The measles virus, Measles morbillivirus, is a highly contagious human pathogen. It causes a systemic illness with symptoms like fever, cough, runny nose, red eyes, and a distinctive rash. Understanding how viruses reproduce within host cells is fundamental to grasping how they cause disease.
Understanding Viral Replication Methods
Viruses employ distinct strategies to multiply inside host cells, categorized into two main cycles: lytic and lysogenic. The lytic cycle involves rapid replication and assembly of new viral particles. This process culminates in the bursting, or lysis, of the host cell, releasing progeny viruses to infect new cells. This destructive process leads to acute infection and the death of the infected cell.
In contrast, the lysogenic cycle integrates viral genetic material into the host cell’s genome. The viral DNA, a prophage, remains dormant and is replicated along with the host cell’s DNA during normal cell division. This allows the virus to persist without immediately destroying the cells. However, under certain conditions, the integrated viral genetic material can reactivate, initiating a lytic cycle and leading to the production of new viruses and host cell destruction.
How Measles Virus Replicates
The measles virus primarily follows a lytic replication cycle within its host cells. As an enveloped, single-stranded, negative-sense RNA virus, Measles morbillivirus produces new viral particles.
The process begins with attachment, where the viral hemagglutinin (H) protein binds to specific receptors on host cells, such as CD150 on immune cells and nectin-4 on epithelial cells. The fusion (F) protein then mediates the merging of the viral envelope with the host cell membrane, allowing the viral genetic material to enter the cytoplasm. Once inside, the viral RNA-dependent RNA polymerase uses the negative-sense RNA genome as a template to produce positive-sense RNA, which serves as messenger RNA for protein synthesis and as an intermediate for creating new negative-sense genomes.
These newly synthesized positive-sense RNAs are translated by host ribosomes into various viral proteins, including the nucleoprotein (N), phosphoprotein (P), matrix (M), fusion (F), hemagglutinin (H), and large (L) proteins. New viral components assemble at the host cell’s plasma membrane, with the matrix (M) protein playing a role in concentrating the ribonucleocapsid and glycoproteins. New measles virions then bud from the cell surface, acquiring a portion of the host cell membrane as their outer envelope. This budding process leads to significant damage and death of the infected host cell, characteristic of a lytic infection, as the measles virus does not integrate its genetic material into the host genome.
Consequences of Measles Replication
The lytic replication strategy of the measles virus directly contributes to the acute symptoms observed during infection. Widespread cell damage and the body’s immune response to this destruction result in the characteristic fever, cough, and rash.
The measles virus initially infects immune cells, such as macrophages, dendritic cells, and lymphocytes, which express the CD150 receptor. This initial infection allows the virus to spread throughout the body, leading to a temporary weakening of the immune system, sometimes referred to as “immune amnesia.” Subsequently, the virus infects epithelial cells in the respiratory tract via the Nectin-4 receptor, leading to virus shedding through respiratory droplets. This rapid replication and cell destruction within the respiratory system make measles highly contagious, as infected individuals can easily transmit the virus through coughing and sneezing. Understanding this lytic replication cycle is important for public health efforts, including the development of vaccines like the MMR (measles, mumps, and rubella) vaccine, which provides protection against the disease.