Abstract
Seoul hantavirus (SEOV) has recently raised concern by causing geographic range expansion of hemorrhagic fever with renal syndrome (HFRS). SEOV infections in humans are significantly underestimated worldwide and epidemic dynamics of SEOV-related HFRS are poorly understood because of a lack of field data and empirically validated models. Here, we use mathematical models to examine both intrinsic and extrinsic drivers of disease transmission from animal (the Norway rat) to humans in a SEOV-endemic area in China. We found that rat eradication schemes and vaccination campaigns, but below the local elimination threshold, could diminish the amplitude of the HFRS epidemic but did not modify its seasonality. Models demonstrate population dynamics of the rodent host were insensitive to climate variations in urban settings, while relative humidity had a negative effect on the seasonality in transmission. Our study contributes to a better understanding of the epidemiology of SEOV-related HFRS, demonstrates asynchronies between rodent population dynamics and transmission rate, and identifies potential drivers of the SEOV seasonality.
Highlights
There are 60,000–100,000 cases of hemorrhagic fever with renal syndrome (HFRS), a rodentborne zoonosis, reported annually, globally [1, 2]
The two predominant hantavirus strains circulating in endemic areas of China are Hantaan virus (HTNV), which is carried by striped field mice (Apodemus agrarius), and Seoul virus (SEOV), which is carried by Norway rat (Rattus norvegicus) [5]
In central China, higher temperature and precipitation in the previous summer led to favorable food conditions for the striped field mouse, the rodent host of HTNV, which led to an autumn peak in incidence of HFRS [14]
Summary
There are 60,000–100,000 cases of hemorrhagic fever with renal syndrome (HFRS), a rodentborne zoonosis, reported annually, globally [1, 2]. China is the main epidemic region for HFRS, and accounts for 90% of cases, globally [1]. The hypothesis posited that favorable climate conditions would lead to more available food, and to greater rodent population sizes, thereby enhancing the risk of hantavirus infections. The 2007 HFRS outbreak in temperate southern Europe may have been caused by increased population density of the bank vole, the vector of Puumala virus (PUUV), which, in turn, may have resulted from abundant food due to preceding warmer than usual autumn and winter weather [12, 13]. In central China, higher temperature and precipitation in the previous summer led to favorable food conditions for the striped field mouse, the rodent host of HTNV, which led to an autumn peak in incidence of HFRS [14]
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