Abstract

Infection with dengue virus presents a broad clinical spectrum, which can range from asymptomatic cases to severe cases that are characterised by haemorrhagic syndrome and/or shock. The reason for such variability remains unknown. This work evaluated the in vitro permissiveness of mouse, rat, hamster and guinea pig macrophages to infection by dengue virus 2 (DENV2). The results established that macrophages derived from the BALB/c mouse strain showed higher permissiveness to DENV2 infection than macrophages from other rodent species, although all rodent species studied had the C820T mutation in the oligoadenylate synthetase 1b gene, indicating no relationship to the different in vitro susceptibilities of mouse cells at this locus. Other molecular mechanisms related to flavivirus susceptibility remain to be explored.

Highlights

  • Infection with dengue virus (DENV) causes dengue and severe dengue

  • Rat Guinea pig Hamster (a) the macrophages into the supernatant was quantified by realtime PCR analysis of the RNA obtained from the supernatant of cells infected for 24, 48, and 72 hours at two different multiplicity of infection (MOI)

  • The differences in the number of viral copies were significant at 24 and 48 hours p.i. (P < 0.01), while the number of viral copies obtained in BALB/c-derived macrophages was similar to that obtained in NIH- and ICR-derived mouse macrophages at 72 hours

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Summary

Introduction

Infection with dengue virus (DENV) causes dengue and severe dengue (formerly dengue fever and dengue haemorrhagic fever). Monocytes/macrophages are the primary target during in vivo infection [1]. Viral entry into these cells enables the virus to spread to different tissues and induces the presentation HLA molecule-associated viral antigens. The presentation of viral antigens by macrophages to memory T cells induces T cell activation and, the proliferation and production of cytokines such as TNF-α, IFN, and IL-2. This set of cytokines and chemokines induces endothelial dysfunction and plasma leakage, both of which are characteristic of more severe manifestations of the disease [2]

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