Abstract
In North America, Sin Nombre virus (SNV) is the main cause of hantavirus cardiopulmonary syndrome (HCPS), a severe respiratory disease with a fatality rate of 35–40%. SNV is a zoonotic pathogen carried by deer mice (Peromyscus maniculatus), and few studies have been performed examining its transmission in deer mouse populations. Studying SNV and other hantaviruses can be difficult due to the need to propagate the virus in vivo for subsequent experiments. We show that when compared with standard intramuscular infection, the intraperitoneal infection of deer mice can be as effective in producing SNV stocks with a high viral RNA copy number, and this method of infection provides a more reproducible infection model. Furthermore, the age and sex of the infected deer mice have little effect on viral replication and shedding. We also describe a reliable model of direct experimental SNV transmission. We examined the transmission of SNV between deer mice and found that direct contact between deer mice is the main driver of SNV transmission rather than exposure to contaminated excreta/secreta, which is thought to be the main driver of transmission of the virus to humans. Furthermore, increases in heat shock responses or testosterone levels in SNV-infected deer mice do not increase the replication, shedding, or rate of transmission. Here, we have demonstrated a model for the transmission of SNV between deer mice, the natural rodent reservoir for the virus. The use of this model will have important implications for further examining SNV transmission and in developing strategies for the prevention of SNV infection in deer mouse populations.
Highlights
Hantaviruses are a family of enveloped, negative sense RNA viruses with a tri-segmented genome of the order Bunyavirales
We first confirmed that a Vero E6-adapted Sin Nombre virus (SNV) (77734, referred to as VE6-SNV) is unable to cause productive infection in deer mice, underscoring the need for working SNV stocks produced in natural rodent hosts (Figure 1A)
To determine whether IM infection results in higher levels of SNV replication than IP infection, groups of deer mice (IM: n = 10, IP: n = 12) were infected with SNV
Summary
Hantaviruses are a family of enveloped, negative sense RNA viruses with a tri-segmented genome of the order Bunyavirales. They are the causative agents of two distinct diseases in humans: hemorrhagic fever with renal syndrome (HFRS) caused by Old World hantaviruses found mainly. Viruses 2019, 11, 183 in Europe and Asia and hantavirus cardiopulmonary syndrome (HCPS) caused by New World hantaviruses in the Americas [1]. While disease caused by hantaviruses was described several decades prior, the first isolation and characterization of a hantavirus occurred in the 1970s when Lee et al. In North America, SNV is the main causative agent of HCPS, responsible for greater than 600 infections in the USA and 120 infections in Canada with fatality rates of 35–40% [4,5]. HCPS is a severe disease characterized by fulminant respiratory failure and cardiogenic shock, and the clinical course begins following an incubation period with a mean of 14–17 days, ranging from 9 to 33 days [1]
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