RSV, or respiratory syncytial virus, is the most prevalent virus infecting children globally, and it is rapidly becoming recognized as a significant pathogen in adults, particularly the elderly.
The most prevalent clinical presentation in RSV infection is an upper respiratory infection; however, in young children, the infection commonly manifests as bronchiolitis and may rarely develop into respiratory failure, apnea, pneumonia, and death.
Most RSV infections are treated with supportive care. However, passive prophylactic immunization is available for at-risk children, such as infants and premature newborns with a history of pulmonary, cardiac, or neuromuscular conditions.
Epidemiology
RSV is considered accountable for over 33 million lower respiratory tract illnesses, 3 million hospitalization, and 199,000 juvenile fatalities worldwide, with the majority of death occurring in resource-limited nations. Seasonal variation in RSV incidence exists, although seasonal effects vary according to global geography; temperate regions have a clear winter-spring predominance, whereas tropical and equatorial climates may have less noticeable spikes with more interseasonal sickness.
Premature newborns, patients with prior pulmonary, cardiac, immunological, and neurologic diseases, and the elderly have much-increased morbidity and death. 90% of children are infected within the first two years of life, while older children and adults are reinfected.
Most RSV patients will develop upper respiratory sickness, but a considerable minority may develop an infection in the lower respiratory tract, most commonly bronchiolitis. Lower respiratory involvement is most common in children under the age of 1, with up to 40% of primary infections progressing in bronchiolitis.
Anatomy
Pathophysiology
RSV is transmitted from human to human by respiratory droplets. The incubation period following RSV inoculation ranges from 2 to 8 days, with a typical incubation period of 4-6 days, depending on host characteristics such as the patient’s age and first RSV infection.
The virus quickly spreads throughout the respiratory tract after being inoculated into the nasopharyngeal or conjunctival mucosa, which targets its favored growing media, apical ciliated epithelial cells. It attaches to cellular receptors with the RSV-G glycoprotein, fuses with host cell membranes, and inserts its nucleocapsid into the host cell to initiate intracellular replication.
When the viral cytotoxicity and the host’s cytotoxic response combine to cause the necrosis of respiratory epithelial cells, the host’s inflammatory immune reaction is triggered, including both humoral and cytotoxic T-cell activation, with the subsequent implications of small airway obstruction and plugging by mucus, cellular waste, and DNA.
An alveolar blockage is a possibility in more challenging cases. Other residual effects include airway edema, decreased lung compliance, and ciliary dysfunction with poor mucus clearance.
Etiology
RSV is a single-stranded RNA virus in the genus Pneumovirus that belongs to the Paramyxoviridae family. The RSV structure consists of a bilipid-layer envelope encasing a ribonucleoprotein core and three membrane proteins, one of which aids host cell attachment and the other in fusion.
RSV only has one serotype; however, it is divided into two strains, A and B, with changes in the structure of essential structural membrane proteins, notably the attachment protein.
Infants are more likely to contract RSV infection during a specific season, an older sibling presence, birth during the RSV season, low birth weight, congenital heart disease, male gender, younger than six months, exposure to smoking, residence in a suburban area, and a young mother are factors associated with RSV infection.
Additionally linked to an increased likelihood of needing hospitalization for an RSV infection are Down Syndrome, Cystic Fibrosis, Cerebral Palsy, and giving birth in September and October close to the RSV season.
Genetics
Prognostic Factors
RSV infection-related hospitalization in children typically results in complete recovery. They are released after three to four days. Infants at high risk spend more time in the hospital, require more mechanical breathing, and are more likely to be transferred to the intensive care unit.
RSV infection can spread from individuals for 3 to 8 days. However, young infants and those with compromised immune systems might continue to transmit the virus for up to 4 weeks after their symptoms disappear.
Note:
Recommended for individuals aged sixty or older as active immunization against lower respiratory tract illness brought on by respiratory syncytial infection (RSV)
Indicated for individuals aged sixty or older as active immunisation against lower respiratory tract illness brought on by respiratory syncytial infection (RSV) :
Administer dose of 0.5 ml intramuscularly as a single dose Dosing Considerations
Limitation of effectiveness: all vaccine individuals may not be protected
Indicated for Prevention of Respiratory Syncytial Virus
Neonates and infants based on body weight (1st RSV season):
Body weight >5 Kg: 100 mg intramuscular injection of one dose
Body weight <5 Kg: 50 mg intramuscular injection of one dose
Children who persist at enhanced risk for severe respiratory Syncytial Virus Disease (2nd RSV season):
Age <2 years:
200 mg intramuscular injection of one dose (i.e., two 100 mg intramuscular injections)
Children who experience cardiac surgery with the cardiopulmonary bypass:
1st RSV season: If surgery <3 months following receiving nirsevimab then the extra dose will be based on body weight at the time of extra dosage
If surgery >3 months following receiving nirsevimab, then an Extra dose of 50 mg nevertheless of body weight
2nd RSV season: If surgery <3 months following receiving nirsevimab, then an Extra dose of 200 mg nevertheless of body weight
If surgery >3 months following receiving nirsevimab, then an Extra dose of 100 mg nevertheless of body weight
RSV, or respiratory syncytial virus, is the most prevalent virus infecting children globally, and it is rapidly becoming recognized as a significant pathogen in adults, particularly the elderly.
