Human respiratory syncytial virus (HRSV) is the most common viral agent of lower respiratory tract infection in children. The virus was first discovered in 1956 from a chimpanzee suffering from coryza and was known as chimpanzee coryza agent. Later it was discovered from infants with respiratory illness and was named respiratory syncytial virus (RSV).

According to the recent ICTV classification, HRSV has been renamed “human orthopneumovirus” and belongs to the genus Orthopneumovirus of family Pneumoviridae.

Morphology of HRSV and HMPV (human metapneumovirus) is similar to human respiroviruses and human rubulaviruses with some important differences in the surface proteins.

RSV and HMPV have three surface glycoproteins projected from the virus envelop—G, F and SH.

Attachment Protein (G)

 • G protein is responsible for attachment of the virus with the host cell.

• There is no structural similarity or sequence homology with corresponding H or HN proteins of other paramyxoviruses.

 • G protein is most variable of all the proteins.

• The variability of G protein is the basis of phylogenetic classification within the species.

Fusion (F) Protein

F protein is structurally similar to F protein of other members of Paramyxoviridae but with limited amino acid similarity. It is synthesized in inactive F0 form which gets cleaved by peptidase to F1 and F2.

It is responsible for fusion of virus membrane with plasma membrane of host cell as described for HPIVs.

Short Hydrophobic (SH) Protein

This is the third transmembrane protein present on the virus surface. The exact function of SH protein is still not known. It has been implicated in impairing the Th1 mediated host antiviral response.

Genetic Diversity

 HRSV has single serotype and two antigenic groups: A and B. The division of two antigenic groups is based on the neutralization with hyperimmune serum and monoclonal antibodies. The two groups can also be differentiated on the basis of nucleotide sequence identity. The difference between the two groups is mainly due to the difference in their G protein which is around 47% amino acid identity difference between the prototype of each group.

F protein has 50% antigenic relatedness between subgroups as compared to 1–7% for G protein.

F protein shows equal protectiveness against both the subgroups, whereas G protein is 13-fold less effective against the heterologous antigenic group.

Genotypes of RSV are classified according to the phylogenetic clustering of G protein gene sequences. Presently there are 8 genotypes within the subgroup A and 11 genotypes within the subgroup B. However, with time, the G protein undergoes so much of sequence variation that the existing classification system gets changed with new genotypes being added.

EPIDEMIOLOGY

 Disease Burden

The global RSV disease burden has been estimated as 64 million cases and 160,000 deaths every year. In a worldwide estimate, it was estimated that 33.8 million new episodes of RSV associated acute lower respiratory tract infection (ALRI) occur worldwide in children below 5 years of age and 66000–199000 RSV associated deaths in children <5 years. In a hospitalized study in India, RSV has been detected in around 17% children.

Primary infection of RSV occurs most commonly during the first year of life (near 70%) and by 24 months age >95% children have been found to be infected with RSV.

Modes of Transmission

• RSV is mostly transmitted by large infected droplets than aerosols.

• The infectivity of the virus remains for a long time in the inanimate environment. This facilitates the transmission of infection through infected fomites.

Seasonality

• In temperate climate seasonal peak of RSV is seen during winter months.

• In tropical and subtropical countries north to equator, RSV peaks are observed during rainy season.

• In Hong Kong, peak activity has been reported during spring and summer months.

• In South America and South Africa, during cold dry months.

• In India, RSV season is mostly observed during fall and winter.

• Thus in general, HRSV activity is observed mainly in two different temperature range—2–4°C and 24–30°C.

Reinfection

 • Reinfection with RSV occurs throughout life. Reinfection can occur even during the same epidemic season.

• Reinfection occurs more commonly due to heterologous antigenic group but can also occur due to the same antigenic group.

 • Repeated infection indicates the ability of RSV to infect even in the presence of preexisting antibodies.

• With repeated infection, the severity becomes less with less risk of developing lower respiratory illness.

Host factors for severe HRSV disease: HRSV is known to cause severe lower respiratory tract illness in the following high-risk group of individuals leading to reduction of pulmonary function, more number of hospitalization and higher mortality.

• Individuals with underlying cardiac or lung disease.

• Elderly individuals with >65 years age.

• Immunocompromised individuals: Patients with T cell deficiency, severe combined immunodeficiency disease (SCID), hematological malignancies, hematological stem cell transplant recipients.

• Children with cystic fibrosis.

Molecular Epidemiology

 Circulation of multiple strains is commonly seen in any given year with predominance of a few genotypes with predominance of either A or B antigenic group. The predominant strain pattern is different in different geographic locations. Replacement of predominant strain usually occurs in every 1–2 years with different strains. Though replacement of strains reflects the advantage of heterologous strains, reinfection with the same genotype is a common phenomenon with HRSV in contrast to influenza virus.

Introduction of new genotype from other geographic location often leads to epidemic.

Unlike influenza, global spread of infection due to new strain is not a common scenario with HRSV. Global spread of HRSV has been observed with a new genotype known as BA of antigenic group B. The unique feature of BA genotype is 60 nucleotide duplication in the G gene, which is thought to be responsible for the spread of the strain across the continents.

PATHOGENESIS

 Humans are the only natural host for HRSV. The incubation period is around 3–5 days. HRSV initially infects the nasopharynx, then spreads to the lower respiratory tract. This occurs most likely due to aspiration of virus in children. The peak virus titer in nasal secretion is around 104–106 infectious virus unit/mL. It apically infects the ciliated cells, inhibits the transport of Na+, resulting in accumulation of fluid in the apical surface. Secretion of mucus in the airways, sloughed epithelial cell debris and accumulation of neutrophils leads to blockage of bronchioles and alveoli. Airway mucus is the hallmark of RSV bronchiolitis. Both type I and type II alveolar cells can be infected by HRSV. In case of pneumonia, there is also infiltration of mononuclear cells leading to interalveolar wall thickening in addition to the accumulation of fluid in the alveolar space.

CLINICAL FEATURES

Rhinorrhea, cough and mild fever are the initial manifestations. This may progress to lower respiratory tract illness. Bronchiolitis and pneumonia are the two manifestations of HRSV infection. Cough, wheeze, poor feeding and breathlessness are the predominant symptoms. Tachypnea, inspiratory crackles and expiratory wheeze are the important findings on examination.

Symptoms are usually mild when infection occurs in the newborns, this could be due to the protective effect of maternal antibody.

ANTIVIRALS

Ribavirin: This is a nucleoside analog, acts as a broad-spectrum antiviral agent mostly against RNA viruses. Ribavirin has been used in severe respiratory viral infections, but the efficacy of the drug is inconclusive. The drug is presently recommended for HRSV infection in immunocompromised and children with significant cardiopulmonary abnormalities.

Palivizumab: This is a humanized mouse monoclonal antibody against the protective epitope of F protein of HRSV. It does not inhibit RSV infection, but reduces the clinical severity. It has been found 50–100% more effective than RSV intravenous immunoglobulin and safe in high-risk children. The drug is recommended in high-risk children like premature babies, children with underlying cardiopulmonary disease.

Motavizumab: It is a humanized monoclonal antibody, derived from palivizumab. The drug is more effective than palivizumab.

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مواضيع ذات صلة

Diagnosis of Respiratory Virus Infection

Human metapneumovirus (HMPV)

Chemical Composition of Viruses

Survey of RNA-Containing Viruses

Survey of DNA-Containing Virus Families

Universal System of Virus Taxonomy

Human parainfluenza viruses (HPIV)

Complications of Influenza virus

Influenza virus

Chikungunya virus

West Nile virus

Transmission Cycle of Japanese encephalitis virus