Journal of General Virology Life-Long Shedding of Puumala Hantavirus in Wild Bank Voles (Myodes glareolus) --Manuscript Draft-- Manuscript Number: JGV-D-14-00201R1 Full Title: Life-Long Shedding of Puumala Hantavirus in Wild Bank Voles (Myodes glareolus) Short Title: Life-long hantavirus shedding by wild rodent hosts Article Type: Standard Section/Category: Animal - Negative-strand RNA Viruses Corresponding Author: Liina Voutilainen, Ph.D. University of Helsinki Helsinki, FINLAND First Author: Liina Voutilainen, Ph.D. Order of Authors: Liina Voutilainen, Ph.D. Tarja Sironen, Ph.D. Elina Tonteri, PhD Anne Tuiskunen Bäck, PhD Maria Razzauti, PhD Malin Karlsson Maria Wahlström Jukka Niemimaa, MSc Heikki Henttonen, PhD Åke Lundkvist, PhD Abstract: The knowledge of viral shedding patterns and viremia 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 (PUUV) hantavirus shedding and viremia in naturally infected, wild bank voles (Myodes glareolus). In a monthly capture-mark-recapture study, we analyzed 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 feces peaked during the first month after seroconversion, but continued throughout the study period with only a slight decline. The quantity of shed PUUV in RT-PCR positive excreta was constant over time. In blood, PUUV RNA was present for up to 7 months but both the probability of viremia and the virus load declined by time. Our findings contradict the current view of a decline in virus shedding after the acute phase and a short viremic period in hantavirus infection - an assumption widely adopted into 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 considerably differ from those observed in laboratory settings. Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation JGV Papers in Press. Published February 20, 2015 as doi:10.1099/vir.0.000076