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Das Humane Metapneumovirus (HMPV, en. Human metapneumovirus) wurde als neuer Vertreter der Familie Paramyxoviridae 2001 erstmals isoliert und 2016 der damals neuen Virusfamilie Pneumoviridae zugeordnet. Es ist dem häufigeren Respiratory-Syncytial-Virus genetisch und klinisch sehr nahe verwandt.
Das HMPV repliziert sich im Respirationstrakt und betrifft vorwiegend Kleinkinder und Kinder. In dieser Altersgruppe macht es bis zu 15 % der jährlichen Bronchiolitisfälle aus. Laut einer sechsjährigen US-Studie ist es bei Kindern der zweithäufigste Erreger der Bronchiolitis.[3]
Bereits im Alter von fünf Jahren haben die meisten Kinder Antikörper gegen das HMPV entwickelt, auch ohne an einer schweren unteren Atemwegsinfektion erkrankt gewesen zu sein.[4]
Außer Menschen kann das Virus erwiesenermaßen auch Schimpansen und Gorillas infizieren. Bis 2011 waren Infektionen an Schimpansen im Tai-Nationalpark in der Elfenbeinküste sowie von Gorillas in Ruanda bekannt geworden.[5]
Das Humane Metapneumovirus (HMPV, en. Human metapneumovirus) wurde als neuer Vertreter der Familie Paramyxoviridae 2001 erstmals isoliert und 2016 der damals neuen Virusfamilie Pneumoviridae zugeordnet. Es ist dem häufigeren Respiratory-Syncytial-Virus genetisch und klinisch sehr nahe verwandt.
Das HMPV repliziert sich im Respirationstrakt und betrifft vorwiegend Kleinkinder und Kinder. In dieser Altersgruppe macht es bis zu 15 % der jährlichen Bronchiolitisfälle aus. Laut einer sechsjährigen US-Studie ist es bei Kindern der zweithäufigste Erreger der Bronchiolitis.
Bereits im Alter von fünf Jahren haben die meisten Kinder Antikörper gegen das HMPV entwickelt, auch ohne an einer schweren unteren Atemwegsinfektion erkrankt gewesen zu sein.
Human metapneumovirus (HMPV) is a negative-sense single-stranded RNA virus of the family Pneumoviridae[1] and is closely related to the Avian metapneumovirus (AMPV) subgroup C. It was isolated for the first time in 2001 in the Netherlands by using the RAP-PCR (RNA arbitrarily primed PCR) technique for identification of unknown viruses growing in cultured cells.[2] It is the second most common cause after Respiratory syncytial virus (RSV) of lower respiratory infection in young children.
The peak age of hospitalization for infants with HMPV occurs between 6–12 months of age, slightly older than the peak of RSV, which is around 2–3 months. The clinical features and severity of HMPV are similar to those of RSV. HMPV is also an important cause of disease in older adults.
Human metapneumovirus was first discovered in 2001 in the Netherlands by Bernadette G. van den Hoogen and her colleagues.[4][5][6][7] 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.[4] 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.[4] It was this close relationship to AMPV that gave rise to this new virus being named human metapneumovirus[4] to reflect both its identity as a metapneumovirus and its use of humans as a host organism.
HMPV is associated with 5% to 40% of respiratory tract infections in hospitalized and outpatient children.[8][9] The virus is distributed worldwide and, in temperate regions, has a seasonal distribution generally following that of RSV and influenza virus during late winter and spring.[8][10] Serologic studies have shown that by the age of five, virtually all children worldwide have been exposed to the virus.[2][11][12][13] Despite near universal infection during early life, reinfections are common in older children and adults.[8][14][12][15] Human metapneumovirus may cause mild upper respiratory tract infection (the common cold). However, premature infants,[16] immunocompromised persons,[17][18][19][20] and older adults>65 years [15][21][22] are at risk for severe disease and hospitalization. In some studies of hospitalizations and emergency room visits, HMPV is nearly as common and as severe as influenza in older adults.[15][21][22][23] HMPV is associated with more severe disease in people with asthma[24][25][26][27] and adults with chronic obstructive pulmonary disease (COPD).[28][29][30] Numerous outbreaks of HMPV have been reported in long-term care facilities for children and adults, causing fatalities.[31][32][33][34][35]
The genomic organisation of HMPV is similar to RSV; however, HMPV lacks the non-structural genes, NS1 and NS2, and the HMPV antisense RNA genome contains eight open reading frames in slightly different gene order than RSV (viz. 3’-N-P-M-F-M2-SH-G-L-5’).[36] HMPV is genetically similar to the avian metapneumoviruses A, B and in particular type C. Phylogenetic analysis of HMPV has demonstrated the existence of two main genetic lineages termed subtype A and B containing within them the subgroups A1/A2 and B1/B2 respectively. Genotyping based on sequences of the F and G genes showed that subtype B was associated with increased cough duration and increased general respiratory systems compared to HMPV-A.[37]
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.[5] 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 epithelial cells of the respiratory tract, using the G protein.[7][38] This G protein contains a hydrophobic region that acts as an uncleaved signal peptide and a membrane anchor to facilitate its binding; however, because recombinant viruses that lack the G protein have still been able to replicate in vitro and in vivo, it seems that attachment via the G protein is not required for rest of the replication cycle.[7]
