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Respiratory Syncytial Virus (A and B)

Virology

Structure of RSV. Fig.1 Structure of RSV. (Bianchini, 2020)

Respiratory syncytial virus (RSV) was first isolated in 1955 from chimpanzees suffering from respiratory illness. It is a non-segmented, negative-sense, single-stranded, enveloped RNA virus. Structurally, the human respiratory syncytial virus is an enveloped, spherical virus with a medium size (120-300 nm diameter). In addition, filamentous species capable of reaching several micrometers in length have also been observed. Like the spherical forms, the filamentous virions are infectious. The RSV genome is 15.2 kb and contains 10 genes encoding 11 proteins: two non-structural (NS1 and NS2) and nine structural proteins (N, P, M, SH, G, F, M2-1, M2-2 and L). RSV has two subtypes, A and B, that are distinguished largely by differences in the viral attachment (G) protein or the nuclear (N) protein. During epidemics, either subtype A or B may predominate, or both subtypes may circulate concurrently.

Epidemiology

RSV outbreaks occur, in moderate climates, in winter/early spring months, and are annual midwinter epidemics. However, RSV circulates throughout longer seasonality in tropical regions. Generally, one of the two genotypes (A and B) predominates in a single season, and they alternate or co-circulate annually, although regional variation occurs. The majority of those who are hospitalized with RSV are infants and toddlers. However, adults with comorbidities and the elderly are also at increased risk from RSV infection. Worldwide, it is estimated that RSV is responsible for approximately 33 million lower respiratory tract illnesses, three million hospitalizations, and up to 199,000 childhood deaths.

Pathogenesis

RSV transmission occurs via air. Once RSV enters the nostrils or mouth, it begins to infect airway epithelial cells (AECs) of the upper respiratory system. RSV binds to cellular receptors using the RSV-G glycoprotein, then uses the RSV-F fusion glycoprotein to fuse with host cell membranes and insert its nucleocapsid into the host cell to begin its intracellular replication. Then, RSV moves down to the lower respiratory system, and reaching the bronchioles where viral replication is more effective. Specifically, ciliated cells in the bronchial epithelia and type 1 pneumocytes in the alveolus, are the main cells targeted by RSV infection, which results mainly in superficial damage to the airway lining. This damage to the airway predisposes the patient to secondary bacterial infections.

Model of RSV pathogenesis in the human respiratory tract. Fig.2 Model of RSV pathogenesis in the human respiratory tract. (Carvajal, 2019)

Symptoms

The clinical manifestations of the pathology caused by human RSV are common to other respiratory viral infections. RSV infection is not clinically distinguishable from other respiratory viruses. The clinical presentation of RSV varies from asymptomatic carriage through cold-like symptoms to acute respiratory distress. RSV clinical manifestation ranges widely from mild upper respiratory infections to severe lower respiratory tract infections (LRTI), mainly bronchiolitis and pneumonia, leading to hospitalization, serious complications (such as respiratory failure) and relevant sequelae in childhood and adulthood (i.e., wheezing, asthma, and hyperreactive airways). The first symptoms of infection are rhinitis, cough, fever, and nasal congestion. The severity of the illness is due both to host and viral factors.

Prophylaxis and Treatment

  • Treatment. Once the disease has occurred, no effective treatment is available for preventing the disease, and only supportive treatment is available. In supportive treatment, corticosteroids, bronchodilators and oxygen supplements are effective to some extent. There are currently only two antivirals for RSV available, palivizumab for prevention and ribavirin for treatment. While many side-effects, such as anemia, lead towards the limited use of ribavirin in RSV treatment. It is necessary to discover the new treatment as well as prophylactic policies.
  • Vaccines. Vaccine development for RSV has been ongoing for over 50 years. At present, there is no approved vaccine is present in the market which can protect from RSV infection. There are currently several recombinant RSV subunit vaccines in clinical trials.

Clinical and laboratory diagnostic tests and assays all need anti-RSV antibodies with high specificity. Based on world-leading technology and antibody platforms, Creative Biolabs is committed to providing a series of ViroAntibody services. We can provide antibodies specifically targeting the RSV or their N protein, M2-1, M2-2 protein, G protein, etc. Our scientists are confident in providing our customers with the most reliable and cost-effective ViroAntibody to facilitate their valuable viral disease research and project development. If you are interested in our antibodies, please feel free to contact us.

References

  1. Bianchini, S.; et al. Role of Respiratory Syncytial Virus in Pediatric Pneumonia. Microorganisms. 2020, 8(12).
  2. Carvajal, J.J.; et al. Host Components Contributing to Respiratory Syncytial Virus Pathogenesis. Front Immunol. 2019, 10: 2152.

All products and services are intended for Research Use Only, and NOT to be used in diagnostic or therapeutic procedures.

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