Abstract
Zika virus (ZIKV) and Dengue virus (DENV) are mosquito-borne viruses of the Flavivirus genus that could cause congenital microcephaly and hemorrhage, respectively, in humans, and thus present a risk to global public health. A preventive vaccine against ZIKV remains unavailable, and no specific antiviral drugs against ZIKV and DENV are licensed. Medicinal plants may be a source of natural antiviral drugs which mostly target viral entry. In this study, we evaluate the antiviral activity of Doratoxylum apetalum, an indigenous medicinal plant from the Mascarene Islands, against ZIKV and DENV infection. Our data indicated that D. apetalum exhibited potent antiviral activity against a contemporary epidemic strain of ZIKV and clinical isolates of four DENV serotypes at non-cytotoxic concentrations in human cells. Time-of-drug-addition assays revealed that D. apetalum extract acts on ZIKV entry by preventing the internalisation of virus particles into the host cells. Our data suggest that D. apetalum-mediated ZIKV inhibition relates to virus particle inactivation. We suggest that D. apetalum could be a promising natural source for the development of potential antivirals against medically important flaviviruses.
Highlights
Zika virus (ZIKV) and the closely related dengue virus (DENV) are mosquito-borne RNA viruses of the genus Flavivirus in the Flaviviridae family [1]
We report that an extract from Dorotoxylon apetalum, an indigenous medicinal plant from the Mascarene Islands, inhibits infection of A549 and Huh7.5 cells by epidemic ZIKV and DENV strains without reducing cell viability
Our results suggest that D. apetalum extract could bind to ZIKV particles, rendering the virus incapable of initiating an infectious viral cycle
Summary
Zika virus (ZIKV) and the closely related dengue virus (DENV) are mosquito-borne RNA viruses of the genus Flavivirus in the Flaviviridae family [1]. Our previous antiviral assays showed that the D. apetalum extract-mediated inhibition of ZIKV is related to a virus inactivation affecting post-attachment step(s) in the infectious virus cycle. Isoquercitrin (Q3G), which is known to inhibit the ZIKV internalisation process in A549 cells, was used as a positive control [22] Both D. apetalum and Q3G showed a similar time-course of ZIKV entry inhibition with a maximum of effect during the first 30 min post-binding (Figure 5C). This result suggests that D. apetalum has the ability to inhibit the early steps of virus internalisation into the host cell. These data provide evidence that D. apetalum extract-mediated inhibition of ZIKV infection occurs early after virus binding to the plasma membrane and could be explained by the inability of the plasma membrane-associated virus to be internalized into the host cell in presence of plant extract
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