The most prevalent clinical presentation in RSV infection is an upper respiratory infection; however, in young children, the infection commonly manifests as bronchiolitis and may rarely develop into respiratory failure, apnea, pneumonia, and death.
Most RSV infections are treated with supportive care. However, passive prophylactic immunization is available for at-risk children, such as infants and premature newborns with a history of pulmonary, cardiac, or neuromuscular conditions.
RSV is considered accountable for over 33 million lower respiratory tract illnesses, 3 million hospitalization, and 199,000 juvenile fatalities worldwide, with the majority of death occurring in resource-limited nations. Seasonal variation in RSV incidence exists, although seasonal effects vary according to global geography; temperate regions have a clear winter-spring predominance, whereas tropical and equatorial climates may have less noticeable spikes with more interseasonal sickness.
Premature newborns, patients with prior pulmonary, cardiac, immunological, and neurologic diseases, and the elderly have much-increased morbidity and death. 90% of children are infected within the first two years of life, while older children and adults are reinfected.
Most RSV patients will develop upper respiratory sickness, but a considerable minority may develop an infection in the lower respiratory tract, most commonly bronchiolitis. Lower respiratory involvement is most common in children under the age of 1, with up to 40% of primary infections progressing in bronchiolitis.
RSV is transmitted from human to human by respiratory droplets. The incubation period following RSV inoculation ranges from 2 to 8 days, with a typical incubation period of 4-6 days, depending on host characteristics such as the patient’s age and first RSV infection.
The virus quickly spreads throughout the respiratory tract after being inoculated into the nasopharyngeal or conjunctival mucosa, which targets its favored growing media, apical ciliated epithelial cells. It attaches to cellular receptors with the RSV-G glycoprotein, fuses with host cell membranes, and inserts its nucleocapsid into the host cell to initiate intracellular replication.
When the viral cytotoxicity and the host’s cytotoxic response combine to cause the necrosis of respiratory epithelial cells, the host’s inflammatory immune reaction is triggered, including both humoral and cytotoxic T-cell activation, with the subsequent implications of small airway obstruction and plugging by mucus, cellular waste, and DNA.
An alveolar blockage is a possibility in more challenging cases. Other residual effects include airway edema, decreased lung compliance, and ciliary dysfunction with poor mucus clearance.
RSV is a single-stranded RNA virus in the genus Pneumovirus that belongs to the Paramyxoviridae family. The RSV structure consists of a bilipid-layer envelope encasing a ribonucleoprotein core and three membrane proteins, one of which aids host cell attachment and the other in fusion.
RSV only has one serotype; however, it is divided into two strains, A and B, with changes in the structure of essential structural membrane proteins, notably the attachment protein.
Infants are more likely to contract RSV infection during a specific season, an older sibling presence, birth during the RSV season, low birth weight, congenital heart disease, male gender, younger than six months, exposure to smoking, residence in a suburban area, and a young mother are factors associated with RSV infection.
Additionally linked to an increased likelihood of needing hospitalization for an RSV infection are Down Syndrome, Cystic Fibrosis, Cerebral Palsy, and giving birth in September and October close to the RSV season.
RSV infection-related hospitalization in children typically results in complete recovery. They are released after three to four days. Infants at high risk spend more time in the hospital, require more mechanical breathing, and are more likely to be transferred to the intensive care unit.
RSV infection can spread from individuals for 3 to 8 days. However, young infants and those with compromised immune systems might continue to transmit the virus for up to 4 weeks after their symptoms disappear.
