACTB or RPL13A is given. That example shows the significance of using suitable reference genes to avoid erroneous normalizations in gene profiling studies for prostate cancer. The use of HPRT1 alone as a reference gene shown in our study was sufficient, but the normalization factors generated from two (HRPT1, ALAS1) or all three genes (HRPT1, ALAS1, K-ALPHA-1) should be considered for an improved reliability of normalization in gene profiling studies of prostate cancer.

1 June 2014 in Emerging Infectious Diseases
Verified
Journal Article
Open access
ARAleksandar Radonic
Aleksandar Radonic
SMSonja Metzger
Sonja Metzger
Piotr Wojciech DabrowskiPiotr Wojciech Dabrowski
Piotr Wojciech Dabrowski
ECEmmanuel Couacy-Hymann
Emmanuel Couacy-Hymann
LSLivia Schuenadel
Livia Schuenadel
ANAndreas Nitsche
Andreas Nitsche
We isolated a monkeypox virus from a wild-living monkey, a sooty mangabey, found dead in Taï National Park, Côte d’Ivoire, in March 2012. The whole-genome sequence obtained from this isolate and directly from clinical specimens showed its close relationship to monkeypox viruses from Western Africa.

24 May 2016 in Gut
Verified
Journal Article
Open access
PDF file
Daniel TodtDaniel Todt
Daniel Todt
AGAnett Gisa
Anett Gisa
ARAleksandar Radonic
Aleksandar Radonic
ANAndreas Nitsche
Andreas Nitsche
PBPatrick Behrendt
Patrick Behrendt
HWHeiner Wedemeyer
Heiner Wedemeyer
Objective Hepatitis E virus (HEV) infection can take chronic courses in immunocompromised patients potentially leading to liver cirrhosis and liver failure. Ribavirin (RBV) is currently the only treatment option for many patients, but treatment failure can occur which has been associated with the appearance of a distinct HEV polymerase mutant (G1634R). Here, we performed a detailed analysis of HEV viral intrahost evolution during chronic hepatitis E infections. Design Illumina deep sequencing was performed for the detection of intrahost variation in the HEV genome of chronically infected patients. Novel polymerase mutants were investigated in vitro using state-of-the-art HEV cell culture models. Results Together, these data revealed that (1) viral diversity differed markedly between patients but did not show major intraindividual short-term variations in untreated patients with chronic hepatitis E, (2) RBV therapy was associated with an increase in viral heterogeneity which was reversible when treatment was stopped, (3) the G1634R mutant was detectable as a minor population prior to therapy in patients who subsequently failed to achieve a sustained virological response to RBV therapy and (4) in addition to G1634R further dominant variants in the polymerase region emerged, impacting HEV replication efficiency in vitro. Conclusions In summary, this first investigation of intrahost HEV population evolution indicates that RBV causes HEV mutagenesis in treated patients and that an emergence of distinct mutants within the viral population occurs during RBV therapy. We also suggest that next-generation sequencing could be useful to guide personalised antiviral strategies.

1 June 2013 in Emerging Infectious Diseases
Verified
Journal Article
Open access
MCMireia Coscollá
Mireia Coscollá
ALAstrid Lewin
Astrid Lewin
SMSonja Metzger
Sonja Metzger
KMKerstin Maetz-Rennsing
Kerstin Maetz-Rennsing
SCSebastien Calvignac-Spencer
Sebastien Calvignac-Spencer
FLFabian H. Leendertz
Fabian H. Leendertz
Tuberculosis (TB) is caused by gram-positive bacteria known as the Mycobacterium tuberculosis complex (MTBC). MTBC include several human-associated lineages and several variants adapted to domestic and, more rarely, wild animal species. We report an M. tuberculosis strain isolated from a wild chimpanzee in Côte d’Ivoire that was shown by comparative genomic and phylogenomic analyses to belong to a new lineage of MTBC, closer to the human-associated lineage 6 (also known as M. africanum West Africa 2) than to the other classical animal-associated MTBC strains. These results show that the general view of the genetic diversity of MTBC is limited and support the possibility that other MTBC variants exist, particularly in wild mammals in Africa. Exploring this diversity is crucial to the understanding of the biology and evolutionary history of this widespread infectious disease.