Type of paper:Â | Essay |
Categories:Â | Medicine Healthcare policy Community health |
Pages: | 7 |
Wordcount: | 1678 words |
Respiratory Syncytial Virus (RSV) was discovered in the year 1956 in a laboratory test involving a chimpanzee with respiratory complications. It was later discovered that the virus originated from humans. RSV exists in two different forms depending on the antigenic makeup. In other words, there are antigenic subtypes A and B (In Anderson & In Graham, 2013). Subtype A is associated with severe illnesses, and it often preponderates respiratory outbreaks. Subtype B, on the other hand, is associated with the asymptomatic strains experienced by most people; it does not cause severe respiratory conditions to individuals. Respiratory Syncytial Virus is the major cause lower respiratory tract infections, especially in children and infants. The severity of RSV is diverse ranging from life-threatening and severe to cold symptoms (In Anderson & In Graham, 2013). Respiratory Syncytial Virus is the main cause of bronchiolitis and pneumonia in newborn children. Also, the virus can cause morbidity and mortality in adults and immunodeficient persons. Most vaccination programs in children target Respiratory Syncytial Virus as it is the main cause of hospitalization among children.
Basic Virus Structure and Function
The sequencing of the haploid set of chromosomes in Respiratory Syncytial Virus was completed in the year 1997 (Gideon Informatics & Berger, 2019). The virus has a single strand Ribonucleic Acid (RNA) with negative sense exhibiting 15,191 base pairs. The genetic materials exist in the helical nucleocapsids, and they encode for eleven structural and non-structural proteins. The entire virus particle or virion is enclosed in a lipid bilayer, which it acquires from the host's plasma membrane. RSV consists of three outer glycoproteins; the fusion protein F, the attachment protein G, as well as the hydrophobic SH protein. The SH proteins are distinct and observable inform of "spikes" jutting out of the virion (Gil-Prieto et al., 2015). On the other hand, glycoproteins are 11 to 20nm in size, while the virion is about 160 to 300 nm in diameter (Gil-Prieto et al., 2015). The Nucleocapsid N protein in Respiratory Syncytial Virus binds to the antigenomic and genomic RNA forming RNAse- resistant nucleocapsid, which gives protection to the viral RNA from the receptors as well as the RNA recognition helicases facilitate immune responses (Gil-Prieto et al., 2015). The major function of the F protein structure is to direct the penetration of the virus through fusion between the host plasma membrane and the virion. Besides, the F protein can mediate fusion with the neighboring cells thereby forming syncytia when expressed within the cell surface (Muralidharan, Li, Wang, & University of Ottawa, 2019). Glycoprotein G aids in the attachment processes of RSV into the host; it forms type II transmembrane glycoprotein. They have a non-enveloped structure that encloses the amino acid present inside. Their shapes assume the icosahedral structure consisting of the plus-sense ssRNA; a structure that keeps on replicating with the surrounding environment. The RSV genome is 7.5kb with an RNA consisting of the single strands (Muralidharan, Li, Wang, & University of Ottawa, 2019).
Epidemiology
Respiratory syncytial virus infection is common among newborn babies, globally, nearly all children are usually affected by the virus at two years of age. Close to 1% to 2% of infants worldwide are hospitalized as a result of lower tract infections (Fordyce et al., 2018). Out of the above number, 55% to 90% suffer from bronchiolitis and 6% to 40% from pneumonia (Fordyce et al., 2018). Mortality and morbidity are common in infants with nosocomial infections as well as those with other medical illnesses including chronic and cardiac lung infections or diseases. Indigenous children from the northern region parts of the world are specifically at high risks for infections and hospitalization from Respiratory syncytial virus. Due to low immunity in children, RSV can easily attack different respiratory cells leading to health complications and even deaths among newborn babies and children. Health education can aid in the eradication of widespread infections caused by RSV (Fordyce et al., 2018). With the absence of the vaccine, palivizumab prophylaxis is the best intervention method that facilitates the reduction of the burden of illnesses and health complications caused by RSV.
There is a substantial increase in the number of admission into the hospitals due to the RSV infections, including pneumonia and bronchitis. For instance, in North American alone, there have been up to 500 deaths and 126, 300 hospitalizations recorded annually as a result of Respiratory syncytial virus (Corry et al., 2015). In Canada, the inpatient care for the illnesses associated with the RSV amounts to $ 18 million annually; the amount accounts for 62% of the total cost of treatment of the disease (Corry et al., 2015). Almost all children are affected by the virus two months after birth leading to the high costs of treatment; on the other hand one percent of children require hospitalization. In developed nations, there exists defined high risk groups possessing chronic underlying disorders (Corry et al., 2015). In these groups, the infections with the RSV is more likely to progress into severe lower respiratory tract infections. Health newborns who are younger than three months are susceptible to similar infections (Corry et al., 2015).