Note:
Recommended for individuals aged sixty or older as active immunization against lower respiratory tract illness brought on by respiratory syncytial infection (RSV)
Indicated for individuals aged sixty or older as active immunisation against lower respiratory tract illness brought on by respiratory syncytial infection (RSV) :
Administer dose of 0.5 ml intramuscularly as a single dose Dosing Considerations
Limitation of effectiveness: all vaccine individuals may not be protected
Indicated for Prevention of Respiratory Syncytial Virus
Neonates and infants based on body weight (1st RSV season):
Body weight >5 Kg: 100 mg intramuscular injection of one dose
Body weight <5 Kg: 50 mg intramuscular injection of one dose
Children who persist at enhanced risk for severe respiratory Syncytial Virus Disease (2nd RSV season):
Age <2 years:
200 mg intramuscular injection of one dose (i.e., two 100 mg intramuscular injections)
Children who experience cardiac surgery with the cardiopulmonary bypass:
1st RSV season: If surgery <3 months following receiving nirsevimab then the extra dose will be based on body weight at the time of extra dosage
If surgery >3 months following receiving nirsevimab, then an Extra dose of 50 mg nevertheless of body weight
2nd RSV season: If surgery <3 months following receiving nirsevimab, then an Extra dose of 200 mg nevertheless of body weight
If surgery >3 months following receiving nirsevimab, then an Extra dose of 100 mg nevertheless of body weight
RSV, or respiratory syncytial virus, is the most prevalent virus infecting children globally, and it is rapidly becoming recognized as a significant pathogen in adults, particularly the elderly.
The most prevalent clinical presentation in RSV infection is an upper respiratory infection; however, in young children, the infection commonly manifests as bronchiolitis and may rarely develop into respiratory failure, apnea, pneumonia, and death.
Most RSV infections are treated with supportive care. However, passive prophylactic immunization is available for at-risk children, such as infants and premature newborns with a history of pulmonary, cardiac, or neuromuscular conditions.
RSV is considered accountable for over 33 million lower respiratory tract illnesses, 3 million hospitalization, and 199,000 juvenile fatalities worldwide, with the majority of death occurring in resource-limited nations. Seasonal variation in RSV incidence exists, although seasonal effects vary according to global geography; temperate regions have a clear winter-spring predominance, whereas tropical and equatorial climates may have less noticeable spikes with more interseasonal sickness.
Premature newborns, patients with prior pulmonary, cardiac, immunological, and neurologic diseases, and the elderly have much-increased morbidity and death. 90% of children are infected within the first two years of life, while older children and adults are reinfected.
Most RSV patients will develop upper respiratory sickness, but a considerable minority may develop an infection in the lower respiratory tract, most commonly bronchiolitis. Lower respiratory involvement is most common in children under the age of 1, with up to 40% of primary infections progressing in bronchiolitis.
RSV is transmitted from human to human by respiratory droplets. The incubation period following RSV inoculation ranges from 2 to 8 days, with a typical incubation period of 4-6 days, depending on host characteristics such as the patient’s age and first RSV infection.
The virus quickly spreads throughout the respiratory tract after being inoculated into the nasopharyngeal or conjunctival mucosa, which targets its favored growing media, apical ciliated epithelial cells. It attaches to cellular receptors with the RSV-G glycoprotein, fuses with host cell membranes, and inserts its nucleocapsid into the host cell to initiate intracellular replication.
When the viral cytotoxicity and the host’s cytotoxic response combine to cause the necrosis of respiratory epithelial cells, the host’s inflammatory immune reaction is triggered, including both humoral and cytotoxic T-cell activation, with the subsequent implications of small airway obstruction and plugging by mucus, cellular waste, and DNA.
An alveolar blockage is a possibility in more challenging cases. Other residual effects include airway edema, decreased lung compliance, and ciliary dysfunction with poor mucus clearance.
RSV is a single-stranded RNA virus in the genus Pneumovirus that belongs to the Paramyxoviridae family. The RSV structure consists of a bilipid-layer envelope encasing a ribonucleoprotein core and three membrane proteins, one of which aids host cell attachment and the other in fusion.
RSV only has one serotype; however, it is divided into two strains, A and B, with changes in the structure of essential structural membrane proteins, notably the attachment protein.
Infants are more likely to contract RSV infection during a specific season, an older sibling presence, birth during the RSV season, low birth weight, congenital heart disease, male gender, younger than six months, exposure to smoking, residence in a suburban area, and a young mother are factors associated with RSV infection.
Additionally linked to an increased likelihood of needing hospitalization for an RSV infection are Down Syndrome, Cystic Fibrosis, Cerebral Palsy, and giving birth in September and October close to the RSV season.
RSV infection-related hospitalization in children typically results in complete recovery. They are released after three to four days. Infants at high risk spend more time in the hospital, require more mechanical breathing, and are more likely to be transferred to the intensive care unit.
RSV infection can spread from individuals for 3 to 8 days. However, young infants and those with compromised immune systems might continue to transmit the virus for up to 4 weeks after their symptoms disappear.
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