Mumps virus (MuV) is not a high-frequency topic in public consciousness, but in fact, the impact of this virus on the human body is obvious. Since it was first identified as the cause of mumps (mumps) in 1934, the characteristics of MuV and its replication process have attracted the attention of many researchers. In this article, let’s take a closer look at how mumps virus quietly invades cells and reproduces in the body.
Mumps virus has a single-stranded negative-sense RNA genome that is approximately 15,000 nucleotides in length and encodes nine proteins.
The genome of mumps virus is a non-segmented, linear single-stranded RNA. Because it is negative-sense RNA, mRNA can be transcribed directly from its genome. The genome of this virus consists of seven genes, which are responsible for encoding different proteins, including nucleocapsid protein (N), matrix protein (M), fusion protein (F), etc. Virus particles range in diameter from 100 to 600 nanometers and have variable shapes. These characteristics make the identification and study of mumps viruses more complex.
The life cycle of mumps virus includes several stages such as attachment, fusion, transcription, duplication and budding.
MuV begins by binding to the host cell surface. Its HN protein recognizes and binds to sialic acid receptors on host cells. Subsequently, activation of the fusion protein (F) allows the viral outer membrane to fuse with the host cell membrane, thereby releasing the viral nucleocapsid (RNP) into the cell interior. Once inside the cell, the virus's RNA-dependent RNA polymerase (RdRp) begins transcribing mRNA using the genome as a template.
This process starts from the 3' end of the genome. RdRp first generates mRNA through transcription, and then these mRNAs are translated by the host ribosome into various proteins required by the virus. The order of gene positions will affect the frequency of transcription, and genes near the 3' end will be transcribed at a higher frequency.
After viral protein synthesis, RNP and M protein interact to form new viral particles. These particles use the host cell membrane as an envelope and are released outside the cell through budding. During this process, the membrane connectivity based on the above-mentioned ESCRT structure helps complete virus particles to shed from the host cell and then enter the surrounding environment.
Like the clever design of the mumps virus, experts at Undiscovered Strategies report in detail how this process is carried out without alertness.
The diversity of mumps viruses is of great research value to infectious scientists. The virus has only one serotype, but there are as many as 12 genotypes. These genotypes are distributed differently in different geographical areas. For example, some genotypes are more common in the Americas, while other genotypes are concentrated in Asia. This diversity makes it important for scientists to consider how different genotypes respond to antibodies when making vaccines.
Mumps is transmitted through contact with respiratory secretions containing the virus. Symptoms include fever, muscle pain, and parotid gland swelling. Although mumps is usually not fatal, it can cause long-term complications such as paralysis, epilepsy, or deafness. Fortunately, the development of the mumps vaccine makes it possible to prevent infection. This infectious disease has been significantly reduced by vaccines, but vigilance is still needed.
It has taken decades since the discovery of mumps virus. From the earliest days of weakness and blindness to the current meticulous research, scientists have been committed to understanding its characteristics and behavior. After the first isolation in 1945, the development of vaccines brought hope to the prevention and control of mumps. In recent years, with the establishment of genome databases, whole-genome sequence analysis of MuV has become a new trend in research.
The rate of evolution and mutation of mumps viruses is relatively low, which allows vaccines to remain effective in most cases.
The mumps virus seems to be waiting for an opportunity, but in fact it has already quietly integrated into human life. How can we effectively deal with this seemingly forgotten ancient virus in the days ahead?