Parainfluenza viruses in adults

INTRODUCTION — Parainfluenza viruses (PIVs) are important respiratory pathogens in adults and children. Although parainfluenza viruses are commonly recognized as a significant cause of morbidity and mortality in children, their impact in adults is less well characterized [1]. In adults, parainfluenza viruses usually cause mild upper respiratory infections (URIs) but can lead to life-threatening lower respiratory tract infections, particularly in immunocompromised patients [2,3].

The virology, clinical manifestations, diagnosis, and treatment of parainfluenza viruses in adults will be reviewed here. Infection with parainfluenza viruses in children is discussed separately. (See "Parainfluenza viruses in children".)

VIROLOGY — PIVs are single-stranded, enveloped RNA viruses belonging to the genus Paramyxovirus in the Paramyxoviridae family [4]. This family also includes mumps, measles, respiratory syncytial viruses, human metapneumovirus, and Nipah and Hendra viruses [5-7].

Structure — Parainfluenza virions are pleomorphic, range in diameter from 150 to 200 nanometers, and contain approximately 15,500 nucleotides [5]. The single strand of negative-sense RNA encodes the following viral proteins: nucleocapsid protein (N), phosphoprotein (P), matrix protein (M), fusion glycoprotein (F), hemagglutinin-neuraminidase glycoprotein (HN), and polymerase (L) (figure 1) [5]. In addition, serotype PIV-3 encodes C, D, and V proteins, PIV-1 encodes a C protein, and PIV-2 encodes a V protein.

●The HN and F proteins project through the lipid envelope and form the major antigenic targets for neutralizing antibody [8].

●The nucleocapsid core is composed of N, P, and L proteins in association with viral RNA. N proteins bind tightly to the viral genome, creating a template for the RNA polymerase composed of the P and L proteins [9].

●The HN glycoproteins are involved in attachment of the virus to the host cell via interactions with sialic acid residues on the cell surface [10]. This interaction allows the F protein to mediate virus-cell membrane fusion, which is required for nucleocapsid entry and infection of the host cell. The neuraminidase portion of the HN protein mediates budding of progeny virions from the surface of infected cells [10,11].

The HN glycoproteins of PIVs are more antigenically stable than those of influenza A viruses. However, the development of antigenic differences over time has been reported [12], and this may hinder production of an effective vaccine. (See "Influenza: Epidemiology and pathogenesis".)

Serotypes — Four major serotypes of human PIVs (PIV-1, -2, -3, and -4) have been described [1,6,7]. PIV-1 and -3 are members of the Respirovirus genera, whereas PIV-2 and -4 are members of the Rubulavirus genera [7]. The classification of the PIVs into two genera is based upon genetic characteristics [5].

In a surveillance study of PIVs in children and adults in the United States from 1990 to 2004 in which more than 40,000 cases were detected, the serotypes were found in the following proportions [13]:

●PIV-3 – 52 percent

●PIV-1 – 26 percent

●PIV-2 – 12 percent

●PIV-4 – 2 percent

●Uncharacterized serotype – 8 percent

Clinical manifestations vary by serotype and the site of viral replication. (See 'Pathogenesis' below and 'Clinical manifestations' below.)

PATHOGENESIS — PIVs initially infect epithelial cells of the nose and oropharynx and can spread distally to the large and small airways [14]. Viral replication rises significantly in the first 24 hours following initial infection, peaking at approximately two to five days [15]. Viral antigen can be detected in the apical portion of respiratory epithelial cells from days 1 to 6 of infection with a decrease on day 7 [16].

The severity of infection appears to correlate with the sites of viral replication and the infecting PIV serotype [17-20]. PIV-1 and PIV-2 replicate efficiently in the upper airway epithelium and are typically associated with upper respiratory infections (URIs) and croup (which results from laryngeal and upper tracheal inflammation) [15,19,20]. PIV-3 replicates in the lower respiratory tract, and infection can lead to bronchiolitis and pneumonia [15]. However, these correlations are not strict; PIV-1 and -2 can cause severe lower tract disease, and PIV-3 can cause self-limited mild URIs.

Pathologic examination of infected tissues in animal models of PIV infection suggests that minimal cellular damage results from direct viral effects [16]. As is the case with other respiratory viruses, the host immune response is likely to play an important role in the pathogenesis of PIV infection [15]. The increase in airway responsiveness (eg, bronchospasm) that is often associated with PIV-3 infection (and other respiratory viruses such as respiratory syncytial virus) may result from increased stromal interleukin-11 production, enhanced acetylcholine release, and increased release of leukotrienes [20-23].

