Abstract
Like all other viruses, a successful egress of functional particles from infected cells is a prerequisite for foamy virus (FV) spread within the host. The budding process of FVs involves steps, which are shared by other retroviruses, such as interaction of the capsid protein with components of cellular vacuolar protein sorting (Vps) machinery via late domains identified in some FV capsid proteins. Additionally, there are features of the FV budding strategy quite unique to the spumaretroviruses. This includes secretion of non-infectious subviral particles and a strict dependence on capsid-glycoprotein interaction for release of infectious virions from the cells. Virus-like particle release is not possible since FV capsid proteins lack a membrane-targeting signal. It is noteworthy that in experimental systems, the important capsid-glycoprotein interaction could be bypassed by fusing heterologous membrane-targeting signals to the capsid protein, thus enabling glycoprotein-independent egress. Aside from that, other systems have been developed to enable envelopment of FV capsids by heterologous Env proteins. In this review article, we will summarize the current knowledge on FV budding, the viral components and their domains involved as well as alternative and artificial ways to promote budding of FV particle structures, a feature important for alteration of target tissue tropism of FV-based gene transfer systems.
Highlights
The step crucial for virus spread within the infected host is the egress of virus particles from the initial and any successively infected cell
For all retroviruses, including foamy viruses, a set of proteins belonging to endosomal sorting complex required for transport (ESCRT) machinery is involved in particle egress
Due to the specific interaction of foamy virus (FV) Gag and Envelope protein (Env) proteins, which is a prerequisite for particle egress, FVs are naturally resistant to pseudotyping by heterologous glycoprotein, even from other retroviruses [12,13,14]
Summary
The step crucial for virus spread within the infected host is the egress of virus particles from the initial and any successively infected cell. The subcellular location of virus budding varies among virus genera and for specific virus species sometimes in dependence of the target tissue type infected [2] It can either take place at the plasma membrane or at an intracellular compartment. Oligomerization of capsid protein leads to formation of the particle, its growth and bending of the plasma membrane, after which the assembled virion pinches off This is characteristic of C-type retroviruses, such as human immunodeficiency virus type 1 (HIV-1) [3] or murine leukemia virus (MuLV) [4]. The budding site can be either plasma membrane or an intracellular compartment (such as endoplasmic reticulum (ER) or Golgi), where the envelope protein is localized This mechanism characterizes B/D-type retroviruses such as Mason-Pfizer monkey virus (MPMV) and mouse mammary tumor virus (MMTV) [5,6,7]. Place of interaction (Capsid-Envelope) plasma membrane plasma membrane trans-Golgi network
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