Human respiratory syncytial virus (hRSV or RSV) is the type species of the genus Pneumovirus. Along with other members of the family Paramyxoviridae, hRSV is an enveloped virus with a negative sense, single-stranded RNA genome. These viruses are 150-200nm in diameter with a helical nucleocapsid
Other members of the family include human parainfluenzavirus 1 (HPIV-1; genus Respirovirus), mumps virus (MuV), human parainfluenzavirus 2 and 4 (HPIV-2 and HPIV-4; genus Rubulavirus), measles virus
(MeV; genus Morbillivirus), Hendravirus and Nipahvirus (genus Henipavirus) and human metapneumovirus (hMPV; genus Metapneumovirus).
A distinguishing feature among genera is the possession (Paramyxovirus) or absence (e.g. Morbilliviruis and Pneumovirus) of neuraminidase (NA).
Figure 1. The hRSV virion enters its target cell by fusion of the hRSV envelope with the cell membrane and release of the viral genome into the cell's cytoplasm where translation will occur. The nucleopretein (N), large (L) and phosphoproteins (P) together with the RNA genome form the nucleoprotein core. These together with the matrix (M), fusion (F), and glycoprotein (G) are classified as structural proteins. The nonstructural proteins include NS1 and 2, small hydrophobic (SH) and M2 (formerly 22-kDa).
The respiratory syncytial virus genome is transcribed from the 3' end into monocistronic (each species only encodes a single protein) mRNA molecules. New viruses are released form the infected cell buy budding. In the presence of newly synthesized hRSV fusion (F) protein, neighbouring infected cells may form a clump whose membranes have fused to form a "giant cell" called a syncytium (Greek syn = with, and kytos = cell), . New virions can then spread more effectively from cell-to-cell.
The disease
Human respiratory syncytial virus (hRSV or RSV) is the most common cause of lower respiratory tract disease in infants and young children. HRSV infects the majority of infants by 2yrs of age usually causing symptoms resembling those of the common cold. In some prematurely born infants or those with chronic lung disease, hRSV can cause life-threatening disease. HRSV infection most commonly occurs in epidemics during the cooler months (exact months will depend on which hemisphere we look at e.g. the Northern hemispahere's peak season occurs from October to March/April while the Southern hemisphere peak is usually around April to October). The majority of cases are seen in children under 4yrs of age, with the peak of severely ill cases found among children less than 6mths of age, particularly in infants with pre-existing heart and lung disease.
The Lab Diagnosis
Virus can be isolated from contiuous cell lines e.g. HeLa cells, which can take 2 to 10 days. A more rapid method is indirect immunofluorescence (IIF) during which viral antigens are detected within the patient's cells present in a nasopharygeal aspirate (NPA) or washing (NPW).
The polymerase chain reaction (PCR) frequently used to provide specific and rapid results using a range of patient specimens, including those with very low cell content.
The Therapies
Oral ("Copegus®", "Rebetol®") and aersol ("Virazole®") ribavirin are antiviral drugs that have been used successfully in some patients to combat both DNA and RNA viruses. Ribavirin is a nucleoside analogue
ith the chemical name of 1-(beta)-D-ribofuranosyl-1 H-1,2,4-triazole-3-carboxamide. the drug interrupts viral protein synthesis by interfering with mRNA transcription.
HRSV intravenous immune globulin (RSV-IVIG) was the first approved immunoprophylactic for hRSV therapy when it was released as Respigam in 1996. RSV-IVIG was prepared from pooled high titre sera containing protective and neutralising antibodies. RSV-IVIG is administered monthly for for 4 to 5mths over the peak season of virus activity to prevent infection. Palivizumab ("Synagis") is next a generation prophylactic consisting of a humanised monoclonal antibody (MAb). Palivizumab is given intramuscularly rather than IV but still requires administration throughout peak hRSV season.
A successful vaccine has not yet been marketed however this area is the focus of much research. In the mid-1960's, a formalin-inactivated whole-virus hRSV vaccine was trialled in infants who had no previous exposure to infection as determined by an absence of anti-hRSV antibodies. When these children were later infected during an hRSV outbreak, the resulting illnesses, especially in children under 2yrs of age, were severe. The incidence of pneumonia (60%) and hospitalisation (21%) was much higher than in children given a placebo (8% and 1.5%, respectively). The cotton-rat animal model has been widely used in studies attempting to explain the nature of enhanced disease. In particular, the lungs of animals immunized with a formalin-inactivated hRSV vaccine and challenged by infection with hRSV have been extensively examined to gain insight into the immune-mediated pathology that occurred.
source :http://www.uq.edu.au/vdu/VDUHumanRespiratorySyncytialVirus.htm
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