MicrobiologyBytes: Virology: Paramyxoviruses Updated: December 7, 2009 Search


Group V: (-)sense RNA Viruses
Order Mononegavirales
Type Species
Bornaviridae Bornavirus Borna disease virus Vertebrates
Filoviridae Marburg-like viruses Marburg virus Vertebrates
Ebola-like viruses Ebola virus Vertebrates


Avulavirus Newcastle disease virus Vertebrates
Henipavirus Hendra virus Vertebrates
Morbillivirus Measles virus Vertebrates
Respirovirus Sendai virus Vertebrates
Rubulavirus Mumps virus Vertebrates
Pneumovirus Human respiratory syncytial virus Vertebrates
Metapneumovirus Avian pneumovirus Vertebrates

Parainfluenzaviruses and RSV produce acute respiratory diseases (c.f. influenza), morbilliviruses and mumps systemic disease = diversity! They also differ from Orthomyxoviruses genetically - non-segmented genome with little genetic variation (c.f. influenza).


Glycoproteins - do not form such prominent spikes as on influenza virus:

HN - haemagglutinin + neuraminidase activities;
Measles - referred to as H protein - no neuraminidase activity;
RSV - G protein - neither activity.

F - consists of 2 disulphide-linked subunits (F1 + F2) - responsible for cell fusion + haemolytic function.

Other proteins:
The M (matrix) protein lines the inner surface of the envelope.
- nucleoprotein.
and P - polymerase activity

Paramyxovirus particle

To view a negatively-stained electron micrograph of paramyxovirus particles, click here.


Non-segmented (-)sense RNA, 17-20kb. The linear arrangement of genes (6) are separated by repeated sequences, a polyadenylation signal at the end of the gene, the intergenic sequence GAA followed by a translation start signal at the beginning of the next gene.

Paramyxovirus gene expression


Very similar for all viruses in this group. Unlike influenza, all the action occurs in the cytoplasm. However, the overall strategy very similar to influenza, although unlike influenza, Paramyxovirus replication is resistant to actinomycin D.

Paramyxovirus replication


A large excess of nucleocapsids are produced in infected cells, which form characteristic cytoplasmic inclusion bodies. Syncytium formation is quite common (F glycoprotein).

Paramyxovirus genome replication


Parainfluenzaviruses 1-4:

Cause acute respiratory infections of man ranging from relatively mild influenza-like illness to bronchitis, croup (narrowing of airways which can result in respiratory distress) and pneumonia; common infection of children. Transmitted by aerosols, virus is usually limited to U.R.T. (no viraemia). Infections of L.R.T. (e.g. in very young children) lead to more serious symptoms. Little serological variation, therefore rare infection in adults.


Recognized by the ancient Greeks, virus first isolated in 1934. Haemagglutination is a valuable assay technique for this virus. Humans are believed to be the only natural reservoir for the virus (possibly primates). Transmission via saliva and respiratory secretions; less infectious than measles/chickenpox - more adult cases.

Symptoms: typically causes painful swelling of parotid glands 16-18 days after infection. This is preceded by primary replication of the virus in epithelial cells of the URT and local lymph nodes, followed by viraemia. In children, mumps is usually self-limited, but in adults (post-puberty) a proportion of cases have more serious sequalae: orchitis (20-30% of males - rarely resulting in sterility); meningitis, encephalitis, pancreatitis, myocarditis, nephritis - <1% adult cases.

Treatment: none (passive immunization has been used).

Mumps virus

Prevention: one invariant serotype therefore vaccines are viable - both formalin-inactivated and live attenuated exist, the latter now being widely used- see below (MMR). Read: MMR vaccine & autism.


Measles virus

Measles virus is believed to have evolved from rinderpest (or a similar animal virus) 4000-5000 years ago - when Babylonian cities grew large enough to support continuous person-to-person transmission and thus maintain the virus. An example of this is phocine (seal) distemper. In the Arctic Sea, seal populations are large/dense enough to maintain the virus, which is sometimes exported to the Baltic/North Sea. Here, it burns itself out and disappears again after an epidemic, since host seal populations are not large enough to maintain it: Devastating seal virus. Dhiman N, et al. (2004) Measles virus receptors: SLAM and CD46. Rev Med Virol. 14: 217-229.

One of the most infectious diseases known! ~500,000 deaths p.a. in children in the third world - part of the W.H.O. expanded programme of immunization (Global Measles Mortality, 2000-2008. MMWR 009 58(47): 1321-1326). Childhood infection almost universal, protection resulting from this is probably lifelong. Both man and wild monkeys are commonly infected, but the virus can also infect rodents (in wild?). In culture, produces characteristic intranuclear inclusion bodies and syncytial giant cells. Transmission and initial stages of disease similar to mumps, but this virus can also infect via the eye and multiply in the conjunctivae. Viraemia following primary local multiplication results in widespread distribution to many organs.

