Yakammaoto inhibits enterovirus 71 infection by reducing viral attachment, internalization, replication, and translation.

Enterovirus 71 (EV71) can cause central nervous system infections with mortality and neurologic sequelae. At present, there is no effective therapeutic modality for EV71 infection. The infection is more common in families with poor socioeconomic status. Therefore, finding a readily available, cost-effective therapeutic modality would be very helpful to these socioeconomically disadvantaged families. Yakammaoto is a cheap and readily available traditional prescription that is proven to have antiviral activity against coxsackievirus B4 (CVB4). CVB4 and EV71 are enteroviruses. In this study, we evaluated the antiviral activity of hot water extract of yakammaoto against EV71. The results of plaque reduction assay and flow cytometry demonstrated that yakammaoto dose dependently inhibited EV71 infection. In addition, reverse transcription-polymerase chain reaction (RT-PCR) and quantitative RT-PCR results showed that yakammaoto reduced viral replication. Western blotting analysis showed that yakammaoto can inhibit viral protein production. Thus, our results suggest that yakammaoto should be considered to manage EV71 infection in the future.

Assessment of the subcellular localization of the herpes simplex virus structural protein VP22 in the absence of other viral gene products.

We previously demonstrated that the herpes simplex virus type 1 (HSV-1) structural protein VP22 exists in the cytoplasm early in infection and migrates to and accumulates in the nucleus late in infection (J. Virol. 73(8) (1999) 6769). The goal of this study is to document the behavior of VP22 in cells in the absence of other viral polypeptides. We characterized the effects of various indirect immunofluorescence sample preparation conditions on the localization of VP22 in cells and have determined the following. (i) Fixing with formaldehyde and permeabilizing with acetone maintains the structure of microtubules in cells, in as much as we observed classic microtubule organizing centers. (ii) Acetone or methanol alone did not completely fix the cells. (iii) Triton X-100 decreased tubulin immunofluorescence signals in our system. (iv) VP22 predominated in the nucleus of cells that were fixed with formaldehyde. Based on our results, we conclude the following. (v) Due to the partial fixation by acetone or methanol alone, microtubules form diffuse irregular shapes. (vi) VP22 is detected in the cytoplasm of cells fixed with acetone or methanol only due to its seepage from the nucleus. Taken together, these findings indicate that (vii) the nuclear localization of VP22 does not require additional viral factors.