Human metapneumovirus

Human metapneumovirus
Human metapneumovirus (hMPV) structure and genome
Virus classification
(unranked):	Virus
Realm:	Riboviria
Kingdom:	Orthornavirae
Phylum:	Negarnaviricota
Class:	Monjiviricetes
Order:	Mononegavirales
Family:	Pneumoviridae
Genus:	Metapneumovirus
Species:	Human metapneumovirus

Human metapneumovirus (HMPV or hMPV) is a negative-sense single-stranded

Human metapneumovirus was first discovered in 2001 in the Netherlands by Bernadette G. van den Hoogen and her colleagues.[5]^[6][7][8] hMPV was first detected in the respiratory secretions of 28 young children in the Netherlands and had initially stood out from other common respiratory viruses because the testing methods van den Hoogen et al. had tried using (immunological assays using virus-specific antibodies and PCR-based methods using virus genome-specific primers) were only able to test for known respiratory viruses and, therefore, were unable to identify the novel virus.^[5] It was not until researchers began applying molecular biology techniques that the genetic characteristics and portions of the genomic sequences of the virus could be identified; these techniques included the randomly primed PCR technique which obtained the limited sequence data needed to reveal a clear relationship between this new virus and the avian pneumovirus.^[5] It was this close relationship to AMPV that gave rise to this new virus being named human metapneumovirus^[5] to reflect both its identity as a metapneumovirus and its use of humans as a host organism.

Epidemiology

HMPV was responsible for 12% of cases of acute

hMPV is estimated to have a 3–6 day incubation period and is often most active during the later winter and spring seasons in temperate climates, overlapping with the RSV and influenza seasons and possibly allowing for repeated infection.^[6] But because it is still a relatively new virus and has not yet been researched very heavily, hMPV and its replication cycle still have a lot of mystery surrounding them. However, researchers have been able to elucidate some principal steps of hMPV's replication cycle, basing their approach and experimentation on the current knowledge we have of the viral life cycles and reproductive measures of the rest of the Paramyxoviridae family.^[38]

With that being said, it has been determined that the first step of the hMPV replication cycle is attachment to the host cell, specifically the

Next in the cycle is the fusion of the viral and host membranes which is likely mediated by the F protein.[8]^[38] Though the fusion mechanism is very similar to that of other Paramyxoviridae family members and involves conformational changes of the F protein, the mechanism for hMPV does not depend on the G protein for fusion like its family members, showing consistency with the previously mentioned idea that the G protein is not necessary for subsequent steps of the hMPV replication cycle.^[8][38] Moreover, the fusion function of the F protein has been proven by its ability to bind to host cells via integrin αvβ1 using an Arginine-Glycine-Aspartate (RGD) motif, which is speculated to be the trigger for membrane fusion events.^[8] One main difference between hMPV and other Paramyxoviridae viruses’ fusion mechanisms though is that hMPV's fusion events occur at acidic pH levels while other viruses’ fusion events occur at neutral pH levels; however, more research needs to be conducted in this area to get a better understanding of what is different about the hMPV fusion mechanism and why.^[38] Although its specific function is uncertain, it is important to note the presence of the SH glycoprotein which seemingly does not have any effects on replication kinetics, cytopathic effects, or plaque formation of hMPV.^[38]

After fusion, the viral

1. detection of hMPV antigens in nasopharyngeal secretions by
   immunofluorescent
   -antibody test
2. the use of immunofluorescence staining with
   monoclonal antibodies
   to detect HMPV in nasopharyngeal secretions and shell vial cultures
3. immunofluorescence assays for detection of hMPV-specific antibodies
4. the use of polyclonal antibodies and direct isolation in cultured cells.

Distribution and habitat

Though hMPV was first discovered and identified in 2001,

So far, peak infection from hMPV in the northern hemisphere is in late winter and early spring, but it can be found globally across all continents[46] and its distribution is very complex and dynamic.^[5] Researchers have found that hMPV is mostly localized and can differ significantly from community to community, allowing for the possibility of the strain in one location one year to be most similar to the strain in a different location the next year.^[5] This phenomenon has actually been recorded with the virus strains in Australia in 2001; in France in 2000 and 2002; in Canada in 1999, 2000, 2001, and 2002; in Israel in 2002; and in the Netherlands in 2001 all being very closely related based on their F gene sequences.^[5] There are at least two major genotypes of hMPV (A and B) that circulate during community outbreaks and each genotype has two of its own,^[5] but as of now, it seems that no one strain is dominant over the others and none of them are known to cause varying levels of severity.^[46]

hMPV is most likely spread from infected individuals to others through 1. secretions from coughing and sneezing, 2. close personal contact (ex. touching, shaking hands, etc), and 3. touching objects with viruses on them then touching your mouth, nose, or eyes.

There are no conclusive studies to date; however, it is likely that transmission occurs by contact with contaminated secretions, via droplet, aerosol, or fomite vectors. Hospital-acquired infections with human metapneumovirus have been reported.^[47] HMPV has been shown to circulate during fall and winter months with alternating predominance of a single subtype each year.^[37]

Treatment

No treatment is yet known,^[48] but ribavirin has shown effectiveness in an animal model.^[49]

Human metapneumovirus was first reported in 2001 and avian metapneumovirus in the 1970s. There are at least four lineages of human metapneumovirus—A1, A2, B1 and B2. Avian metapneumovirus has been divided into four subgroups—A, B, C and D. Bayesian estimates suggest that human metapneumovirus emerged 119–133 years ago and diverged from avian metapneumovirus around 1800.[52]

References