Chickenpox, known medically as varicella, is a highly contagious disease caused by the Varicella-Zoster Virus (VZV). This pathogen is responsible for the characteristic itchy rash and fluid-filled blisters that mark the primary infection. Studying VZV under high magnification reveals its highly structured particle and the cellular changes it induces in the host.
The Varicella-Zoster Virus Structure
The Varicella-Zoster Virus is classified as a member of the Herpesviridae family, a group of large, enveloped viruses. Its complex structure consists of four main layers, visible only using powerful electron microscopy. The core of the virion contains the viral genetic material, a linear, double-stranded DNA molecule.
Surrounding the DNA is the capsid, a rigid protein shell shaped like an icosahedron. This structure is composed of 162 individual protein units and measures about 100 to 110 nanometers in diameter. The entire VZV particle, when fully assembled, measures between 150 and 200 nanometers in diameter.
The capsid is encased by the tegument, an amorphous layer of proteins containing enzymes essential for the virus’s early replication cycle. The outermost layer is a lipid envelope, a membrane derived from the host cell. Embedded within this envelope are multiple viral glycoproteins that facilitate the virus’s entry into new cells.
VZV Replication and Cellular Effects
Under a light microscope, VZV infection is identified by the changes the virus causes within infected cells, known as cytopathic effects. Once VZV enters a host cell, its DNA is transported to the nucleus where replication and assembly occur. This process disrupts normal cellular function and modifies the cell’s internal structure.
A notable result is the formation of multinucleated giant cells, or syncytia, which are large cells containing multiple nuclei. VZV promotes the fusion of infected cells with neighboring cells, creating these characteristic structures. This cell-to-cell spread allows the virus to bypass the host’s immune response and spread throughout the tissue.
Another distinct feature visible is the presence of intranuclear inclusion bodies. These appear as dense, eosinophilic (pink-staining) masses within the nucleus of the infected cells, often pushing the cell’s chromatin to the periphery. These inclusion bodies represent the accumulation of viral proteins, serving as a clear marker of herpesvirus infection.
Methods for Microscopic Identification
Microscopic identification of VZV relies on two distinct approaches. To observe the intricate structure of the virion itself, scientists employ electron microscopy (EM). EM uses a beam of electrons instead of light, providing the high magnification necessary to visualize objects as small as 150 nanometers. EM is reserved for research or specialized cases due to its complexity and cost.
A more practical, rapid method for clinical diagnosis is the Tzanck smear, which uses standard light microscopy. This technique involves scraping the base of a fresh skin lesion and staining the collected cells.
The Tzanck smear identifies the cytopathic effects, not individual VZV particles. A positive result is the observation of multinucleated giant cells and prominent intranuclear inclusion bodies. While rapid, the Tzanck smear cannot differentiate VZV from other herpesviruses, as both produce similar cellular changes.