Transmission
The transmission of Respiratory syncytial virus usually occurs through sneezing and coughing. The virus can also get into the host if droplets from the sneeze and cough get into the nose, eye or mouth (Cooper & Brodersen, 2010). Besides, getting in contact with the contaminated surfaces such as doorknobs and then touching the face before washing hands may aid in the transmission of RSV. When infected with RSV, infants and children often become contagious for about three to eight days. Children or newborns with low immune system may continue spreading the virus even after the deterioration of the symptoms and for as long as four weeks (Cooper & Brodersen, 2010). Children usually become exposed to the RSV outside homes including childcare centers and in schools. When entering the body, the virus attaches itself to the receptors inside the host body; the above procedure induces the process of endocytosis (Cooper & Brodersen, 2010). The process of replication is initiated by the single-stranded RNA that takes the positive side mechanism. When it enters the body of the host, the virus replicates and changes the RNA contents of the host, then assumes the components of the hosts through change in the chemical contents (Karron & Black, 2017). The viruses can stay for long hours when exposed to the surrounding environment. The replication nature of the viruses also accounts for their effective transmission and long survival. When it enters the body, the viral agent can reproduce a million times in a second resulting in high infections (Cooper & Brodersen, 2010).
Pathophysiology
Ones it enters the body, Respiratory syncytial virus causes severe damages and injuries to the bronchiolar ciliary apparatus and epithelial tissues within the respiratory structures. The destruction leads to an increase in fluid within the alveoli and bronchioles (Sande, 2012). The above results, therefore, lead to the obstruction of the alveoli and bronchioles, leading to the collapse of the airway of a condition called emphysema. Respiratory syncytial virus replication, if not treated earlier, can results in the destruction of the entire respiratory system and progress into the lungs (Sande, 2012). The time of infection and the beginning of illnesses is about four to five days. The virus often spread from the upper part of the respiratory tract to the lower end through the spread of respiratory epithelium and inhalation of secretions (Sande, 2012). There are cases when the virus can spread to other organs such as liver, causing more health complications. Children who encounter the virus for the first time may only show mild symptoms including rhinorrhea, coughing, and the reduction in appetite (Sande, 2012). At the initial stages, sneezing, wheezing, as well as low-grade fever are common symptoms. Continuous coughing may lead to difficulty in breathing and pain along the throat.
Treatment with Medications
In most cases, viral diseases do not respond well to medications due to their replicative nature. The application of medications in the treatment, therefore, remains a contentious issue as there are biochemists and pharmaceutical professionals who prefer treatment of the virus with beta-agonists, antibodies, and antivirals (Kinnear, Tregoning, Shattock, & Imperial College, London, 2016). On the other hand, the prophylactic antibody can be employed to the populations at risk during the peak seasons or during the disease outbreak. Specifically, some of the best or recommended drugs may include ribavirin, which is commonly used in severe or high-risk cases. Bronchodilators may also be employed to reduce the symptoms including blockages within the airways However, the efficiency of bronchodilators in the treatment process remains contentious as it is unapproved (Karron & Black, 2017).
The current control measures mainly involve the use of antivirals, which are mainly given as vaccines before the infections to increase the immune system to fight the virus ones it enters the body. However, there are new vaccines that are being developed that target the F protein, as well as virus-like particles.
References
Cooper, V. L., & Brodersen, B. W. (2010). Bovine Respiratory Disease, An Issue of Veterinary Clinics: Food Animal Practice - E-Book.
Corry, J. D., Peeples, M. E., Ohio State University., & Ohio State University,. (2015). Prevention of respiratory syncytial virus attachment protein cleavage in vero cells rescues infectivity of progeny virions for primary human airway cultures.
Fordyce, E. A. F., Fraser, H. S., Crepin, D., Onions, S. T., Parra, G. F., Sleigh, C. J., King-Underwood, J., ... Murray, J. (2018). Conformationally restricted benzothienoazepine respiratory syncytial virus inhibitors: their synthesis, structural analysis and biological activities1. (MedChemComm.)
Gideon Informatics, Inc., & Berger, S. (2019). Respiratory Syncytial Virus. Los Angeles: Gideon Informatics, Incorporated.
Gil-Prieto, R., Gonzalez-Escalada, A., Marin-Garcia, P., Gallardo-Pino, C., Gil-de-Miguel, A., & Wang, S.-M. (2015). Respiratory Syncytial Virus Bronchiolitis in Children up to 5 Years of Age in Spain. (Medicine.)
In Anderson, L. J., & In Graham, B. S. (2013). Challenges and opportunities for respiratory syncytial virus vaccines.
Karron, R. A., & Black, R. E. (2017). Determining the burden of respiratory syncytial virus disease: the known and the unknown. (Lancet.)
Kinnear, E., Tregoning, J., Shattock, R., & Imperial College, London,. (2016). DNA vaccination against Respiratory Syncytial Virus (RSV).
Muralidharan, A., Li, S., Wang, L., & University of Ottawa. (2019). Towards Better Understanding of Respiratory Syncytial Virus (RSV) Vaccine-Induced Enhanced Disease.
Sande, C. J. (2012). The effects of strain variation on respiratory syncytial virus infection and immunity. n.p.
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