Respiratory Syncytial Virus (RSV)- An Overview

Respiratory syncytial virus (RSV) is a common and contagious virus that infects the respiratory tract of humans and animals. It belongs to the genus Orthopneumovirus within the family Pneumoviridae and order Mononegavirales. It has a single-stranded, negative-sense RNA genome that encodes 11 viral proteins.

RSV usually causes mild, cold-like symptoms in adults and older children, such as runny nose, cough, fever, sore throat, sneezing and headache . However, RSV can also cause severe infections of the lower respiratory tract, such as bronchiolitis (inflammation of the small airways in the lung) and pneumonia (infection of the lungs), especially in infants, young children, older adults and people with weakened immune systems . RSV is the most common cause of bronchiolitis and pneumonia in children younger than 1 year of age in the United States.

RSV spreads from person to person through respiratory droplets that are produced when an infected person coughs or sneezes. The virus can also be transmitted by touching contaminated surfaces or objects, such as toys, cups or utensils, and then touching the eyes, nose or mouth. RSV can survive on hard surfaces for several hours and on soft surfaces for shorter periods . The incubation period of RSV is about 4 to 6 days, and the virus can be shed for up to 8 days after the onset of symptoms.

There is no specific treatment or vaccine for RSV infection. Most cases are mild and resolve on their own with supportive care, such as rest, fluids and fever-reducing medications. However, some people may need hospitalization for oxygen therapy, intravenous fluids or mechanical ventilation if they develop severe breathing difficulties or complications . Prevention of RSV infection mainly relies on good hygiene practices, such as washing hands frequently, avoiding close contact with sick people, covering coughs and sneezes, and disinfecting surfaces and objects. For high-risk groups, such as premature infants or children with chronic lung or heart conditions, a monthly injection of a monoclonal antibody called palivizumab may be given during the RSV season to reduce the risk of severe disease .

RSV is a major public health problem worldwide. It is estimated that RSV causes about 33 million acute lower respiratory infections (ALRI) annually in children under 5 years of age, resulting in about 3 million hospitalizations and 120,000 deaths. RSV also causes significant morbidity and mortality in older adults, especially those with chronic obstructive pulmonary disease (COPD) or cardiovascular disease. RSV infections show seasonal patterns that vary by geographic region and climate. In temperate regions, RSV outbreaks typically occur during winter months, while in tropical regions, RSV activity may be year-round or associated with rainy seasons.

RSV is a complex virus that has evolved various strategies to evade the host immune system and cause recurrent infections throughout life. Understanding the molecular mechanisms of RSV pathogenesis and immunity is essential for developing effective vaccines and antiviral therapies against this important respiratory pathogen.

The RSV virion is an enveloped, non-segmented, negative-sense RNA virus that belongs to the family Pneumoviridae and the genus Orthopneumovirus. The virus has a variable shape and size, ranging from spherical particles of 100-350 nm in diameter to long filaments of 60-120 nm in diameter and up to 10 μm in length. The virus envelope consists of a lipid bilayer derived from the host cell membrane, which contains three transmembrane glycoproteins: the fusion protein (F), the attachment protein (G), and the small hydrophobic protein (SH) .

The F protein mediates the fusion of the viral membrane with the host cell membrane, allowing the release of the viral nucleocapsid into the cytoplasm. The F protein also forms syncytia, which are large multinucleated cells that result from the fusion of infected cells with neighboring cells . The F protein is a type I glycoprotein that forms homotrimers on the viral surface. Each F monomer consists of two disulfide-linked subunits: F1 and F2. The F1 subunit contains two heptad repeat regions (HR1 and HR2) that are involved in the conformational changes of the protein during fusion.

The G protein is responsible for the attachment of the virus to its receptors on the host cell surface. The G protein is a type II glycoprotein that forms homotetramers on the viral surface. The G protein has a short cytoplasmic tail, a transmembrane domain, and a large ectodomain that contains multiple N- and O-linked glycans. The G protein is highly variable among different strains of RSV and can elicit strain-specific neutralizing antibodies . The G protein binds to various molecules on the host cell surface, such as heparan sulfate proteoglycans, CX3CR1 (a chemokine receptor), and nucleolin .

