Life-long shedding of Puumala hantavirus in wild bank voles (Myodes glareolus)
Author(s) -
Liina Voutilainen,
Tarja Sironen,
Elina Tonteri,
Anne Tuiskunen Bäck,
Maria Razzauti,
Malin Karlsson,
Maria Wahlström,
Jukka Niemimaa,
Heikki Henttonen,
Åke Lundkvist
Publication year - 2015
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/vir.0.000076
Subject(s) - biology , bank vole , viral shedding , hantavirus , puumala virus , seroconversion , virology , hantavirus infection , bunyaviridae , host (biology) , arvicolinae , disease reservoir , population , hantavirus pulmonary syndrome , virus , zoology , ecology , demography , microtus , sociology
The knowledge of viral shedding patterns and viraemia in the reservoir host species is a key factor in assessing the human risk of zoonotic viruses. The shedding of hantaviruses (family Bunyaviridae) by their host rodents has widely been studied experimentally, but rarely in natural settings. Here we present the dynamics of Puumala hantavirus (PUUV) shedding and viraemia in naturally infected wild bank voles (Myodes glareolus). In a monthly capture-mark-recapture study, we analysed 18 bank voles for the presence and relative quantity of PUUV RNA in the excreta and blood from 2 months before up to 8 months after seroconversion. The proportion of animals shedding PUUV RNA in saliva, urine and faeces peaked during the first month after seroconversion, but continued throughout the study period with only a slight decline. The quantity of shed PUUV in reverse transcription quantitative PCR (RT-qPCR) positive excreta was constant over time. In blood, PUUV RNA was present for up to 7 months but both the probability of viraemia and the virus load declined with time. Our findings contradict the current view of a decline in virus shedding after the acute phase and a short viraemic period in hantavirus infection - an assumption widely adopted in current epidemiological models. We suggest the life-long shedding as a means of hantaviruses to survive over host population bottlenecks, and to disperse in fragmented habitats where local host and/or virus populations face temporary extinctions. Our results indicate that the kinetics of pathogens in wild hosts may differ considerably from those observed in laboratory settings.
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