Herpes simplex virus type 1 (HSV-1) is an important factor for vision loss in developed countries. A challenging aspect of the ocular infection by HSV-1 is that common treatments, such as acyclovir, fail to provide effective topical remedies. Furthermore, it is not very clear whether the viral glycoproteins, required for HSV-1 entry into the host, can be targeted for an effective therapy against ocular herpes in vivo. Here, we demonstrate that HSV-1 envelope glycoprotein gD, which is essential for viral entry and spread, can be specifically targeted by topical applications of a small DNA aptamer to effectively control ocular infection by the virus. Our 45-nt-long DNA aptamer showed high affinity for HSV-1 gD (binding affinity constant [Kd] = 50 nM), which is strong enough to disrupt the binding of gD to its cognate host receptors. Our studies showed significant restriction of viral entry and replication in both in vitro and ex vivo studies. In vivo experiments in mice also resulted in loss of ocular infection under prophylactic treatment and statistically significant lower infection under therapeutic modality compared to random DNA controls. Thus, our studies validate the possibility that targeting HSV-1 entry glycoproteins, such as gD, can locally reduce the spread of infection and define a novel DNA aptamer-based approach to control HSV-1 infection of the eye.
Chrysanthemum stunt viroid (CSVd), a noncoding RNA, is known to cause chrysanthemum stunt disease, which affects the yield of flowers. To gain insights into CSVd replication, infection, and the reasons for the spreading of CSVd disease in chrysanthemum plants, we prepared linear CSVd RNA and analyzed its ability to cause disease in chrysanthemum plants. We found that linear CSVd replicated as efficiently as CSVd RNA isolated from the infected chrysanthemum plants. Additionally, the linear CSVd RNA was evaluated for its ability to infect other plants as well, which revealed that CSVd has a wide host range for its replication. Importantly, the CSVd isolated from these hosts is infectious to chrysanthemum plants, and thus potentially contributes to the spreading of the disease to chrysanthemum plants.
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