The SH protein is a small type I glycoprotein that forms homopentamers on the viral surface. The SH protein has a long cytoplasmic tail, a transmembrane domain, and a short ectodomain that contains one N-linked glycan. The SH protein is conserved among different strains of RSV and can elicit cross-reactive neutralizing antibodies . The SH protein modulates the fusion activity of the F protein and may also interfere with the innate immune response of the host cell .

The viral nucleocapsid consists of a single-stranded, negative-sense RNA genome that is approximately 15.2 kb in size and encodes 11 structural and nonstructural proteins . The RNA genome is tightly associated with the nucleoprotein (N), which protects it from degradation and recognition by host cell receptors. The RNA genome also remains bound to the RNA polymerase complex, which consists of the large polymerase protein (L), the phosphoprotein (P), and the transcription processivity factor M2-1 . The matrix protein (M) lies underneath the lipid envelope and interacts with both the nucleocapsid and the cytoplasmic tails of the envelope glycoproteins. The M protein plays a role in viral assembly and budding .

The RNA genome has a leader region at its 3` end and a trailer region at its 5` end, which are involved in RNA replication and transcription. The RNA genome contains 10 open reading frames (ORFs) that are separated by intergenic regions. The ORFs are arranged in the following order from 3` to 5`: NS1, NS2, N, P, M, SH, G, F, M2, and L . The NS1 and NS2 proteins are nonstructural proteins that modulate host cell responses to viral infection. The N, P, M, SH, G, F, M2-1, and L proteins are structural proteins that constitute the viral particle. The M2 ORF encodes two proteins: M2-1 and M2-2. M2-1 is a transcription processivity factor that enhances mRNA synthesis by binding to nascent transcripts. M2-2 is an antitermination factor that regulates mRNA transcription by binding to L-P complexes .

The RSV genome consists of a single-stranded, negative-sense RNA that contains 10 open reading frames (ORFs) and is approximately 15.2 kilobases in size . The RNA encodes 11 structural and nonstructural proteins: NS1, NS2, N, P, M, SH, G, F, M2-1, M2-2, and L. A complementary copy of the genome called the antigenome is involved in RNA replication.

Both the genome and antigenome lack 5’ caps or 3’ poly(A) tails. Instead, they have a leader region and a trailer region at the 3’ and 5’ ends respectively. The leader region is a noncoding sequence that acts as a promoter for RNA synthesis. The trailer region is a noncoding sequence that contains signals for polyadenylation and termination of RNA synthesis.

The ORFs are arranged in the following order from the 3’ to the 5’ end: leader-NS1-NS2-N-P-M-SH-G-F-M2-L-trailer. Each ORF is flanked by conserved gene start (GS) and gene end (GE) sequences that act as transcription signals for the viral polymerase. The GS and GE sequences are complementary to each other and form a panhandle structure that initiates transcription.

The NS1 and NS2 proteins are nonstructural proteins that interfere with the host immune response by inhibiting type I interferon production and signaling. The N protein binds to the viral RNA and forms a helical nucleocapsid that protects the RNA from degradation and recognition by host receptors. The P protein associates with the N protein and acts as a cofactor for the viral polymerase. The M protein is a matrix protein that lies underneath the lipid envelope and interacts with the cytoplasmic tails of the envelope glycoproteins. The SH protein is a small hydrophobic protein that forms ion channels in the viral envelope. The G protein is an attachment glycoprotein that binds to cellular receptors such as CX3CR1. The F protein is a fusion glycoprotein that mediates the fusion of the viral envelope with the host membrane. The M2-1 protein is a transcription processivity factor that enhances the synthesis of long mRNAs. The M2-2 protein is a transcription antitermination factor that regulates the synthesis of short mRNAs. The L protein is the large subunit of the viral polymerase that catalyzes RNA synthesis.

