Measles is a highly contagious viral illness known for its characteristic rash. The measles virus interacts with the host’s body at a cellular level, causing significant changes within infected cells that are central to the disease’s progression. Understanding these cellular alterations provides insight into the virus’s lifecycle and its effects on human tissues.
Defining Measles-Specific Cells
A hallmark of a measles infection is the formation of unique structures known as Warthin-Finkeldey giant cells. These are the body’s own cells structurally altered by the virus. Found primarily in lymphoid tissues like the tonsils, appendix, and lymph nodes, these giant cells are a pathological indicator of the disease. They are large, multinucleated cells, sometimes containing up to 100 nuclei within a single shared cytoplasm.
These altered cells also feature eosinophilic inclusion bodies, which are abnormal protein aggregates composed of viral nucleoprotein strands, direct evidence of the virus replicating inside the host cell. The presence of Warthin-Finkeldey cells is so characteristic of measles that they can be identified in tissue samples before other classic symptoms like the rash appear. The formation of these giant cells occurs during the prodromal stage of the infection.
Viral Mechanisms Affecting Host Cells
The measles virus initiates infection by targeting specific proteins on the surface of host cells. The virus uses its surface proteins to attach to receptors on human cells, such as SLAMF1 on immune cells and nectin-4 on epithelial cells. This attachment allows the virus to fuse with the cell membrane and inject its RNA into the cell’s cytoplasm.
Once inside, the virus hijacks the cell’s machinery to replicate its RNA and produce new viral proteins. The viral fusion protein is transported to the surface of the infected cell, causing it to fuse with its uninfected neighbors. This cell-to-cell fusion creates the large, multinucleated Warthin-Finkeldey giant cells, also referred to as syncytia. This process of fusing cells allows the virus to spread efficiently throughout a tissue without being exposed to the host’s immune defenses in the bloodstream.
Primary Cell Types Infected by Measles
The measles virus demonstrates a preference for certain cell types, which dictates the course of the infection. The initial targets are immune cells located in the respiratory tract, including lymphocytes, dendritic cells, and macrophages. The virus’s ability to infect these cells leads to a temporary but potent suppression of the immune system, making the host more vulnerable to other infections.
Following this primary infection, a secondary viremia, or wave of virus in the bloodstream, occurs. This disseminates the virus throughout the body, allowing it to infect other cell types.
Epithelial cells lining the respiratory tract become major targets, and their destruction contributes directly to symptoms such as a persistent cough and coryza. The virus also infects endothelial cells, which line the blood vessels, contributing to the characteristic maculopapular rash. In some cases, the virus can reach neuronal cells, leading to rare but serious neurological complications.
Role in Measles Diagnosis and Disease Progression
The identification of measles-altered cells plays an important part in diagnosing the illness, sometimes even before the most recognizable symptoms emerge. The presence of Warthin-Finkeldey giant cells in tissue samples is a pathognomonic sign of measles, meaning it is specifically characteristic of the disease. For instance, these cells can be found in an appendix removed due to inflammation, allowing for a measles diagnosis during its prodromal stage, prior to the rash.
This early histological diagnosis can be valuable for timely intervention and management of the patient, potentially minimizing the severity of symptoms and preventing complications. The cellular changes caused by the virus are directly linked to the progression of the disease. Understanding how the measles virus infects and alters specific cells provides a clear picture of its pathogenesis. It connects the microscopic events of viral replication and cell fusion to the macroscopic symptoms and potential complications experienced by an infected individual.