Dynamics of Puumala hantavirus infection in naturally infected bank voles (Clethrinomys glareolus)

1999 ◽  
Vol 144 (12) ◽  
pp. 2415-2428 ◽  
Author(s):  
A. D. Bernshtein ◽  
N. S. Apekina ◽  
T. V. Mikhailova ◽  
Yu. A. Myasnikov ◽  
L. A. Khlyap ◽  
...  
2002 ◽  
Vol 8 (9) ◽  
pp. 924-929 ◽  
Author(s):  
Gert E. Olsson ◽  
Neil White ◽  
Clas Ahlm ◽  
Fredrik Elgh ◽  
Ann-Christin Verlemyr ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Liina Voutilainen ◽  
Eva R. Kallio ◽  
Jukka Niemimaa ◽  
Olli Vapalahti ◽  
Heikki Henttonen

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Liina Voutilainen ◽  
Eva R. Kallio ◽  
Jukka Niemimaa ◽  
Olli Vapalahti ◽  
Heikki Henttonen

Abstract Understanding the dynamics of zoonotic pathogens in their reservoir host populations is a prerequisite for predicting and preventing human disease epidemics. The human infection risk of Puumala hantavirus (PUUV) is highest in northern Europe, where populations of the rodent host (bank vole, Myodes glareolus) undergo cyclic fluctuations. We conducted a 7-year capture-mark-recapture study to monitor seasonal and multiannual patterns of the PUUV infection rate in bank vole populations exhibiting a 3-year density cycle. Infected bank voles were most abundant in mid-winter months during years of increasing or peak host density. Prevalence of PUUV infection in bank voles exhibited a regular, seasonal pattern reflecting the annual population turnover and accumulation of infections within each year cohort. In autumn, the PUUV transmission rate tracked increasing host abundance, suggesting a density-dependent transmission. However, prevalence of PUUV infection was similar during the increase and peak years of the density cycle despite a twofold difference in host density. This may result from the high proportion of individuals carrying maternal antibodies constraining transmission during the cycle peak years. Our exceptionally intensive and long-term dataset provides a solid basis on which to develop models to predict the dynamic public health threat posed by PUUV in northern Europe.


1993 ◽  
Vol 132 (3-4) ◽  
pp. 359-367 ◽  
Author(s):  
Irina Gavrilovskaya ◽  
N. Apekina ◽  
N. Okulova ◽  
V. Demina ◽  
A. Bernshtein ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maxime Bélondrade ◽  
Simon Nicot ◽  
Charly Mayran ◽  
Lilian Bruyere-Ostells ◽  
Florian Almela ◽  
...  

AbstractUnlike variant Creutzfeldt–Jakob disease prions, sporadic Creutzfeldt–Jakob disease prions have been shown to be difficult to amplify in vitro by protein misfolding cyclic amplification (PMCA). We assessed PMCA of pathological prion protein (PrPTSE) from 14 human sCJD brain samples in 3 substrates: 2 from transgenic mice expressing human prion protein (PrP) with either methionine (M) or valine (V) at position 129, and 1 from bank voles. Brain extracts representing the 5 major clinicopathological sCJD subtypes (MM1/MV1, MM2, MV2, VV1, and VV2) all triggered seeded PrPTSE amplification during serial PMCA with strong seed- and substrate-dependence. Remarkably, bank vole PrP substrate allowed the propagation of all sCJD subtypes with preservation of the initial molecular PrPTSE type. In contrast, PMCA in human PrP substrates was accompanied by a PrPTSE molecular shift during heterologous (M/V129) PMCA reactions, with increased permissiveness of V129 PrP substrate to in vitro sCJD prion amplification compared to M129 PrP substrate. Combining PMCA amplification sensitivities with PrPTSE electrophoretic profiles obtained in the different substrates confirmed the classification of 4 distinct major sCJD prion strains (M1, M2, V1, and V2). Finally, the level of sensitivity required to detect VV2 sCJD prions in cerebrospinal fluid was achieved.


2016 ◽  
Vol 49 (3) ◽  
pp. 348-350 ◽  
Author(s):  
Carla Julia da Silva Pessoa Vieira ◽  
David José Ferreira da Silva ◽  
Eriana Serpa Barreto ◽  
Carlos Eduardo Hassegawa Siqueira ◽  
Vivaldo Gomes da Costa ◽  
...  

2019 ◽  
Vol 94 (3) ◽  
Author(s):  
Wanda Christ ◽  
Janne Tynell ◽  
Jonas Klingström

ABSTRACT Virus infection frequently triggers host cell stress signaling resulting in translational arrest; as a consequence, many viruses employ means to modulate the host stress response. Hantaviruses are negative-sense, single-stranded RNA viruses known to inhibit host innate immune responses and apoptosis, but their impact on host cell stress signaling remains largely unknown. In this study, we investigated activation of host cell stress responses during hantavirus infection. We show that hantavirus infection causes transient formation of stress granules (SGs) but does so in only a limited proportion of infected cells. Our data indicate some cell type-specific and hantavirus species-specific variability in SG prevalence and show SG formation to be dependent on the activation of protein kinase R (PKR). Hantavirus infection inhibited PKR-dependent SG formation, which could account for the transient nature and low prevalence of SG formation observed during hantavirus infection. In addition, we report only limited colocalization of hantaviral proteins or RNA with SGs and show evidence indicating hantavirus-mediated inhibition of PKR-like endoplasmic reticulum (ER) kinase (PERK). IMPORTANCE Our work presents the first report on stress granule formation during hantavirus infection. We show that hantavirus infection actively inhibits stress granule formation, thereby escaping the detrimental effects on global translation imposed by host stress signaling. Our results highlight a previously uncharacterized aspect of hantavirus-host interactions with possible implications for how hantaviruses are able to cause persistent infection in natural hosts and for pathogenesis.


Vaccine ◽  
2021 ◽  
Author(s):  
Tiitus Lamponen ◽  
Iivo Hetemäki ◽  
Heikki J. Niemi ◽  
Hanna Jarva ◽  
Eliisa Kekäläinen ◽  
...  
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