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“10 Reasons Why ‘HMPV’ Movie is a Must-Watch in 2025”

A single-stranded, negative-polarity virus belonging to the Pneumoviridae family is the human metapneumovirus (hMPV). It is closely related to the avian metapneumovirus (aMPV) subgroup C. It was first identified in the Netherlands in 2001 when RAP-PCR (RNA Arbitrarily Primed PCR) technology was used to detect an unknown virus growing in cultured cells.
In a major U.S. outpatient clinic, hMPV surpassed respiratory syncytial virus (RSV) as the second most prevalent cause of acute respiratory tract disease in otherwise healthy children under five by 2016. Hospitalization for hMPV in neonates peaks between 6 and 12 months, which is a little later than the peak for RSV, which occurs between 2 and 3 months. RSV and hMPV are similar in clinical symptoms and severity. In older people, hMPV is also a major source of sickness. By the end of 2024, there was a significant hMPV outbreak in Northeast Asia.
Classification: Genus Metapneumovirus

hmpv

Virus Species (shorthand)NCBI Classification Number
Avian Metapneumovirus (aMPV) 38525 is the name of the virus.
162145 Human Metapneumovirus (hMPV) Metapneumovirus in Humans

Discovery and Naming.
The first discovery of human metapneumovirus was made in 2001 by Bernadette G. van den Hoogen and her associates in the Netherlands. When hMPV was initially identified in the respiratory secretions of 28 young children, van den Hoogen et al.’s novel testing techniques made it possible to distinguish it from other prevalent respiratory viruses. After molecular biology techniques showed the virus’s genetic properties and showed that it closely resembled avian pneumovirus, it was called “human metapneumovirus” to indicate its classification and human hosts.

Epidemiology hmpv.


In outpatient clinics in the United States, responsible for about 12% of acute respiratory tract infections in otherwise healthy children. Furthermore, 15% of hospitalized instances of community-acquired pneumonia are caused by it. Following influenza and RSV, the virus mainly appears in late winter and spring and has a global distribution with seasonal trends. Studies show that almost all children worldwide are exposed to hMPV by the time they are five years old. Even if exposure happens early in childhood, reinfections are common in older children and adults.
Mild upper respiratory tract infections, such as the common cold, can be caused by the virus. For those over 65, immunocompromised people, and premature babies, it presents serious hazards that frequently result in serious diseases and hospitalization. In older populations, hMPV has been found to be as common and severe as influenza in certain investigations. Additionally, those who have asthma or chronic obstructive lung disease (COPD) are at increased risk from the infection.

Genomic Structure.
Despite lacking the non-structural genes NS1 and NS2, hMPV shares a similar genomic structure to RSV. It features eight open reading frames, albeit in a somewhat different order than RSV. Using phylogenetic analysis, two main genetic lineages are discovered as subtypes A and B. These are further separated into subgroups A1/A2 and B1/B2.

Lifecycle and Replication.
The seasons of influenza and RSV correspond with the winter and spring seasons in temperate countries, when hMPV is most active. Three to six days are thought to be the incubation period. Even though research on hMPV is still developing, significant understanding of its replication cycle has been attained:
Attachment: The virus attaches itself to respiratory tract epithelial cells using the G protein.
F protein mediates the fusing of the host and viral membranes to initiate viral entry.
Replication: Viral RNA mimics the production of mRNA and antigenomic cRNA.
Assembly and Release: Once viral proteins have passed through the Golgi apparatus, the virus can assemble at the cell surface and infect neighboring cells.
Further research is required to fully understand how the virus replicates.

Virology.
hMPV infects the epithelial cells in the nasal passages and lungs. It is believed to cling to host cells through glycosaminoglycans, including heparan sulfate.

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