Abstract
As obligate intracellular pathogens, viruses depend on the host cell machinery to complete their life cycle. Kaposi’s sarcoma-associated herpes virus (KSHV) is an oncogenicvirus causally linked to the development of Kaposi’s sarcoma and several other lymphoproliferative malignancies. KSHV entry into cells is tightly regulated by diverse viral and cellular factors. In particular, KSHV actively engages cellular integrins and ubiquitination pathways for successful infection. Emerging evidence suggests that KSHV hijacks both actin and microtubule cytoskeletons at different phases during entry into cells. Here, we review recent findings on the early events during primary infection of KSHV and its closely related primate homolog rhesus rhadinovirus with highlights on the regulation of cellular cytoskeletons and signaling pathways that are important for this phase of virus life cycle.
Highlights
Entry into cells is the first step in a successful viral infection [1]
Multiple receptors including Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), integrins, ephrin receptor tyrosine kinase A2 (EphA2) and xCT are involved in Kaposi’s sarcoma-associated herpesvirus (KSHV) entry and fusion, which might result in the activation of distinct signaling pathways and entry kinetics depending on the cell types
This study suggests that KSHV infection in endothelial cells might occur through macropinocytosis, which contradicts our observation that KSHV infection in human umbilical vein endothelial cells (HUVEC) is mainly through clathrin-mediated endocytosis [136]
Summary
Entry into cells is the first step in a successful viral infection [1]. A myriad of dynamic interactions between the virus and cell occurs during this complex process [2]. Studies in the last decade have illustrated the pathways of KSHV entry into different cells, and identified viral and cellular factors that regulate this process. Some of these events have been discussed in previous reviews [4,5]. There is emerging evidence that KSHV actively modulates and engages cytoskeletons during its entry into cells, and these dynamic virus–cell interactions are essential for KSHV infection. We focus on the role of cellular cytoskeletons, actin, in the early events of KSHV infection, and discuss the latest updates on the involvement of cellular cytoskeletons and related signaling pathways in these processes. We make comparison of the early events of infection of KSHV with those of other viruses, rhesus rhadinovirus (RRV), a KSHV closely related primate gammaherpesvirus
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call