Next in the cycle is the fusion of the viral and host membranes which is likely mediated by the F protein.[7][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.[7][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.[7] 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] Though we are unsure of its specific function, 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 ribonucleoprotein (RNP) containing negative-sense viral RNA (vRNA) genome is released into the cytoplasm and acts as a template for mRNA and antigenomic cRNA synthesis.[7] From here, most of our knowledge about hMPV transcription is derived from what we already know about RSV and other Paramyxoviridae viruses, including that leader and trailer sequences in the genome are partially complementary and act as promoters for transcription.[7] We see that proteins N, P, and L dissociate from the vRNA and bind to each other to form the polymerase complex so that the genomic RNA can act as a matrix for viral transcription and replication in the cytoplasm.[38] The final step in the replication process of hMPV we are relatively sure of is the journeying of the envelope glycoproteins (F, G, and SH) to zones of membranous accumulation via the Golgi apparatus to be exposed at the surface of infected cells.[38] This allows infected cells to merge with adjacent cells through the action of viral fusion proteins on the surface, effectively spreading the virus’s genome.[38] As of now, the rest of the replication cycle following RNA and viral protein synthesis are unclear and require further research.[7]
HMPV infects airway epithelial cells in the nose and lung. HMPV is thought to attach to the target cell via the glycoprotein (G) protein interactions with heparan sulfate and other glycosaminoglycans. The HMPV fusion (F) protein encodes an RGD (Arg-Gly-Asp) motif that engages RGD-binding integrins as cellular receptors,[39][40][41][42] then mediates fusion of the cell membrane and viral envelope in a pH-independent fashion, likely within endosomes.[43][44]
The identification of HMPV has predominantly relied on reverse-transcriptase polymerase chain reaction (RT-PCR) technology to amplify directly from RNA extracted from respiratory specimens. Alternative more cost-effective approaches to the detection of HMPV by nucleic acid-based approaches have been employed and these include:
Though hMPV was first discovered and identified in 2001, serological studies showed that hMPV, or a close relative of it, had already been circulating for at least 50 years.[4][45] From this information, it is clear that the virus had not just “jumped” from birds, or some other animal reservoir, to humans shortly before its discovery.[4]
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[45] and its distribution is very complex and dynamic.[4] 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.[4] 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.[4] 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,[4] 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.[45]
We suspect that 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.[5] We have yet to develop a reliable antiviral therapy treatment or vaccine to prevent the spread of hMPV, but there do seem to be promising developments in that area.[4][5] In some vaccine trials, researchers have observed how a live recombinant human parainfluenza virus that contains the hMPV F gene can induce hMPV-specific antibodies and can protect experimental animals from hMPV.[4] Another similar study demonstrated how a chimeric bovine/human parainfluenza virus 3 expressing the hMPV F gene allows for neutralizing antibodies against both parainfluenza and hMPV.[4] However promising these results and trials may seem, it is important to note that these experiments have limitations including their small-population animal models.[4] Overall, while vaccines and antiviral therapy treatments are in the works, the biggest difficulty that researchers face at the moment is the limited data available about the development of hMPV in the natural host.[4]
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.[46] HMPV has been shown to circulate during fall and winter months with alternating predominance of a single subtype each year.[37]
No treatment is yet known,[47] but ribavirin has shown effectiveness in an animal model.[48]
American pharmaceutical corporation Moderna has conducted a clinical trial for a candidate modRNA vaccine against metapneumovirus.[49] As of October 2019, the vaccine candidate has passed through phase I, with reports that the vaccine is well-tolerated at all dose levels at two months, and provokes an immune response which boosts the production of neutralising antibodies.[50]
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.[51]
Human metapneumovirus (HMPV) is a negative-sense single-stranded RNA virus of the family Pneumoviridae and is closely related to the Avian metapneumovirus (AMPV) subgroup C. It was isolated for the first time in 2001 in the Netherlands by using the RAP-PCR (RNA arbitrarily primed PCR) technique for identification of unknown viruses growing in cultured cells. It is the second most common cause after Respiratory syncytial virus (RSV) of lower respiratory infection in young children.
