Epidemiology: RSV plays a major role in respiratory infection among the childhood population, especially infants and younger children. It is the leading viral agent respiratory tract disease worldwide, causing bronchiolitis and pneumonia in infants and young children. There are about 100,000 cases and 4,500 deaths yearly of RSV infections in the United States (1). Typically, all children are infected with RSV by age 2 to 3; however, the infections can reemerge up to 5 to 6 per year. RSV was first extracted from chimpanzees that were showing upper respiratory tract disease as an agent in 1956 (1). The chimpanzees had an upper respiratory tract illness in addition to coryza, runny nose, and malaise. The humans that interacted with these …show more content…
How RSV works: . The F (fusion) glycoprotein is responsible for membrane fusion such as viral penetration and syncytium formation. The G (glycoprotein) protein is responsible for viral attachment and a major antigenic determinant of RSV since it induces protective antibodies (3). The SH (small hydrophobic) protein, matrix protein (M), and the M2 protein are envelope-associated proteins that are not involved in viral attachment or syncytium formation (3). Other proteins such as the nucleoprotein (N), phosphoprotein (P), and the large nucleoprotein (L) are in the nucleocapsid. NS-1 and NS-2 are non-structure protein that is only found in the infected cells but not present in virions (3). RSV activation: RSV comes into the airway epithelium from the apical side only and aims to destroy the ciliated epithelia cells (4). Then RSV buds and releases the virus from the apical surface (4). RSV is caused by TLR3 activation. It initiates infections by binding to a cellular receptor and then the viral envelope fuses with the plasma membrane. The virus attaches the cell through the main protein, the G protein and fuses with the plasma membrane of the host cell through the F protein. After penetration, the nucleocapsid of the virus is released into the cytoplasm where replication occurs (3). The viral RNA is like a template for mRNA (3). The mRNA’s job is to translate the viral proteins and complementary RNA serves as a template for virion RNA
RSV infection is limited to the respiratory tract. Respiratory Syncytial Virus affects the respiratory system causing an interruption of the normal physiology of the lungs which are the main organs affected. The lungs are a pair of cone-shaped bodies that occupy the thorax. The lungs have two vital functions air distribution and gas exchange. In addition to attending as an air distribution pathway and gas exchange surface the components of the respiratory tract cleanse, warm and humidify inspired air. RSV affects the lungs by inflaming the small airways and decreasing the oxygen flow in and out, thereby affecting the capacity for normal oxygen exchange. Initial infection in young infants or children frequently involves the LRT and most often manifests as the clinical entity of bronchiolitis. Inoculation of the virus occurs in the URT in respiratory epithelial cells [ (Leonard R Krilov, 2010) ]. Spread of the virus down the respiratory tract occurs by
Viruses are microscopic particles that invade and take over both eukaryotic and prokaryotic cells. They consist of two structures, which are the nucleic acid and capsid. The nucleic acid contains all genetic material in the form of DNA or RNA, and is enclosed in the capsid, which is the protein coating that helps the virus attach to and penetrate the host cell. In some cases, certain viruses have a membrane surrounding the capsid, called an envelope. This structure allows viruses to become more stealthy and protected. There are two cycles in which a virus can go into: lytic and lysogenic. The lytic cycle consists of the virus attaching to a cell, injecting its DNA, and creating more viruses, which proceed to destroy the host. On the other hand, the lysogenic cycle includes the virus attaching to the cell, injecting its DNA, which combines with the cell’s DNA in order for it to become provirus. Then, the provirus DNA may eventually switch to the lytic cycle and destroy the host.
Respiratory Synctial Virus (RSV) is an infection that is contagious that resembles the common cold a lot of times. RSV is the most common viral pathogen that causes lower respiratory tract infections in infants. RSV infection in infancy cause severe bronchiolitis and pneumonia and may incline children to the following development of asthma, the most common chronic illness of childhood. RSV is the most single related cause of pneumonia and bronchiolitis. Epidemics of the virus are seen each winter, 80% of infections typically occur during a three-month period. The virus is not typically severe during infancy but it is rare if it happens. (As, in my case I was born with the RSV virus and was hospitalized for eighteen days and was put on assisted ventilation.) In infants RSV infection can spread to the bronchial tubes and lungs. The virus can also infect adults, in where the infection can cause viral pneumonia, which is sometimes followed by a bacterial infection of the lower respiratory system.
The respiratory syncytial pathogen is a non-segmented negative -sense single stranded RNA virus that falls under the paramyxoviridae family. The virus is comprised of 10 genes the encode 11 proteins and is divided into two subtypes A and B, which further divide into multiple genotypes. Genetic studies have tried
RSV enters a cell through fusion at the plasma membrane. Initiation emerges when the G protein of the RSV binds to a specific long unbranched polysaccharide of the
On encountering a host cell, the retrovirus attaches itself to receptors on the surface of the host cell’s membrane. Once inside the cell, the capsid opens, releasing RNA and reverse transcriptase into the cell’s cytoplasm.
The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.
