Susceptibility to and transmission of H5N1 and H7N1 highly pathogenic avian influenza viruses in bank voles (Myodes glareolus)

Abstract

The study of influenza type A (IA) infections in wild mammals populations is a critical gap in our knowledge of how IA viruses evolve in novel hosts that could be in close contact with avian reservoir species and other wild animals. The aim of this study was to evaluate the susceptibility to infection, the nasal shedding and the transmissibility of the H7N1 and H5N1 highly pathogenic avian influenza (HPAI) viruses in the bank vole (Myodes glareolus), a wild rodent common throughout Europe and Asia. Two out of 24 H5N1-infected voles displayed evident respiratory distress, while H7N1-infected voles remained asymptomatic. Viable virus was isolated from nasal washes collected from animals infected with both HPAI viruses, and extra-pulmonary infection was confirmed in both experimental groups. Histopathological lesions were evident in the respiratory tract of infected animals, although immunohistochemistry positivity was only detected in lungs and trachea of two H7N1-infected voles. Both HPAI viruses were transmitted by direct contact, and seroconversion was confirmed in 50% and 12.5% of the asymptomatic sentinels in the H7N1 and H5N1 groups, respectively. Interestingly, viable virus was isolated from lungs and nasal washes collected from contact sentinels of both groups. The present study demonstrated that two non-rodent adapted HPAI viruses caused asymptomatic infection in bank voles, which shed high amounts of the viruses and were able to infect contact voles. Further investigations are needed to determine whether bank voles could be involved as silent hosts in the transmission of HPAI viruses to other mammals and domestic poultry.

Figure 1

Nasal shedding of infected voles at different time points of infection. Mean of the viral shedding (viral copies/μL) recorded on nasal washes collected on days 3, 5, 7 and 9 pi from intranasally infected voles with 10^3.75 EID₅₀/0.1 mL of the Os/H7N1 strain (group Os/H7N1) and 10^4.4 EID₅₀/0.1 mL of the Tk/H5N1 strain (group Tk/H5N1).

Figure 2

Immunohistochemical detection of HPAI viruses in paraffin-embedded tissue sections from infected voles. Positive staining by IHC in trachea (A) (red arrow) and lungs (B) collected on day 3 pi from two voles intranasally infected with 10^3.75 EID₅₀/0.1 mL of the Os/H7N1 virus.

Figure 3

Mean body weight changes of control voles and voles infected with HPAI viruses. Body weight of bank voles intranasally inoculated with (A) 10^3.75 EID₅₀/0.1 mL of Os/H7N1 virus and (B) 10^4.4 EID₅₀/0.1 mL of Tk/H5N1 virus (group I-Tk/H5N1). Data shown are the mean ± SD (error bars) of body weight changes of inoculated voles in comparison to the control group. No significant difference (p > 0.05) was noticed between the body weight recorded at different points in all experimental groups.