Figure 1.
A typical baculovirus replication cycle.
Nucleocapsids are produced in the nucleus of infected cells, but two forms of enveloped virions are produced. The first, budded virus (BV), is formed when single nucleocapsids exit the nucleus and bud from the cell, acquiring an envelope from the plasma membrane. The BV attachment and fusion protein, either GP64 or F depending on the type of baculovirus, is concentrated at one end of the virion in structures that are visible by electron microscopy, known as peplomers. Later, the second type of virion, called occlusion-derived virus (ODV), is formed when nucleocapsids obtain an envelope from the inner nuclear membrane. ODV become embedded in large proteinaceous crystals that are primarily composed of a single viral protein called polyhedrin, and are known as occlusion bodies. The occlusion bodies remain within the nucleus until they are liberated by cell lysis. The ODV of some baculoviruses, known as multiple nucleopolyhedroviruses (MNPVs), contain multiple nucleocapsids within a single-enveloped virus particle, as is illustrated here. In nature, the baculovirus replication cycle begins when a susceptible insect larva consumes viral occlusion bodies contaminating their food source. The occlusion bodies dissolve in the highly alkaline environment of the larval midgut, releasing ODV, which attach to the microvillar membranes of midgut epithelial cells. Attachment and fusion occurs via the PIF proteins, found in the ODV envelope. Infected midgut epithelial cells produce BV, which bud from the basal side and infect tracheal epithelial cells. Infection of tracheal cells is thought to be one mechanism that allows BV to escape across the midgut basal lamina (BL) and spread infection throughout the insect. The majority of tissues become infected, producing large amounts of ODV and BV. The infected insects liquefy after death, allowing dispersal of occlusion bodies and promoting subsequent infections.
Figure 2.
Baculovirus-induced climbing behavior, historically known as “Wipfelkrankheit” (tree top disease), has been attributed to the viral egt gene.
Gypsy moth (Lymantria dispar) larvae that were infected with wild type L. dispar MNPV (LdMNPV) (A) demonstrated increased climbing behavior compared to a mutant of LdMNPV lacking the egt gene (B) [8]. This evolutionary adaptation is thought to aid in virus dispersal after death of the larvae, resulting in increased dispersal of occluded virus to the rest of the vegetation below.