%0 Journal Article
%T Comparative Evaluation of Permissiveness to Dengue Virus Serotype 2 Infection in Primary Rodent Macrophages
%A Jeanette Prada-Arismendy
%A Ver¨®nica Rinc¨®n
%A Jaime E. Castellanos
%J Journal of Tropical Medicine
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/950303
%X 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. 1. Introduction Infection with dengue virus (DENV) causes dengue and severe dengue (formerly dengue fever and dengue haemorrhagic fever). DENV belongs to the Flaviviridae family, flavivirus genus. DENV is an enveloped virus, and its genome consists of a positive polarity, single-stranded RNA of around 11£¿kb that encodes ten proteins. DENV can replicate in several types of cells, including dendritic cells, B and T lymphocytes, endothelial cells, hepatocytes, and neuronal cells. However, 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, consequently, the proliferation and production of cytokines such as TNF-¦Á, 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]. Several studies have addressed the relationship between human genes and the susceptibility to dengue virus infection. For example, the HLA-A*0203 allele correlated with dengue fever (DF) in Thai children, while HLA-A*0207 correlated with dengue haemorrhagic fever (DHF). Moreover, the alleles HLA-B44, B62, B76, and B77 confer protection against DHF in secondary infections [3]. Other polymorphisms associated with DHF have been found in the genes for DC-SIGN1, TNF-¦Á, Fc-¦Ã receptors, vitamin D receptors, and mannose binding lectin [4, 5]. In addition to these host factors, there is evidence that DENV serotypes 2 and 3 cause DHF more frequently [6], supporting the belief that both host and
%U http://www.hindawi.com/journals/jtm/2012/950303/