RSV is a virus that is hard to diagnosis because the signs and symptoms are a lot like the common cold. One may start to develop a runny nose or decrease in appetite the first couple of days when having this virus; but coughing, sneezing, and wheezing may also occur. In young infants, they may experience irritability or difficulties with breathing (“CDC,” 2014). One may have this virus before realizing the symptoms like a dry cough, low grade fever, sore throat or headache (Mayo Clinic, 1998). Someone with an upper respiratory tract infection may have a fever, headache, sore throat or wheezing; whereas someone with a lower respiratory tract infection may have a cough, increased breathing rate, tightness in the chest. While both tract infections should be taken seriously, they both can lead to RSV.
Molecular Cell Biology, 7th Edition, 2013, Lodish, Berk, Kaiser, Krieger, Bretscher. Ploegh, Amon, and Scott. W.H. Freeman and Company (ISBN-13: 978-1-4292-3413-9)
Some viruses also have an outer bag of lipo-protein called an envelope. After a virus attaches to a living cell, it either enters the cell to release the genetic information, or, the virus injects the information through the cells outer lining. Thus changing the cells natural functions and forcing the cell to spend its energy to create copies of the virus. The cell will go on making copies of the virus until the cell is used up and dies. The virus then leaves the dead cell and invades a nearby cell and the process starts all over. There are five types of human herpes virus: Varicella zoster which causes chickenpox, Epstein Barr virus which causes infectious mononucleosis, cytomegalovirus which can cause cytomegalic inclusion disease in infants, and herpes simplex viruses 1 and 2.
When a virus invades the human body there is an assortment of responses from the immune system relying largely on the particular pathogen type. Viruses invade the host with the purpose of replication to ensure survival. My cytosolic virus is a single stranded RNA virus. The virus is surrounded by an envelope with a lipid membrane. Inside the envelope are matrix proteins, integrase, protease, reverse transcriptase and the RNA genome. All viruses contain three proteins necessary for their survival; one for replication, one for packaging and delivering it to more host cells and a protein that modifies the function or structure of the host
Rapid virological testing for RSV is recommended in order to guide isolation and allocate Liam into cohorts in hospital (Fitzgerald, 2011).
Gardner’s Respiratory Virus (GRV) is an enveloped, single-stranded RNA (ssRNA) virus that has been shown to cause both upper and lower respiratory tract infections. This virus is an intracellular virus capable of replicating free within the cytoplasm of host cells. Spread through small, airborne viral droplets, GRV invades the physical barrier that is the mucosal surface lining the lungs and respiratory tract. The cells that line this surface are mostly epithelial cells, and GRV enters these cells by being transported across their membranes through receptor mediated endocytosis. Once inside the host cell, GRV replicates and begins its cytopathic effects on the host cells; the infected epithelial cells undergo structural changes that lead to irritation, inflammation, and eventual lysis that can weaken these mucosal surfaces, making the host more susceptible to further pathogenic attack. As with similar viruses, once the first line of defense is breached and GRV is transported into the host cells, the immune response, involving both the innate and adaptive branches of the immune system is initiated and attempts to remove the virus as well as prevent future infection. GRV however, is highly evolved and possesses various evasion mechanisms that prevent the immune system from accomplishing its job; luckily, a drug does exist to help eliminate the virus.
The HIV-1 virion is approximately 120 nm in diameter, roughly spherical, and is composed of two copies of a single stranded positive sense RNA enclosed by a capsid (24). The HIV-1 genome is less than 10 kb and encodes for more than nine different gene products. It encodes for 3 major structural protein genes: gag (group-specific antigen), pol (DNA polymerase), and env (Envelope), which code for major structural proteins and essential enzymes. Gag generates the mature Gag protein matrix (MA or p17), capsid (CA or p24), nucleocapsid (NC or p7), and p6, which encompass proteins for the basic infrastructure of the virus such as the inner core of the viral particle (25). Pol encodes for reverse transcriptase (RT), which enables the virus to reproduce, integrase (IN), which is necessary to integrate the viral double stranded DNA into the host genome, RNAse H, and HIV protease, which are all encapsulated in the core of the inner particle formed by the viral capsid protein p24 (25). Env encodes for glycoproteins of the outer membrane such as outer gp120 (which enables the virus to attach and fuse to cells of the host), and transmembrane gp41 that anchors the glycoprotein complex to the surface of the virion (25). Between the core and the envelope is the HIV matrix proteins which are composed of the viral protein p17 (23). HIV-1 also encodes for proteins with important regulatory elements (tat (Trans-Activator of Transcription) and rev
Rubella virus is a member of the Togaviridae family though is its own genus, Rubivirus. Rubella is caused by the Rubella virus which can be found in the blood, stool, or throat of an infected individual (change). There is currently only one genetically stable serotype of Rubella, however a phylogenetic tree analysis of nine virus strains confirms the existence of a minimum of three distinct genetic lineages (Parkman, 1996). The virus is spherical in shape with a diameter of 50-80nm and is a 20-faced nucleocapsid. The core surrounding the single-stranded, positive-sense RNA genome has hemagglutinin-containing surface projections and is also surrounded by a lipoprotein envelope. There are three major structural polypeptides: E1 and E2 membrane glycoproteins, and a single nonglycosylated capsid protein associated with RNA. The first envelope protein, E1, is responsible for viral hemagglutinination and neutralization while E2 is categorized into two forms: E2a and E2b. There are two forms because of the differences in glycosylation and these differences indicate different strains of Rubella (Parkman, 1996).