The peak age of hospitalization for infants with HMPV occurs between 6–12 months of age, slightly older than the peak of RSV, which is around 2–3 months. The clinical features and severity of HMPV are similar to those of RSV. HMPV is also an important cause of disease in older adults.
El metapneumovirus humano es un virus ARN de la familia Paramyxoviridae, género metapneumovirus. Puede provocar enfermedad respiratoria de gravedad variable, sobre todo en niños. Se diagnostica mediante la reacción en cadena de la polimerasa o cultivo celular.[1] Está emparentado con el metapneumovirus aviar que causa enfermedad de vías respiratorias en aves.[2]
Fue descubierto en Países Bajos, en el año 2001.
El metapneumovirus humano suele causar enfermedad respiratoria de carácter leve, sin embargo los niños pequeños, ancianos y personas con inmunodeficiencia pueden presentar complicaciones severas, como neumonía y precisar hospitalización.
El ser humano es el único huésped conocido del metapneumovirus humano. Se transmite de una persona a otra mediante la inhalación de pequeñas gotas provenientes de las secreciones respiratorias. Se encuentra extendido por todo el mundo.
Datos: Q743338
Especies: Human metapneumovirus
El metapneumovirus humano es un virus ARN de la familia Paramyxoviridae, género metapneumovirus. Puede provocar enfermedad respiratoria de gravedad variable, sobre todo en niños. Se diagnostica mediante la reacción en cadena de la polimerasa o cultivo celular. Está emparentado con el metapneumovirus aviar que causa enfermedad de vías respiratorias en aves.
O Metapneumovírus humano (hMPV) é um RNA vírus da família Paramyxoviridae e está estreitamente aparentado com o metapneumovírus das aves (aMPV). Foi isolado em 2001 na Holanda.[1] É um dos vírus mais frequentes das infeções do trato respiratório nas crianças, depois do virus sincicial respiratório.
O Metapneumovírus humano (hMPV) é um RNA vírus da família Paramyxoviridae e está estreitamente aparentado com o metapneumovírus das aves (aMPV). Foi isolado em 2001 na Holanda. É um dos vírus mais frequentes das infeções do trato respiratório nas crianças, depois do virus sincicial respiratório.
Človeški metapnevmovirus (hMPV) je enovijačni virus RNK iz družine paramiksovirusov in je soroden ptičjemu metapnevmovirusu. Virus so prvič odkrili leta 2001 na Nizozemskem. Vzrok razmeroma poznega odkritja je verjetno slabo in počasno razmnoževanje na celičnih kulturah, uporabljenih za diagnostiko drugih respiratornih virusov, ter posebne zahteve za gojenje.
Od odkritja hMPV pa do danes je bil virus opisan po vsem svetu kot eden izmed pomembnejših povzročiteljev okužb dihal pri ljudeh vseh starosti in naj bi povzročil od 4-16 % vseh okužb dihal. Izbruhi okužb potekajo sezonsko v spomladanskih in zimskih mesecih, tj. na severni polobli od januarja do marca ter na južni polobli od junija do julija.
Klinična slika okužbe s hMPV je zelo podobna okužbi z respiratornim sincicijskim virusom (RSV), zaradi česar je bil hMPV morda tudi spregledan. Tako se pogosto kaže kot blaga okužba zgornjih dihal, vendar lahko povzroči nevarno okužbo spodnjih dihal, kot sta bronhiolitis in pljučnica. hMPV povzroči od 5-10 % hospitalizacij otrok zaradi akutnih okužb dihal. Prevladujejo predvsem dojenčki, mlajši od 6 mesecev. Približno 40 % vseh hospitaliziranih otrok ima določen dejavnik tveganja za okužbo, kot so astma in ostale kronične bolezni dihal. Poleg tega lahko pride do naknadne okužbe, ki se pojavi po prvotni okužbi z drugim virusom ali bakterijo; najbolj nevarna naj bi bila naknadna okužba po okužbi z RSV-jem. Poleg otrok sta ogroženi skupini še starejši ljudje, še posebej v primeru kronične obstruktivne pljučne bolezni (KOPB), ter bolniki z oslabljenim imunskim sistemom, kot so bolniki na imunosupresivnem zdravljenju in bolniki z obolenjem krvotvornih organov (npr. z levkemijo).