EPIDEMIOLOGY

Prevalence — Human PIVs are among the most common causes of respiratory tract infections worldwide [24-26].

The burden and severity of illness vary with age and the infecting PIV serotype. The majority of PIV-associated illnesses that come to clinical attention occur in young children [27]. Although upper respiratory infections (URIs) are the most common form of PIV infection in children, croup and lower respiratory tract infections account for substantial disease burden. In a surveillance study in the United States, PIV-associated croup, bronchiolitis, and pneumonia accounted for 1.1 hospitalization per 1000 children aged <5 years old [28]. PIV-3 accounted for the majority of cases, followed by PIV-1 and PIV-2. (See "Parainfluenza viruses in children".)

By adulthood, >90 percent of individuals have antibodies to PIVs [6]. However, these antibodies are only partially protective and reinfection can occur [6]. Among adults, URIs and pneumonia are the most common clinical manifestations; PIV-3 is the predominant infecting serotype [19]. Likewise, PIV-3 is most frequently detected among adults hospitalized with PIV with peak incidence in the late spring and early summer [29].

In a large epidemiologic survey of over 2000 patients with community-acquired pneumonia in the United States, PIVs were detected in approximately 3 percent of cases [25]. Similar prevalence rates have been reported in other studies [30-32]. The severity of illness is greatest in older adults (particularly residents of long-term care facilities) and immunocompromised adults [33]. (See 'Risk factors for severe disease' below.)

Trends in PIV infections in the United States are monitored by the National Respiratory and Enteric Virus Surveillance System and can be found on the United States Centers for Disease Control and Prevention website [24]. Like other respiratory viral infections, the incidence of PIV infection dropped during the COVID-19 pandemic when infection control practices were in place and has since rebounded.

Transmission

Route of transmission — PIVS are transmitted from person to person, primarily via inhalation of large droplets or fomites [34]. Virus can be transmitted from patients with symptomatic infections or from those with subclinical infections [35-37]. The latter population is presumed to play a role in the development of outbreaks and can make infection control in health care facilities challenging. (See 'Outbreaks' below and 'Infection control' below.)

Seasonality — PIV infections occur throughout the world and throughout the year, with certain serotypes predominating during the spring or fall [27,38]. In the United States, peak seasonal activity for PIV-1 seems to occur biennially during the fall of odd-numbered years (figure 2) [13,39]. PIV-2 transmission tends to peak annually each fall [13]. PIV-3 is endemic and its transmission patterns are least predictable, though seasonal activity tends to peak in the spring and early summer [6,13,29]. Seasonal patterns of PIV-4 infections have not been established since the disease is usually mild and the virus is difficult to detect. In tropical countries, PIVs do not exhibit seasonal variation [40].

Outbreaks — Although most PIV infections are community acquired, outbreaks can occur within health care facilities and other close-contact settings and can be particularly severe when older individuals and immunocompromised patients are affected. [33,41-48].

As an example, an outbreak involving 26 patients on an inpatient hematology unit was traced to a single admission from the community and persisted over a two-month period [44]. The majority of affected patients developed lower respiratory tract infections, and the case-fatality rate was 38 percent. In one retrospective review of >100 immunocompromised patients in a hematology and stem cell transplantation (SCT) unit, nosocomial transmission was prominent, occurring in 63 percent of SCT recipients [49].

Although few studies have been performed in homeless shelters, one study found PIV transmission to be common and that shelter-specific prevention may be needed to mitigate infections [50].

Risk factors for severe disease — Factors associated with the development of lower respiratory tract infection and severe disease in adults include [30,38,51-54]:

●Immunocompromise (particularly hematopoietic stem cell and lung transplantation)

●Older age

●Cardiac and pulmonary comorbidities

●Infection with PIV serotype 3 (PIV-3)

Among immunocompromised patients, the highest morbidity and mortality has been described in hematopoietic cell transplant (HCT) recipients, patients with leukemia, and lung transplant recipients [51,55-59]. In these patient populations, glucocorticoid (≥1 mg/kg/day prednisone equivalent) use has been linked to the development of lower respiratory tract infections and mortality [51,60-62]. Whether glucocorticoids play a direct role in driving disease severity or whether their use is a marker for a sicker patient population (eg, patients with graft-versus-host disease, organ rejection) is unclear. Among solid organ transplantation, clinically significant disease is most common among lung transplant recipients [54].