The RNA encapsidation by the N protein and the association of other proteins with the nucleocapsid allow RSV to replicate and transcribe its genome in the cytoplasm of infected cells.

Respiratory syncytial virus (RSV) is a widespread human pathogen that causes frequent reinfections. It is the most common cause of bronchiolitis and pneumonia in children younger than 1 year of age in the United States. It is also the leading global cause of respiratory infections in infants and the second most frequent cause of death during the first year of life.

According to the CDC, RSV affects an estimated 64 million people and causes 160,000 deaths annually worldwide. In the United States, RSV causes about 2.1 million outpatient visits and 58,000 hospitalizations among children younger than 5 years old each year. RSV also causes about 177,000 hospitalizations and 14,000 deaths among adults older than 65 years old each year.

RSV infections show seasonal variations in different geographical areas of the world. In temperate climates, RSV outbreaks typically occur during the winter months, while in tropical and subtropical regions, RSV activity may peak during the rainy season or throughout the year .

Some groups of people are at higher risk of developing severe RSV disease, such as:

• Premature infants
• Infants and children with chronic lung or heart conditions
• Infants and children with weakened immune systems
• Children exposed to secondhand smoke
• Adults with chronic obstructive pulmonary disease (COPD) or congestive heart failure
• Elderly adults

RSV infection can also cause complications such as otitis media, asthma exacerbation, respiratory failure, and secondary bacterial infections. RSV infection can also increase the risk of developing asthma later in life.

Currently, there is no vaccine available for RSV prevention, although several candidates are under development. The only approved prophylactic treatment for RSV is palivizumab, a monoclonal antibody that can reduce the risk of hospitalization due to RSV in high-risk infants and young children. However, palivizumab is expensive and has limited availability and efficacy. Therefore, other preventive measures such as hand hygiene, avoiding contact with sick people, and covering coughs and sneezes are recommended to reduce the transmission of RSV.

RSV spreads from person to person through respiratory droplets that are produced when an infected person coughs or sneezes. These droplets can enter the eyes, nose, or mouth of another person who is in close contact with the infected person. RSV can also spread through direct contact with the virus, such as kissing an infected person or touching a contaminated surface and then touching the face .

RSV has an incubation period of 2 to 8 days, usually 4 to 6 days. People infected with RSV are usually contagious for 3 to 8 days and may become contagious a day or two before they start showing signs of illness. However, some infants, and people with weakened immune systems, can continue to spread the virus even after they stop showing symptoms, for as long as 4 weeks.

Children are often exposed to and infected with RSV outside the home, such as in school or childcare centers. They can then transmit the virus to other members of the family. RSV can survive for many hours on hard surfaces such as tables and crib rails. It typically lives on soft surfaces such as tissues and hands for shorter amounts of time.

People are typically infected with RSV for the first time as an infant or toddler and nearly all children are infected before their second birthday. However, repeat infections may occur throughout life, and people of any age can be infected. Infections in healthy children and adults are generally less severe than among infants and older adults with certain medical conditions.

People at highest risk for severe disease include:

• Premature infants
• Young children with congenital (from birth) heart or chronic lung disease
• Young children with compromised (weakened) immune systems due to a medical condition or medical treatment
• Children with neuromuscular disorders
• Adults with compromised immune systems
• Older adults, especially those with underlying heart or lung disease

In the United States and other areas with similar climates, RSV circulation generally starts during fall and peaks in the winter. The timing and severity of RSV circulation in a given community can vary from year to year.

