Reply: To PMID 22871625.

I read with interest the comment of Uma and associates on the report of “Dengue retinochoroiditis.”1 I highly appreciate their comments in which they highlight four points: (1) the genetic predisposition to dengue virus infection, (2) the protective effects of ACE inhibitors, (3) additional investigations of platelet functions, and (4) molecular mimicry between vascular endothelial cells and dengue virus.

Dengue virus is composed of four distinct serotypes related to flaviviruses which represent the most important emerging viral disease at the present time. First, in response to the genetic predisposition: genetic determinants of dengue virus susceptibility include human leukocyte antigens, blood type, and single nucleotide type polymorphisms in immune response genes.2 At the same time, one has to consider other factors such as viral genetic determinants, age, ethnicity and the nutritional status of the individual related to dengue virus susceptibility. It is, therefore, conceded that functional genetic studies to complement available data would certainly help in defining the dengue virus susceptibility. Second, in reference to the ACE inhibitors protective effect in dengue, there are no clinical trials that have been reported on this subject and the hypothesis need to be verified by future studies. Third, our two patients had thrombocytopenia and we did not perform studies on antibodies against thrombocytes or platelet receptor polymorphism. Fourth, the concept of molecular mimicry that has been proposed by Liu and associates3 is intriguing. They have found that dengue virus complex-specific mAb (DB16-1) targeted the same epitope in the dengue virus non-structural protein 1 (NS1) and lysine-rich CEACAM1 (LYRIC) protein in human endothelial cells suggesting that it may play a role in the pathogenesis of dengue hemorrhagic fever and dengue shock syndrome.3 The role of this molecular mimicry in ocular and retinal vasculopathy remains to be determined. Furthermore, future studies on the role of anti-NS1 antibody as a cause of vascular permeability should be studied in individuals with endothelial cell dysfunction in dengue fever.