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Geraniin extracted from the nephelium lappaceum (rambutan) rind i | 4013
Drug Designing: Open Access

Drug Designing: Open Access
Open Access

ISSN: 2169-0138

+44 1223 790975

Geraniin extracted from the nephelium lappaceum (rambutan) rind inhibits dengue virus type-2


International Conference and Expo on Drug Discovery & Designing

August 11-13, 2015 Frankfurt, Germany

Siti Aisyah Abdul Ahmad, Uma Palanisamy, Bimo A Tejo and Sharifah Syed Hassan

Posters-Accepted Abstracts: Drug Des

Abstract :

The fast spread of dengue pandemic especially in tropical countries is worrisome. The number of occurrences and amount of
individuals being infected with dengue fever is growing every year. Despite its fast spread, there is yet no effective vaccine
or antiviral drugs available. Nephelium lappaceum, or rambutan, is a type of fruit which can be found in abundance in Malaysia
and other regions of tropical Southeast Asia. Consumption of rambutan results in the production of waste from its seed and rind.
Currently, many reports have shown the various biological activities such as antioxidant, antimicrobial and anti-inflammatory of
geraniin extracted from natural sources. Geraniin has also been shown to be the major compound found in the extract of rambutan
rind. In this study, the antiviral activity of geraniin extracted from the rambutan rind against dengue virus type-2 (DENV-2) was
investigated. Using plaque reduction assay, it was shown that geraniin possessed inhibitory potential towards DENV-2 with the
mechanism of inhibiting its attachment to cells. The stage of DENV-2 replication cycle where geraniin impose its inhibitory action
was also determined through the time-of-addition assay. Through this assay, it was shown that geraniin exhibits its inhibitory potential
on DENV-2 at the early stage of DENV-2 life cycle, which primarily involves the envelope (E) protein. Docking study showed that
geraniin interacts with this major protein. In conclusion, geraniin from the rind of Nephelium lappaceum possesses antiviral activity
against DENV-2 through the mechanism of inhibiting viral attachment, most probably by binding to the E protein, hence disrupting
the infection process.

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