RSV replicates in the cytoplasm of infected cells by using its negative-sense RNA genome as a template for transcription and replication. The replication cycle of RSV involves the following steps:

• Attachment: The RSV attaches to its receptors on the apical surface of ciliated epithelial cells through the attachment glycoprotein (G protein). The G protein binds to various molecules on the host cell surface, such as heparan sulfate, CX3CR1, and nucleolin .
• Fusion: The fusion protein (F) mediates the fusion of the viral membrane with the host membrane and releases the nucleocapsid into the host cell cytoplasm. The F protein undergoes a conformational change from a prefusion to a postfusion state, bringing the viral and cellular membranes closer together.
• Biosynthesis: The negative-sense RNA genome serves as a template for the RSV polymerase complex, consisting of the large protein (L) and the phosphoprotein (P), to synthesize mRNAs and genome progeny. The polymerase complex recognizes the gene start and gene end signals on the genome and transcribes each gene sequentially from 3` to 5` end. The mRNAs are capped and polyadenylated by viral enzymes. The surface glycoproteins (G, F, and SH) are produced, post-translationally modified, and transported through the endoplasmic reticulum and Golgi apparatus to the host cell membrane. The structural and nonstructural proteins (N, P, M, M2, NS1, NS2, and L) are synthesized by translation of the mRNAs. Progeny of genome and antigenome (a positive-sense copy of the genome) are also synthesized by the polymerase complex.
• Assembly: The matrix protein (M) associates with the replication complex and interacts with the cytoplasmic tail of F protein to form viral filaments, allowing the viral nucleocapsid to be packaged into viral filament particles. The M protein also regulates viral transcription and replication by modulating the activity of the polymerase complex.
• Release: The RSV is released from the cells by budding through the plasma membrane, taking up the surface glycoproteins with the membrane that constitutes the viral envelope. The virus particles can be spherical or filamentous in shape.

RSV pathogenesis is a complex and variable process affected by many host and viral factors. The disease can range from mild rhinitis to severe diseases of the upper and lower respiratory tract like bronchiolitis and pneumonia .

After the virus enters the host body through the transmission routes, the virus rapidly spreads into the respiratory tract, where it multiplies in the apical ciliated epithelial cells. In typical RSV primary infection, host response is dominated by IFN-γ produced by NK, CD4+, and CD8+ T cells. RSV infection after immunization with formalin-inactivated RSV (FI-RSV) or RSV G glycoprotein induces an immune response dominated by type 2 cytokines and is associated with lung eosinophilia and airway mucus production. RSV infection with allergic inflammation or absence of STAT1-mediated signaling induces airway epithelial mucus with the expression of IL-17 cytokine.

Both the humoral and cytotoxic T-cell activation is triggered which results in viral cytotoxicity as well as cytotoxicity from the host’s immune response causing necrosis of respiratory epithelial cells . It can lead to small airway obstruction by mucus, cellular debris as well as alveolar obstruction. Other effects may include ciliary dysfunction with impaired mucus clearance, airway edema, and decreased lung compliance .

The severity of RSV infection depends on various factors such as age, prematurity, underlying lung or heart diseases, immunosuppression, viral strain, viral load, and coinfection with other pathogens . Infants are more susceptible to severe RSV infection due to their immature immune system, narrow airways, and lack of maternal antibodies. Older adults and immunocompromised patients are also at risk of severe RSV infection due to their declining immune function and comorbidities.

Some possible additional sentences to conclude the point are:

• RSV pathogenesis is still not fully understood and requires further research to elucidate the molecular mechanisms involved in viral replication, host immune response, and tissue damage.
• A better understanding of RSV pathogenesis may help to develop effective vaccines and antiviral therapies to prevent and treat RSV infection .
• RSV pathogenesis also provides insights into other respiratory viral infections such as influenza, coronavirus, and parainfluenza that share some common features with RSV infection.
  
  
  

  Clinical Manifestations of Respiratory Syncytial Virus (RSV)

  
  

The symptoms of RSV infection usually appear about four to six days after exposure to the virus . In adults and older children, RSV usually causes mild cold-like signs and symptoms. These may include:

• Congested or runny nose
• Dry cough
• Low-grade fever
• Sore throat
• Sneezing
• Headache

In very young infants with RSV, the only symptoms may be irritability, decreased activity, and breathing difficulties.

