TY  - JOUR
A1  - Schmidt, Sabrina
A1  - Saxenhofer, Moritz
A1  - Drewes, Stephan
A1  - Schlegel, Mathias
A1  - Wanka, Konrad M.
A1  - Frank, Raphael
A1  - Klimpel, Sven
A1  - von Blanckenhagen, Felix
A1  - Maaz, Denny
A1  - Herden, Christiane
A1  - Freise, Jona
A1  - Wolf, Ronny
A1  - Stubbe, Michael
A1  - Borkenhagen, Peter
A1  - Ansorge, Hermann
A1  - Eccard, Jana
A1  - Lang, Johannes
A1  - Jourdain, Elsa
A1  - Jacob, Jens
A1  - Marianneau, Philippe
A1  - Heckel, Gerald
A1  - Ulrich, Rainer Günter
T1  - High genetic structuring of Tula hantavirus
JF  - Archives of virology
N2  - Tula virus (TULV) is a vole-associated hantavirus with low or no pathogenicity to humans. In the present study, 686 common voles (Microtus arvalis), 249 field voles (Microtus agrestis) and 30 water voles (Arvicola spec.) were collected at 79 sites in Germany, Luxembourg and France and screened by RT-PCR and TULV-IgG ELISA. TULV-specific RNA and/or antibodies were detected at 43 of the sites, demonstrating a geographically widespread distribution of the virus in the studied area. The TULV prevalence in common voles (16.7 %) was higher than that in field voles (9.2 %) and water voles (10.0 %). Time series data at ten trapping sites showed evidence of a lasting presence of TULV RNA within common vole populations for up to 34 months, although usually at low prevalence. Phylogenetic analysis demonstrated a strong genetic structuring of TULV sequences according to geography and independent of the rodent species, confirming the common vole as the preferential host, with spillover infections to co-occurring field and water voles. TULV phylogenetic clades showed a general association with evolutionary lineages in the common vole as assessed by mitochondrial DNA sequences on a large geographical scale, but with local-scale discrepancies in the contact areas.
Y1  - 2016
U6  - https://doi.org/10.1007/s00705-016-2762-6
SN  - 0304-8608
SN  - 1432-8798
VL  - 161
SP  - 1135
EP  - 1149
PB  - Springer
CY  - Wien
ER  - 
TY  - JOUR
A1  - Maaz, Denny
A1  - Rausch, Sebastian
A1  - Richter, Dania
A1  - Kruecken, Juergen
A1  - Kuehl, Anja A.
A1  - Demeler, Janina
A1  - Bluemke, Julia
A1  - Matuschka, Franz-Rainer
A1  - von Samson-Himmelstjerna, Georg
A1  - Hartmann, Susanne
T1  - Susceptibility to Ticks and Lyme Disease Spirochetes Is Not Affected in Mice Coinfected with Nematodes
JF  - Infection and immunity
N2  - Small rodents serve as reservoir hosts for tick-borne pathogens, such as the spirochetes causing Lyme disease. Whether natural coinfections with other macroparasites alter the success of tick feeding, antitick immunity, and the host's reservoir competence for tick-borne pathogens remains to be determined. In a parasitological survey of wild mice in Berlin, Germany, approximately 40% of Ixodes ricinus-infested animals simultaneously harbored a nematode of the genus Heligmosomoides. We therefore aimed to analyze the immunological impact of the nematode/tick coinfection as well as its effect on the tick-borne pathogen Borrelia afzelii. Hosts experimentally coinfected with Heligmosomoides polygyrus and larval/nymphal I. ricinus ticks developed substantially stronger systemic type 2 T helper cell (Th2) responses, on the basis of the levels of GATA-3 and interleukin-13 expression, than mice infected with a single pathogen. During repeated larval infestations, however, anti-tick Th2 reactivity and an observed partial immunity to tick feeding were unaffected by concurrent nematode infections. Importantly, the strong systemic Th2 immune response in coinfected mice did not affect susceptibility to tick-borne B. afzelii. An observed trend for decreased local and systemic Th1 reactivity against B. afzelii in coinfected mice did not result in a higher spirochete burden, nor did it facilitate bacterial dissemination or induce signs of immunopathology. Hence, this study indicates that strong systemic Th2 responses in nematode/tick-coinfected house mice do not affect the success of tick feeding and the control of the causative agent of Lyme disease.
Y1  - 2016
U6  - https://doi.org/10.1128/IAI.01309-15
SN  - 0019-9567
SN  - 1098-5522
VL  - 84
SP  - 1274
EP  - 1286
PB  - American Society for Microbiology
CY  - Washington
ER  -