Secondary bacterial or fungal pneumonia complicating PIV lower respiratory tract infection is also a significant contributor to morbidity and mortality, particularly in immunocompromised hosts [51,62]. As an example, in a cohort of 253 HCT recipients with PIV infection, infection with a second pulmonary pathogen occurred in 29 of 55 patients (53 percent) with PIV-3 pneumonia [51]. The 30-day mortality was higher among those with pulmonary copathogen when compared with those without copathogens (48 versus 19 percent; p = 0.024). A similar trend was observed at 180 days, with a mortality rate of 96 percent in those with pulmonary copathogen compared with 50 percent in those without copathogens.

Among hospitalized adults overall, death is uncommon (5.1 percent) with bacterial coinfection, fungal coinfection, decreased body mass index, and increased respiratory rate being most strongly associated with mortality [29].

CLINICAL MANIFESTATIONS — The clinical manifestations of PIV infections in adults vary based on the patient's age and immune status as well as the infecting PIV serotype. The spectrum ranges from asymptomatic infections and mild upper respiratory infections (URIs) to severe and fatal pneumonia.

URI and acute bronchitis — Upper respiratory infections (URIs) and acute bronchitis are the most common clinical manifestation of PIV infection in adults. The clinical features associated with URI and acute bronchitis caused by PIVs are similar to those caused by other pathogens.

Signs and symptoms of PIV-associated URI include fever, rhinorrhea, cough, and/or sore throat [41]. Other upper respiratory tract manifestations of PIV infection, such as croup, occur more commonly in children. (See "Parainfluenza viruses in children", section on 'Clinical presentation'.)

As with other forms of acute bronchitis, prolonged cough is typically a dominant symptom of PIV-associated acute bronchitis. Wheezing and mild dyspnea may accompany the cough. (See "Acute bronchitis in adults".)

Most cases of URI and acute bronchitis caused by PIV are self-limited. Rarely, infection progresses to involve the lower respiratory tract, particularly in older and immunocompromised adults [51,56,62,63].

Pneumonia — Lower respiratory tract infections can evolve from URIs or may be the initial presenting manifestation of PIV infection [29,51,60]. Pneumonia and acute bronchitis are the most common PIV-associated lower tract infection in adults. Bronchiolitis occurs more commonly in children and is discussed separately. (See "Bronchiolitis in infants and children: Clinical features and diagnosis".)

As with other forms of pneumonia, the most common symptoms and signs associated with pneumonia due to PIV include fever, cough, sputum production, and dyspnea [29]. Wheezing due to bronchospasm is common. PIV pneumonia can be severe. In a retrospective review of 550 adults hospitalized with PIV infection, over 50 percent required supplemental oxygen, approximately 10 percent intensive care, and approximately 7 percent ventilatory support [29]. Severe disease tends to occur more commonly in older and immunocompromised adults.

Radiographic findings are nonspecific, similar to other viral pneumonias, and include tree-in-bud opacities, interstitial infiltrates, ground-glass opacities, bronchial wall thickening, and peribronchial consolidation (image 1) [36,64,65].

Bacterial and fungal coinfection — Secondary bacterial and fungal coinfections are not uncommon in patients with PIV pneumonia and are major contributors to mortality [29,51,66]. Coinfection should be suspected if imaging is not consistent with a purely viral pneumonia (ie, lobar or nodular pneumonia) or if there is a biphasic illness with initial improvement followed by clinical or radiologic worsening.

In one retrospective review of hospitalized patients with PIV infection, coinfection with any pathogen occurred in 136 of 550 patients (25 percent) [29]. The majority of coinfections involved the respiratory tract (83 percent). Of those, approximately 40 percent were bacterial, 13 percent fungal, and the remainder viral. Mortality was higher in patients with bacterial and fungal coinfection when compared with patients without coinfections. The severity of illness was higher in patients with viral coinfections compared with those without, but mortality was not significantly increased.