In severe cases, RSV infection can spread to the lower respiratory tract, causing pneumonia or bronchiolitis — inflammation of the small airway passages entering the lungs. Signs and symptoms may include:

• Fever
• Severe cough
• Wheezing — a high-pitched noise that`s usually heard on breathing out (exhaling)
• Rapid breathing or difficulty breathing — the person may prefer to sit up rather than lie down
• Bluish color of the skin due to lack of oxygen (cyanosis)
• Middle ear infection (otitis media)

Most children and adults recover in one to two weeks, although some might have repeated wheezing. Severe or life-threatening infection requiring hospitalization may occur in premature infants or in anyone who has chronic heart or lung problems .

RSV can also cause more severe infections in people who are at high risk for complications, such as:

• Infants younger than 6 months of age
• Infants and children with underlying lung diseases, such as bronchopulmonary dysplasia or congenital heart diseases
• Infants exposed to secondhand smoking
• Immunocompromised patients (e.g., patients with immune disorders, or who have recently undergone organ transplantation)
• Individuals with asthma
• Individuals with cardiopulmonary disease
• Elderly patients having a chronic obstructive pulmonary disease (COPD)

Call your healthcare professional if you or your child is having difficulty breathing, not drinking enough fluids, or experiencing worsening symptoms.

Diagnosis of Respiratory Syncytial Virus (RSV)

RSV infection can be difficult to diagnose based on the symptoms alone, as they can be similar to those of other respiratory viruses. Therefore, laboratory tests are often needed to confirm the diagnosis. Some of the common tests used for RSV diagnosis are:

• Rapid antigen detection tests (RADTs): These tests check for certain proteins from the RSV virus called antigens in a fluid sample from the nose. Antigens trigger the immune system to attack the virus. RADTs can provide results in an hour or less . However, they may sometimes give false-negative results, especially in older children and adults who have lower levels of viral shedding. Therefore, a more sensitive test (such as PCR) may be needed to confirm the diagnosis in some cases.
• Direct fluorescent antibody (DFA): This test uses fluorescent dyes to detect RSV antigens in a nasal swab or aspirate sample under a microscope. DFA is more sensitive and specific than RADTs, but it requires specialized equipment and trained personnel. It is also more expensive and time-consuming than RADTs.
• Polymerase chain reaction (PCR): This test amplifies and detects the genetic material of the RSV virus (RNA) in a nasal swab or aspirate sample. PCR is the most sensitive and specific test for RSV diagnosis, and it can also distinguish between different strains of the virus. It is particularly useful for older children and adults, as well as for hospitalized and immunocompromised patients who are at higher risk of severe RSV infection. However, PCR is more costly than other tests and may have a longer turnaround time in some laboratory settings.
• Viral culture: This test involves growing the RSV virus in a cell culture medium and observing its growth under a microscope. Viral culture is highly specific and allows for the storage of the virus for further studies. However, it is not recommended for initial clinical management due to its low sensitivity and slow turnaround time of about 3 to 5 days . It may also miss coinfections with other respiratory viruses.

Other laboratory tests that may be used to diagnose complications of RSV infection include:

• Blood tests: These tests may check for white blood cell counts or detect viruses, bacteria, or other germs in the blood that may cause secondary infections or sepsis.
• Chest X-rays: These tests may check for lung inflammation or signs of pneumonia or bronchiolitis caused by RSV infection.
• Pulse oximetry: This test uses a painless skin monitor to measure the oxygen levels in the blood. Low oxygen levels may indicate respiratory distress or failure due to RSV infection .

Treatment of RSV

Mild infections usually do not require any treatment and antibiotics or bronchodilators are not used during RSV infections. Supportive treatment may include :

• Acetaminophen (Tylenol and other medications) may be given to the patient to reduce fever. However, aspirin should never be given to a child.
• Nasal saline drops and suctioning can be used to help clear a stuffy nose.
• Antibiotics can be prescribed in case of bacterial infection, such as bacterial pneumonia.
• It is important to drink enough fluids to prevent dehydration and also look out for signs of dehydration like dry mouth, little to no urine output, sunken eyes, and extreme fussiness or sleepiness.

