Introduction

Dengue transmission requires the simultaneous presence of three factors; susceptible humans, a
competent mosquito vector, and DV [1]. Studies of DF endemic zones have shown that low income
groups have a higher incidence of disease. Two and one-half billion people in more than one
hundred countries are at risk of infection, with an estimated 50 million cases per year.[2] DV is a
mosquito-borne flavivirus and the most prevalent arbovirus in tropical and subtropical regions of the
globe [3]. DF may result from infection with any of the four antigenically related dengue virus
serotypes (DEN-1-4)[4] of the genus Flavivirus [5]. DENV-2 was the predominant serotype in the
Tamaulipas outbreak that occurred in 2005 [6]. An Immunoglobulin M (IgM)-capture enzyme-linked
immunosorbent assay (ELISA) confirms recent dengue infection.[7]
Among both DF and DHF cases, more than 98 percent of the patients had serologic evidence for a
secondary dengue virus infection from another serotype of dengue virus or a non-dengue flavivirus
[8]. Epidemiological studies indicate that homologous immunity provides nearly permanent
protection against re-infection with a previously experienced serotype; in contrast, heterologous
immunity does not provide protection against re-infection in the long term [9]. The antibody-
dependent enhancement (ADE) theory states that cross-reactive, yet non-neutralizing