Human respiratory syncytial virus: Difference between revisions

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==Ecology==
==Ecology==
Habitat; symbiosis; contributions to the environment.
Respiratory Syncytial Virus is spread through person to person contact by infected respiratory secretions.  It requires the close contact of infected individuals, contact with infected nasal secretions, or contamination of hands or objects which have been introduced to such secretions.    Outbreaks of the disease occur at particular seasons yearly which usually last up to 5 months.  Epidemics usually occur in the late fall, winter or spring seasons, with most outbreaks in February or March.  RSV is commonly acquired by patients who are hospitalized and the likelihood of RSV infection increases with the duration of the stay.  The hospital staff plays a major role in the spread of RVS infection.  To reduce the risk of infection precautions must be in effect such as hand washing.


==Pathology==
==Pathology==

Revision as of 02:48, 16 December 2008

A Microbial Biorealm page on the genus Human respiratory syncytial virus

Classification

Higher order taxa

Viruses; ssRNA viruses; ssRNA negative-strand viruses; Mononegavirales; Paramyxoviridae; Pneumovirinae; Pneumovirus

Species

NCBI: Taxonomy

Genus species

Description and significance

Human Respiratory Syncytial Virus was first isolated in 1956 from a laboratory chimpanzee with a respiratory illness and was later discovered to be of human origin. RSV consists of two antigenic subtypes, A and B. Subtype B is characterized as the asymptomatic strains that of which the majority of individuals experiences. The more severeillnesses and which usually predominate during outbreaks are associated with subtype A strains. RSV was determined to be the leading cause of lower respiratory tract infections particularly in young infants. The severity of the disease is very diverse ranging from mild cold symptoms to severe and life-threatening. It's the leading cause of pneumonia and bronchiolitis in infants. It may cause mortality or morbidity in the elderly as well as immunodeficient individuals. It is the most common pathogen leading to hospitalization in young children up to the age of 5. Approximately two thirds of infants are infected with RSV within their first year and 90% have been infected by the age of 2.

Genome Structure and Virion Structure

The genome of RSV was completely sequenced in 1997. It is a linear single stranded negative-sense RNA consisting of 15,191 base pairs. The genome is found in the helical nucleocapsid. The genome encodes for 11 proteins including structural and non-structural.

The virion of the RSV is enveloped with a lipid bilayer, which is obtained from the host’s plasma membrane. It contains three surface glycoproteins, the attachment protein G, fusion protein F, and the small hydrophobic SH protein, which are separated from each other and can be seen as “spikes” that project out of the virion. The glycoproteins can be measured to be about 11-20nm in size, while the virion appears to be about 150-300nm in diameter.

The major function of the F protein is to direct viral penetration by the fusion between the virion and the host plasma membrane. The F protein is also able to mediate fusion with other neighboring cells forming syncytia, when it is expressed on the cell surface. The glycoprotein, G, is a type II transmembrane glycoprotein and is the major RSV attachment protein. It contains a single hydrophobic region which serves as a signal peptide and also as a membrane anchor. The small hydrophobic SH protein is a short integral membrane protein whose function is unknown. However, it is suggested that the SH protein enhances the function of the attachment protein and or fusion protein. Another RSV protein is the matrix protein M, located in the inner layer of the lipid bilayer, and is found to play a role in the formation of virus-like particles. These four proteins are used to form the viral envelop. The non-structural proteins are NS1 and NS2, these proteins enhance viral growth but are not essential.

The virion consists of a nucleocapsid which is contained in the lipid bilayer. The nucleocapsid has a symmetrical helix shape and is measured to be about 12-15nm in diameter. There are four nucleocapsid proteins inside the virion which carry out the replication and transcription of the RSV genome, the nucleocapsid protein N, the phosphoprotein P, the antitermination factor M2-1, and the large polymerase subunit L.

The RSV nucleocapsid N protein binds to genomic and antigenomic RNA and forms an RNAse-resistant nucleocapsid. This provides protection of the viral RNA from the toll-like receptors and RNA recognition helicases that initiate immune responses. In order for the N protein to encapsidate minigenome RNAs the help of the P protein is required. The P protein acts as a chaperonin for the N protein, without it the N protein would be incapable to binding to minigenome RNA. The L protein is responsible for all enzymatic activity and the M2-1 protein is a transcription antitermination factor which is crucial for viral viability. Proteins M2-1 and M2-1 are both play important roles in balancing transcription and RNA replication.

Virus Life Cycle and metabolism

Respiratory Syncytial Virus enters the cell through fusion at the plasma membrane. The initiation step occurs when the G protein of the RSV binds to a certain long unbranched polysaccharide of the extracellular matrix consisting of disaccharide subunits called GAGs. GAGs are often involved in the interaction between cells and various viruses. The F protein then interacts with the protein RhoA and mediates the attachment of the virus. RhoA may act as a receptor for the fusion protein or by may play a role in viral infection; the actual role of RhoA is unknown. Viral gene expression and replication occurs in the cytoplasm. Once the virus is in the cytoplasm the nucleocapsid and the genome is released. The M2-2 gene governs the transition from transcription to production of genomic RNA. The polymerase then enters the genome at its 3’ end and the genes are transcribed into mRNAs by the start-stop-restart synthesis. This creates a polar transcription gradient in which the promoter starting genes are transcribed more frequently than the genes which are downstream. Replication generates a complete positive-sense RNA complement of the genome called the antigenome, which acts as a template for genome synthesis. The genome and the antigenome are both coated with the N protein at all time which serves as the template for RNA synthesis. The M protein regulates the assembly of the RSV by interacting with the envelope proteins F and G and with the nucleocapsid proteins N, P, and M2-1. The new synthesized proteins then self-assembly and budding occurs, acquiring an envelop from the membrane.

Ecology

Respiratory Syncytial Virus is spread through person to person contact by infected respiratory secretions. It requires the close contact of infected individuals, contact with infected nasal secretions, or contamination of hands or objects which have been introduced to such secretions. Outbreaks of the disease occur at particular seasons yearly which usually last up to 5 months. Epidemics usually occur in the late fall, winter or spring seasons, with most outbreaks in February or March. RSV is commonly acquired by patients who are hospitalized and the likelihood of RSV infection increases with the duration of the stay. The hospital staff plays a major role in the spread of RVS infection. To reduce the risk of infection precautions must be in effect such as hand washing.

Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

Current Research

Enter summarries of the most rescent research here--at least three required

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Edited by student of Emily Lilly at University of Massachusetts Dartmouth.