Bacterial respiratory pathogens are similar to those that cause community-acquired and hospital-acquired pneumonia and include Streptococcus pneumoniae, Staphylococcus aureus, Pseudomonas aeruginosa, and gram-negative rods [3,29,51]. Fungal coinfections are more common in immunocompromised hosts; the most common fungal coinfection is aspergillosis, followed by infection with Candida spp. Viral respiratory copathogens, such as influenza, rhinovirus, adenovirus, respiratory syncytial virus, and human metapneumovirus, typically are present initially and are generally associated with more severe courses.

Other manifestations — Otitis media and sinusitis can occur as either primary PIV infections or secondary bacterial superinfections [67]. Nonrespiratory complications of PIV are rarely reported but include meningitis [68], myocarditis and/or pericarditis [69], and Guillain-Barré syndrome [70].

Chronic airway diseases

Asthma and COPD exacerbations — PIV infection is associated with exacerbations of asthma and chronic obstructive pulmonary disease (COPD) [23,71,72]. In patients with asthma, PIV infections are common triggers for exacerbations and may also play a role in asthma pathogenesis. (See "Role of viruses in wheezing and asthma: An overview", section on 'Asthma exacerbations' and "Role of viruses in wheezing and asthma: An overview", section on 'Development of asthma'.)

In patients with COPD, PIV account for approximately 8 percent of acute exacerbations [73]. As with asthma, PIV infections have a putative role in COPD pathogenesis [19]. (See "Evaluation for infection in exacerbations of chronic obstructive pulmonary disease".)

Pulmonary dysfunction in transplant recipients — PIV infections have been associated with significant short- and long-term pulmonary dysfunction in both lung transplant and hematopoietic cell transplant (HCT) recipients [53].

In lung transplant recipients, PIV infections (particularly lower respiratory tract infections) have been associated with lung allograft dysfunction (chronic lung rejection) and graft loss [56,57,74-77]. As an example, in a cohort study evaluating 139 lung transplant recipients, pneumonia caused by community-acquired respiratory viruses was associated with an increased risk of chronic lung allograft dysfunction (CLAD; hazard ratio [HR] 1.64, 95% CI 1.17-2.28). Among respiratory viruses, the risk was highest among those with adenoviral infection followed by PIV infections (HR 13.42, 95% CI 2.81-64.59 and HR 2.18, 95% CI 1.34-3.56, respectively). A recent meta-analysis of available studies demonstrated that PIV was associated with relatively low pooled 30-day mortality (0 to 3 percent), but CLAD progression 180 to 360 days postinfection was substantial (pooled incidences 19 to 24 percent). Progression to CLAD is associated with more severe infections involving the lower respiratory tract [78]. While the pathogenesis is not well understood, both direct viral cytopathic effects and resultant inflammation within the allograft are thought to contribute to development of rejection and chronic graft dysfunction. (See "Chronic lung allograft dysfunction: Bronchiolitis obliterans syndrome", section on 'Etiology and risk factors'.)

Similarly, PIV and other respiratory viral infections have been associated with chronic pulmonary impairment in HCT recipients, characterized by persistent airflow obstruction based on spirometry [79,80]. This chronic impairment has been associated with increased mortality, particularly among HCT recipients with graft-versus-host disease.

DIAGNOSIS — The need to pursue a specific microbiologic diagnosis of PIV infection varies with severity of illness, patient immune status, and treatment setting.

●For most immunocompetent outpatients with mild respiratory tract infections (ie, upper respiratory infection [URI], acute bronchitis, or mild community-acquired pneumonia [CAP]), testing for PIV or other pathogens is not necessary, as results generally do not change management.

●For hospitalized patients with CAP, we generally include testing for PIV in our initial diagnostic evaluation during respiratory virus season (late fall to early spring in the northern hemisphere) and during known outbreaks.

●For most immunocompromised patients presenting with fever or symptoms of upper or lower respiratory tract infection, we generally test for PIV and other respiratory viruses as part of our evaluation regardless of treatment setting.

Polymerase chain reaction (PCR) is the preferred testing method [81,82]. Usually, we obtain a nasopharyngeal swab for testing. However, PCR can also be performed on nasal washings (which may enhance sensitivity) and lower respiratory tract specimens, such as bronchoalveolar lavage fluid [83]. PCR for PIV can be performed directly as a single assay or as part of a multiplex panel [84-87]. The availability of each assay varies from institution to institution.