Najobičajnejša preiskava je dokaz virusa s pomočjo verižne reakcije s polimerazo (PCR), čeprav se lahko uporabi posebne celične kulture. Zdravljenje je v glavnem podporno, npr. z uporabo dodatnega kisika, vendar nekatere raziskave nakazujejo možnost zdravljenja s protivirusnimi zdravili, kot je ribavirin, ter preventive s cepljenjem.
Človeški metapnevmovirus (hMPV) je enovijačni virus RNK iz družine paramiksovirusov in je soroden ptičjemu metapnevmovirusu. Virus so prvič odkrili leta 2001 na Nizozemskem. Vzrok razmeroma poznega odkritja je verjetno slabo in počasno razmnoževanje na celičnih kulturah, uporabljenih za diagnostiko drugih respiratornih virusov, ter posebne zahteve za gojenje.
Od odkritja hMPV pa do danes je bil virus opisan po vsem svetu kot eden izmed pomembnejših povzročiteljev okužb dihal pri ljudeh vseh starosti in naj bi povzročil od 4-16 % vseh okužb dihal. Izbruhi okužb potekajo sezonsko v spomladanskih in zimskih mesecih, tj. na severni polobli od januarja do marca ter na južni polobli od junija do julija.
Klinična slika okužbe s hMPV je zelo podobna okužbi z respiratornim sincicijskim virusom (RSV), zaradi česar je bil hMPV morda tudi spregledan. Tako se pogosto kaže kot blaga okužba zgornjih dihal, vendar lahko povzroči nevarno okužbo spodnjih dihal, kot sta bronhiolitis in pljučnica. hMPV povzroči od 5-10 % hospitalizacij otrok zaradi akutnih okužb dihal. Prevladujejo predvsem dojenčki, mlajši od 6 mesecev. Približno 40 % vseh hospitaliziranih otrok ima določen dejavnik tveganja za okužbo, kot so astma in ostale kronične bolezni dihal. Poleg tega lahko pride do naknadne okužbe, ki se pojavi po prvotni okužbi z drugim virusom ali bakterijo; najbolj nevarna naj bi bila naknadna okužba po okužbi z RSV-jem. Poleg otrok sta ogroženi skupini še starejši ljudje, še posebej v primeru kronične obstruktivne pljučne bolezni (KOPB), ter bolniki z oslabljenim imunskim sistemom, kot so bolniki na imunosupresivnem zdravljenju in bolniki z obolenjem krvotvornih organov (npr. z levkemijo).
Najobičajnejša preiskava je dokaz virusa s pomočjo verižne reakcije s polimerazo (PCR), čeprav se lahko uporabi posebne celične kulture. Zdravljenje je v glavnem podporno, npr. z uporabo dodatnega kisika, vendar nekatere raziskave nakazujejo možnost zdravljenja s protivirusnimi zdravili, kot je ribavirin, ter preventive s cepljenjem.
人類偏肺病毒（hMPV）是副黏液病毒科下的一種單鏈核糖核酸病毒，於2001年在荷蘭被首度發現。病毒主要令兒童受急性呼吸道感染，病徵包括發燒、咳嗽、氣促及呼吸困難等。抵抗力弱的成年人也有機會受感染。
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사람 메타뉴모바이러스(human metapneumovirus, hMPV)는 뉴모바이러스과에 속하는 음성 단일가닥 RNA 바이러스이다.[1] 조류 메타뉴모바이러스 C형과 계통학적으로 매우 밀접하다. 2001년에 네덜란드에서 RAP-PCR(RNA Arbitrarily Primed -)기술을 통해 처음으로 분리되었다.[2] 근래에 유아의 호흡기 세포융합 바이러스 감염이 감소함에 따라 현재 유아 급성 호흡기 감염에 있어서 두 번째로 흔한 감염원이다.
hMPV는 2개월에서 3개월 사이의 유아에게서 피크를 찍는 호흡기 세포융합 바이러스보다 살짝 늦은 6개월에서 12개월 사이의 유아에게서 피크를 찍는다. 호흡기 세포융합 바이러스와 hMPV의 위험성과 의료적 증상은 서로 유사하다. 노인 역시 hMPV에 취약한 대상이다.