For further complications, treatments at the hospital may include :

• Intravenous (IV) fluids
• Humidified oxygen
• A breathing machine (mechanical ventilation in extreme cases)

Currently, there are no vaccines licensed and used for RSV infections but a number of vaccine candidates are in their clinical trial phases testing the safety and efficacies of these vaccines. However, palivizumab can be administered to infants and young children who are at high risk for severe disease.

Prevention and Control of RSV

As RSV is highly contagious, suitable preventive interventions must be taken to prevent its spread. Some of the measures include :

• Avoiding close contact with infected people
• Hand washing when handling the baby
• Covering the mouth while sneezing or coughing with a tissue or upper shirt sleeve and not with the hand
• Cleaning frequently touched surfaces such as doorknobs and mobile devices
• Avoiding sharing cups, bottles, towels, toys, utensils, etc. that have been contaminated with the virus
• Limiting the time children spend in childcare centers or other potentially contagious settings during periods of high RSV activity
• Educating parents, caregivers, and health care providers about the risk, transmission, preventive measures, and other factors associated with RSV infections

People with flu-like symptoms should avoid contact with children at high risk for severe RSV diseases, including premature infants, children younger than 2 years of age with chronic lung or heart conditions, children with weakened immune systems, or children with neuromuscular disorders. If this is not possible, they should carefully follow the prevention steps mentioned above and wash their hands before interacting with such children. They should also refrain from kissing high-risk children while they have cold-like symptoms.

Parents of children at high risk for developing severe RSV disease should help their child, when possible, do the following:

• Avoid close contact with sick people
• Wash their hands often with soap and water for at least 20 seconds
• Avoid touching their face with unwashed hands

Researchers are working to develop RSV vaccines, but none are available yet. A drug called palivizumab (pah-lih-VIH-zu-mahb) is available to prevent severe RSV illness in certain infants and children who are at high risk for severe disease. This could include, for example, infants born prematurely or with congenital (present from birth) heart disease or chronic lung disease. The drug can help prevent serious RSV disease, but it cannot help cure or treat children already suffering from serious RSV disease, and it cannot prevent infection with RSV. If your child is at high risk for severe RSV disease, talk to your healthcare provider to see if palivizumab can be used as a preventive measure.

Some additional points are:

• Palivizumab is given as an injection once a month during the RSV season (usually November to April) and can reduce the risk of hospitalization due to RSV by about 50%.
• Palivizumab is not recommended for healthy infants or children older than 24 months of age.
• Palivizumab does not interfere with routine childhood vaccinations and can be given at the same time.

RSV infection can be difficult to diagnose based on the symptoms alone, as they can be similar to those of other respiratory viruses. Therefore, laboratory tests are often needed to confirm the diagnosis. Some of the common tests used for RSV diagnosis are:

• Rapid antigen detection tests (RADTs): These tests check for certain proteins from the RSV virus called antigens in a fluid sample from the nose. Antigens trigger the immune system to attack the virus. RADTs can provide results in an hour or less . However, they may sometimes give false-negative results, especially in older children and adults who have lower levels of viral shedding. Therefore, a more sensitive test (such as PCR) may be needed to confirm the diagnosis in some cases.
• Direct fluorescent antibody (DFA): This test uses fluorescent dyes to detect RSV antigens in a nasal swab or aspirate sample under a microscope. DFA is more sensitive and specific than RADTs, but it requires specialized equipment and trained personnel. It is also more expensive and time-consuming than RADTs.
• Polymerase chain reaction (PCR): This test amplifies and detects the genetic material of the RSV virus (RNA) in a nasal swab or aspirate sample. PCR is the most sensitive and specific test for RSV diagnosis, and it can also distinguish between different strains of the virus. It is particularly useful for older children and adults, as well as for hospitalized and immunocompromised patients who are at higher risk of severe RSV infection. However, PCR is more costly than other tests and may have a longer turnaround time in some laboratory settings.
• Viral culture: This test involves growing the RSV virus in a cell culture medium and observing its growth under a microscope. Viral culture is highly specific and allows for the storage of the virus for further studies. However, it is not recommended for initial clinical management due to its low sensitivity and slow turnaround time of about 3 to 5 days . It may also miss coinfections with other respiratory viruses.