In general, PCR has higher sensitivity than culture or antigen detection assays [84,88-90]. Most PCR assays detect serotypes 1, 2, and 3 reliably. However, both the overall sensitivity and the sensitivity for certain PIV serotypes may be reduced when using multiplex assays [91-95]. As a practical note, not all multiplex assays include PIV in their panels, so it is important to select one that does or use an adjunct single assay when diagnosis is needed.

A positive PCR result confirms the diagnosis of PIV infection. However, because PIV infection can be asymptomatic or occur concurrently with other respiratory pathogens, we perform a thorough evaluation for other contributors of the patient's symptoms and signs as part of our diagnostic approach. This is particularly important for severely ill and immunocompromised patients who are at higher risk for bacterial and fungal coinfections and/or when radiology suggests possible coinfection. (See 'Bacterial and fungal coinfection' above.)

Other tests have limited value for the diagnosis of PIV infection. Culture and serology are not widely available and have long turnaround times. Rapid antigen testing kits are also not routinely available and have only moderate sensitivity [6,96].

TREATMENT — There are no antiviral agents with proven efficacy for the treatment of PIV infections [3]. Fortunately, most immunocompetent patients with parainfluenza virus infections have mild, self-limited illnesses and recover with supportive care alone.

For adults with pneumonia caused by PIV, the cornerstones of treatment include:

●Supportive care – Supplemental oxygen and/or ventilatory support may be needed for patients with severe pneumonia. Use of inhaled bronchodilators (eg, albuterol) can help with airway hyper-responsiveness and wheezing [29]. Because airway hyper-responsiveness can be profound, corticosteroids are sometimes used to help reduce inflammation, though this is controversial, particularly in immunocompromised patients [97].

●Reduction of immunosuppression (if immunocompromised) – For immunocompromised patients with severe disease, immunosuppression should be reduced when feasible [2]. Because glucocorticoid use has been associated with the development of severe PIV infections, we generally discontinue or taper glucocorticoid use when possible. However, the best approach to reducing immunosuppression varies from patient to patient and needs to be individualized.

●Close monitoring and prompt treatment for secondary infections – Patients with PIV are at increased risk of bacterial and fungal infections. Thus, we monitor patients closely for any clinical or radiographic worsening (eg, development of progressive dyspnea or new consolidations on chest imaging). Our threshold for pursuing a thorough diagnostic evaluation (eg, serum fungal markers and/or bronchoscopy) and initiating empiric antibiotics for secondary bacterial and fungal pneumonia is low, particularly in immunocompromised patients. Antifungal prophylaxis is not routinely recommended for patients at risk for secondary fungal infections; however, some experts do use antifungal prophylaxis (with anti-mold activity) for 30 to 90 days after diagnosis of viral lower respiratory tract infections for severely immunocompromised individuals.

We generally do not use ribavirin for the treatment of PIV infections because of lack of proven efficacy and the high side effect profile of this drug [53]. Case reports and small case series have shown variable results for the use of aerosolized, oral, or intravenous ribavirin for the treatment of PIV infection in hematopoietic cell transplant (HCT) and solid organ transplant recipients [51,63,98-102]. Ribavirin is often considered for treatment of PIV infection in lung transplant recipients because of the association between PIV infection and chronic lung allograft dysfunction (CLAD). However, evidence supporting its use is limited. While some individual observational studies suggest benefit, in a systematic review of observational studies in lung transplant recipients, ribavirin did not appear to prevent progression to CLAD (OR 0.61 [0.27-1.18], P = 0.16) [78].

The use of intravenous immune globulin (IVIG) for treatment of severe PIV infections is controversial. We generally do not use IVIG for treatment, as there are insufficient data to support its use [51,103]. However, some experts favor IVIG use for patients with severe infections, particularly in patients with hypogammaglobulinemia [104,105].

DAS181 (an inhaled recombinant sialidase fusion protein) is a promising investigational agent for the treatment of parainfluenza infections. In vitro, DAS181 has been shown to inhibit PIV infection by enzymatically removing the sialic acid moiety of the PIV receptor [106]. Case reports and case series in HCT and solid organ transplant recipients suggest that DAS181 is well tolerated and may improve symptoms, pulmonary function, and need for supplemental oxygen as well as reduce PIV viral loads [97,107-109]. In a posthoc analysis of a randomized trial comparing DAS181 versus placebo in immunocompromised patients, DAS181 was associated with improved oxygenation in a selected group of severely immunocompromised patients with lower respiratory tract infections; however, a statistically significant improvement in oxygenation was not found in the total trial population [110]. Further study is underway. Additional agents under investigation include hemagglutinin neuraminidase inhibitors [111,112] and short interfering RNAs [113].