Symptoms: After a 10-12 day incubation period, dry cough, sore throat, conjunctivitis (virus may be excreted during this phase!), followed a few days later by the characteristic red, maculopapular rash and Koplik's spots - raised red spots with white centres in the mouth. Towards the end of the disease, there is extensive, generalized virus infection in lymphoid tissues and skin.
Complications include bronchopneumonia and otitis media (with or without secondary bacterial infections) (relatively common), and encephalitis (~1:2000 cases).
Subacute schlerosing pan encephalitis (SSPE) results from a rare (~1 : 3x105 cases of measles), chronic infection in which the virus multiplies in the brain with the expression of a limited repertoire of virus genes, resulting in neurodegenerative disease. Rima BK, Paul Duprex W. Molecular mechanisms of measles virus persistence. Virus Res, 2005.
Several recent reports have suggested that measles infection before full immunological competence (e.g. younger then 2 years) may be linked to ulcerative colitis and Crohn's disease. This idea is plausible since measles virus can infect and persist in endothelial cells in the gastrointestinal tract and cause an immune response with giant cell formation. However, more evidence needs to be obtained before this can be verified.

Treatment: None

Prevention: Both live and killed vaccines exist. Vaccination with the live attenuated vaccine has been practised in the US since the 1960's with a dramatic decline in the incidence of the disease, but has only been used more recently in the UK. Trivalent live attenuated vaccine (MMR) usually given - all of these viruses best avoided during pregnancy! The present WHO target for eradication of measles is the year 2015.



Bestsellers - Music - DVDs - Videos - Electronics
Search for ... (keywords):
Search for ... (keywords):

Bestsellers - Music - DVDs - Videos - Electronics


Respiratory syncytial virus (RSV):

RSV was first isolated in 1956 and subsequently recognized as a major cause of L.R.T. disease in infants and young children. Shows typical seasonal peak of respiratory virus infections. RSV infects man, monkeys and some rodents with disease production, but inapparent infections (resulting in spread of virus) may occur in many mammals. In culture, causes characteristic syncytial masses - hence the name.

RSV is highly infectious, transmission by respiratory secretions. Causes 100,000 hospitalizations and up to 4,500 deaths per year in the USA. Primary multiplication occurs in epithelial cells of URT producing a mild illness. In ~50% children less than 8 months old, virus subsequently spreads into the L.R.T. causing bronchitis, pneumonia and croup. RVS has been suggested as a possible factor in cot death and asthma.


Mumps virus

RSV may be linked to epidemics of asthma and has been identified as an exacerbating factor in nephrotic disease, cystic fibrosis, and opportunistic infections in the immunocompromised. Bone marrow transplant patients develop lower respiratory tract disease with RSV, which carries a mortality of up to 50%. RSV infection in the elderly causes up to 14% of community-acquired pneumonia, especially in those with underlying cardiopulmonary disease. Children who have been hospitalized in infancy with respiratory syncytial virus (RSV) bronchiolitis are at significantly increased risk of asthma and allergy by the time they reach the age of 13 years (Sigurs N, et al. Severe respiratory syncytial virus bronchiolitis in infancy and asthma and allergy at age 13. Am J Respir Crit Care Med. 2005 171: 137-141).

Prevention:  Currently no effective vaccine! Also, infection does not result in lasting protection (c.f. mumps, measles) therefore repeated infections ('colds') occur throughout life - usually without serious consequences in adults. Ribavirin has some activity against L.R.T. RSV infections.

Respiratory Syncytial Virus (RSV): Overview, Treatment, and Prevention Strategies


Human Metapneumovirus (HMPV):

HMPV was first isolated from children in the Netherlands and assigned to the pneumovirus genus on the basis of clinical data, sequence homology and gene organization (A Newly Discovered Human Pneumovirus Isolated From Young Children With Respiratory Tract Disease. van den Hoogen BG, et al. Nat Med. 7: 719-724, 2001). HMPV produces RSV-like illnesses in children, ranging from upper respiratory tract disease to severe bronchiolitis and pneumonia. Serological studies showed that by the age of five years, virtually all children have been exposed to HMPV and that the virus has been circulating in humans for at least 50 years. In the UK, ~2% of non-hospitaized patients with a respiratory infection are positive for HMPV (Stockton J, et al. Human metapneumovirus as a cause of community-acquired respiratory illness. Emerg Infect Dis. 2002;8:897-90). All recent data suggests that hMPV infections are not limited to young children or to the upper respiratory tract and that this virus causes severe lower respiratory tract diseases in high-risk subjects. However, although a frequent cause of hospitalization in young children, HPMV infections may be less severe then those caused by RSV and influenza A (Boivin et al. Human metapneumovirus infections in hospitalized children. Emerg Infect Dis. 2003 9:634-40).

HMPV: Latest News

Nipah and Hendra Viruses:

Nipah and Hendra viruses have emerged as new pathogens in Malaysia and Australia respectively in recent years:
Nipah virus

© MicrobiologyBytes 2009.