*모식종
어린이 입원환자 및 외래환자의 기도 감염 원인에서 hMPV는 6%에서 40%를 차지한다.[4][5][6][7][8][9][10][11][12][13] 전세계적으로 퍼져있으며, 온대지방에서는 늦겨울에서 봄 사이에 호흡기 세포융합 바이러스, 인플루엔자와 함께 계절성 바이러스로 따라온다.[4][14][15] 또한 5세 이하의 어린이의 대부분이 이 바이러스에 노출되어있음이 혈청학 연구로 밝혀졌다.[2][16][17][18][19][20][21] 이처럼 거의 모든 사람이 어린 시절에 이 바이러스에 감염되지만, 이후에 다시 이 바이러스에 재감염되는 일이 빈번하게 일어난다.[4][22][20][23]
인간 메타뉴모바이러스로 인해 야기되는 대표적 질병은 감기(상부 기도 감염)이다. 그러나 미숙아,[24] 65세 이상의 노인,[23][25][26] 면역결핍 환자의[27][28][29][30] 경우 감기보다 더 치명적인 질병이 걸려 입원환자로 전환되는 경우가 있다. 노인에게 hMPV가 인플루엔자만큼 치명적인 바이러스로 작용함이 입원환자와 응급실 방문환자를 대상으로 한 연구를 통해 밝혀졌다.[23][25][26][31] 또한 천식 환자나[32][33][34][35] 만성 폐쇄성 폐질환[36][37][38] 환자의 경우 hMPV 감염은 더욱 치명적일 수 있다. 장기 간호시설의 환자들 사이에서 hMPV가 급증해 사망자가 발생한 사례가 다수 있다.[39][40][41][42][43] 2020년 일본 아와시의 한 노인시설에서는 17명의 hMPV환자가 발생해 5명이 사망했다.[44]
hMPV의 유전체 구조는 호흡기 세포융합 바이러스와 유사하나 몇 가지 차이점이 존재한다. 첫째로 hMPV에는 비구조유전자 NS1, NS2가 존재하지 않으며, 둘째로 hMPV의 안티센스 RNA 유전체에 있는 8개의 오픈 리딩 프레임이 호흡기 세포융합 바이러스의 3’-N-P-M-F-M2-SH-G-L-5’과는 다르다.[45] 이보다는 조류 메타뉴모바이러스와 훨씬 유사하며, 특히 조류 메타뉴모바이러스 C와 유사하다. 계통학적 분석을 통해 hMPV에 소분류로 A와 B가 존재하며, 각각은 또 A1/A2와 B1/B2의 아류형으로 구성됨이 밝혀졌다.
hMPV는 코와 허파의 상피세포를 감염시키는데, 당단백질을 통해 헤파란황산염 및 글리코사미노글리칸과 반응하여 세포막에 부착할 것으로 추측된다. 또한 hMPV의 융합 단백질에 있는 아르기닌-글라이신-아스파라긴(RGD) 모티프가 인테그린을 세포 수용체삼아[46][47][48][49] 바이러스가 세포 내부에 엔도솜의 형태로 침투할 수 있도록 한다.[50][51]
hMPV는 역전사 중합효소 연쇄반응(RT-PCR)을 통해 호흡기 표본으로부터 RNA를 증폭하여 검출한다. 이외에도 핵산을 이용해서 저렴하게 검출할 수 있는데, 구체적인 방법은 다음과 같다.
전염 경로가 완전히 밝혀지지는 않았으나, 감염된 분비물, 비말, 에어로졸, 혹은 매개물을 통해 전염될 것으로 여겨진다. 병원에서 hMPV에 감염된 사례도 보고되었다.[52]
아직 뚜렷한 치료법이 개발되지 않았으나,[53] 모형동물에서는 리바비린이 효과를 보인다.[54]
조류 메타뉴모바이러스가 1970년대에 보고된 것에 비해, hMPV는 2001년이 되어서야 알려졌다. 베이즈 추론법에 의하면 hMPV는 대략 1800년대에 조류 메타뉴모바이러스에서 분리되었으며 궁극적으로는 119년에서 133년 전에 발생한 것으로 보인다.[55]
|date= (도움말) 사람 메타뉴모바이러스(human metapneumovirus, hMPV)는 뉴모바이러스과에 속하는 음성 단일가닥 RNA 바이러스이다. 조류 메타뉴모바이러스 C형과 계통학적으로 매우 밀접하다. 2001년에 네덜란드에서 RAP-PCR(RNA Arbitrarily Primed -)기술을 통해 처음으로 분리되었다. 근래에 유아의 호흡기 세포융합 바이러스 감염이 감소함에 따라 현재 유아 급성 호흡기 감염에 있어서 두 번째로 흔한 감염원이다.
hMPV는 2개월에서 3개월 사이의 유아에게서 피크를 찍는 호흡기 세포융합 바이러스보다 살짝 늦은 6개월에서 12개월 사이의 유아에게서 피크를 찍는다. 호흡기 세포융합 바이러스와 hMPV의 위험성과 의료적 증상은 서로 유사하다. 노인 역시 hMPV에 취약한 대상이다.