PREVENTION

Vaccine development — There is no licensed vaccine to prevent infection with PIVs, although vaccine development is underway [3,114-116]. Natural immunity to PIV is incomplete, and reinfection is common. Thus, a protective PIV vaccine may have value, particularly among children and immunocompromised individuals. Vaccine development is discussed in detail separately. (See "Parainfluenza viruses in children", section on 'Vaccine development'.)

Infection control — The United States Centers for Disease Control and Prevention (CDC) recommends that infants and young children hospitalized with PIV infection should be placed on standard and contact precautions and should have a private room when possible [117]. Standard precautions alone are recommended for adults [117]. However, to minimize nosocomial spread, we generally use standard and contact precautions plus isolation for PIV-infected adults as well [44,118]. Respiratory precautions are not considered necessary because the droplets that spread virus are large and do not aerosolize. (See "Infection prevention: Precautions for preventing transmission of infection".)

There are also instances in which an immunocompromised patient may be in close proximity to a contact with PIV infection (ie, an immunocompromised parent exposed to an infected child). In these cases, minimizing exposure would be ideal but is not always feasible. When exposure is unavoidable, both careful hand hygiene and face masks should be used to minimize the risk of transmission.

SUMMARY AND RECOMMENDATIONS

●Background – In adults, parainfluenza viruses (PIVs) usually cause mild upper respiratory infections (URIs) but can lead to life-threatening lower respiratory tract infections, particularly in immunocompromised and older adult patients. (See 'Introduction' above and 'Clinical manifestations' above.)

●Virology – PIVs are single-stranded, enveloped RNA viruses belonging to the genus Paramyxovirus. (See 'Virology' above.)

●Pathogenesis – The extent of infection correlates well with the severity of disease: mild upper respiratory tract infections are associated with limited infection of the nasopharynx, whereas more severe disease involves spread of infection to the large and small airways. (See 'Pathogenesis' above.)

●Epidemiology – In the United States, serotype PIV-1 usually causes outbreaks biennially during the fall of odd-numbered years. In contrast, PIV-2 and PIV-3 occur in annual epidemics in the fall and spring, respectively. In tropical countries, PIVs do not exhibit seasonal variation. (See 'Epidemiology' above.)

●Diagnosis

•Immunocompetent patients – For most immunocompetent outpatients with mild respiratory tract infections (ie, URI, acute bronchitis, or mild community-acquired pneumonia [CAP]), testing for PIV or other pathogens is not necessary, as results generally do not change management. (See 'Diagnosis' above.)

•Immunocompromised patients – We generally test any immunocompromised patient with fever and respiratory tract symptoms and signs as infection can quickly progress. In addition, we test most hospitalized patients with CAP for PIV as part of our initial evaluation, particularly during respiratory virus season and/or during known outbreaks. (See 'Diagnosis' above.)

•PCR preferred – Polymerase chain reaction (PCR) is the preferred testing method. A positive PCR result confirms the diagnosis of PIV infection. However, because coinfection is common, we perform a thorough evaluation for other contributors to the patient's symptoms as part of our diagnostic approach. This is particularly important for severely ill and immunocompromised patients who are at higher risk for bacterial and fungal coinfection. (See 'Diagnosis' above.)

●Treatment

•Supportive care – Supportive care (eg, supplemental oxygen, bronchodilators), reduction of immunosuppressive medications (for immunocompromised patients), and close monitoring for the development of secondary bacterial and fungal infections are the cornerstones of management. (See 'Treatment' above.)

•Limited efficacy for other therapies – There are no antiviral agents with proven efficacy for PIV infections. We generally do not use ribavirin for the treatment of PIV infections because of lack of proven efficacy and the adverse effects of this drug. Use of intravenous immune globulin is controversial. (See 'Treatment' above.)

●Vaccine development – There is no licensed vaccine to prevent infection with parainfluenza viruses, although vaccine development is underway. (See 'Vaccine development' above.)

●Infection control – Hospitalized patients with PIV infection should be placed on standard and contact precautions and should have a private room whenever possible. (See 'Infection control' above.)

ACKNOWLEDGMENT — The views expressed in this topic do not necessarily represent the views of the National Institutes of Health or the United States government.