Anti-HSV Polyclonal antibody

Purpose of review To review the principles of oncolytic virotherapy and summarize the recent preliminary evidence on the efficacy of oncolytic virotherapy for cholesteatoma (CHST) treatmentin vitroin human CHST cells and in a gerbil CHST model. Recent findings The use of oncolytic virotherapy for nonmalignant lesions is innovative. In-vitro results showed that oncolytic herpes simplex virus 1 (oHSV) selectively targets and kills CHST cells. In a gerbil model of CHST, local oHSV injections were associated with a decrease in CHST volume and modulation of bony changes. Surgical treatment options for CHST are limited by high morbidity and recidivism, emphasizing the need for developing treatment alternatives. Preliminary results support the potential therapeutic effect of oncolytic virotherapy on CHST, yet further research is needed to evaluate this novel approach.

Herpes simplex virus type 1 (HSV-1) is a very common human pathogenic virus among the world's population. The lytic replication cycle of HSV-1 is, amongst others, characterized by a tripartite viral gene expression cascade, the assembly of nucleocapsids involving their subsequent nuclear egress, tegumentation, re-envelopment and the final release of progeny viral particles. During productive infection of a multitude of different cell types, HSV-1 generates not only infectious heavy (H-) particles, but also non-infectious light (L-) particles, lacking the capsid. In monocyte-derived mature dendritic cells (mDCs), HSV-1 causes a non-productive infection with the predominant release of L-particles. Until now, the generation and function of L-particles is not well understood, however, they are described as factors transferring viral components to the cellular microenvironment. To obtain deeper insights into the L-particle composition, we performed a mass-spectrometry-based analysis of L-particles derived from HSV-1-infected mDCs or BHK21 cells and H-particles from the latter one. In total, we detected 63 viral proteins in both H- and L-particle preparations derived from HSV-1-infected BHK21 cells. In L-particles from HSV-1-infected mDCs we identified 41 viral proteins which are differentially distributed compared to L-particles from BHK21 cells. In this study, we present data suggesting that L-particles modify mDCs and suppress their T cell stimulatory capacity. Due to the plethora of specific viral proteins incorporated into and transmitted by L-particles, it is tempting to speculate that L-particles manipulate non-infected bystander cells for the benefit of the virus.