Other laboratory tests that may be used to diagnose complications of RSV infection include:

• Blood tests: These tests may check for white blood cell counts or detect viruses, bacteria, or other germs in the blood that may cause secondary infections or sepsis.
• Chest X-rays: These tests may check for lung inflammation or signs of pneumonia or bronchiolitis caused by RSV infection.
• Pulse oximetry: This test uses a painless skin monitor to measure the oxygen levels in the blood. Low oxygen levels may indicate respiratory distress or failure due to RSV infection .

Mild infections usually do not require any treatment and antibiotics or bronchodilators are not used during RSV infections. Supportive treatment may include :

• Acetaminophen (Tylenol and other medications) may be given to the patient to reduce fever. However, aspirin should never be given to a child.
• Nasal saline drops and suctioning can be used to help clear a stuffy nose.
• Antibiotics can be prescribed in case of bacterial infection, such as bacterial pneumonia.
• It is important to drink enough fluids to prevent dehydration and also look out for signs of dehydration like dry mouth, little to no urine output, sunken eyes, and extreme fussiness or sleepiness.

For further complications, treatments at the hospital may include :

• Intravenous (IV) fluids
• Humidified oxygen
• A breathing machine (mechanical ventilation in extreme cases)

Currently, there are no vaccines licensed and used for RSV infections but a number of vaccine candidates are in their clinical trial phases testing the safety and efficacies of these vaccines. However, palivizumab can be administered to infants and young children who are at high risk for severe disease.

As RSV is highly contagious, suitable preventive interventions must be taken to prevent its spread. Some of the measures include :

• Avoiding close contact with infected people
• Hand washing when handling the baby
• Covering the mouth while sneezing or coughing with a tissue or upper shirt sleeve and not with the hand
• Cleaning frequently touched surfaces such as doorknobs and mobile devices
• Avoiding sharing cups, bottles, towels, toys, utensils, etc. that have been contaminated with the virus
• Limiting the time children spend in childcare centers or other potentially contagious settings during periods of high RSV activity
• Educating parents, caregivers, and health care providers about the risk, transmission, preventive measures, and other factors associated with RSV infections

People with flu-like symptoms should avoid contact with children at high risk for severe RSV diseases, including premature infants, children younger than 2 years of age with chronic lung or heart conditions, children with weakened immune systems, or children with neuromuscular disorders. If this is not possible, they should carefully follow the prevention steps mentioned above and wash their hands before interacting with such children. They should also refrain from kissing high-risk children while they have cold-like symptoms.

Parents of children at high risk for developing severe RSV disease should help their child, when possible, do the following:

• Avoid close contact with sick people
• Wash their hands often with soap and water for at least 20 seconds
• Avoid touching their face with unwashed hands

Researchers are working to develop RSV vaccines, but none are available yet. A drug called palivizumab (pah-lih-VIH-zu-mahb) is available to prevent severe RSV illness in certain infants and children who are at high risk for severe disease. This could include, for example, infants born prematurely or with congenital (present from birth) heart disease or chronic lung disease. The drug can help prevent serious RSV disease, but it cannot help cure or treat children already suffering from serious RSV disease, and it cannot prevent infection with RSV. If your child is at high risk for severe RSV disease, talk to your healthcare provider to see if palivizumab can be used as a preventive measure.

Some additional points are:

• Palivizumab is given as an injection once a month during the RSV season (usually November to April) and can reduce the risk of hospitalization due to RSV by about 50%.
• Palivizumab is not recommended for healthy infants or children older than 24 months of age.
• Palivizumab does not interfere with routine childhood vaccinations and can be given at the same time.

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