Parainfluenza Virus

Virology

Fig.1 Schematic of the parainfluenza virion (Falsey, 2012)

Parainfluenza virus (PIV) is a negative-sense single-stranded RNA virus that belongs to the Paramyxoviridae family. PIV is a common respiratory virus and includes four different serotypes (PIV-1, -2, -3, -4a, and 4b). PIV1 and PIV3 are members of the genus Respirovirus while PIV-2 and PIV-4 belong to the genus Rubulavirus. The virus particle is pleomorphic and ranges from 150 to 250 nm in size. The RNA genome, unlike influenza, is nonsegmented, ~15,000 nucleotides in length, and encodes six structural proteins: the nucleocapsid protein (NP), the phosphoprotein (P), the matrix protein (M), the fusion glycoprotein (F), the hemagglutinin-neuraminidase glycoprotein (HN), and RNA polymerase (L). The HN and F proteins are surface proteins that mediate attachment to the sialic acid residues on the surface of host epithelial cells (HN) and fusion of the viral envelope with the host cell membrane (F), respectively. The HN and the F protein form the antigenic targets for neutralization and protection through host antibodies and may act as targets that can be utilized for vaccine development.

Pathogenesis

PIV initially infects the pseudostratified mucociliary airway epithelium of the nose and oropharynx with subsequent spread to the large and small airways. The parainfluenza viruses replicate in the epithelium of the upper respiratory tract and spread from there to the lower respiratory tract. High levels of viral replication can cause respiratory epithelial changes. Epithelial cells of the small airways become infected, and this is followed by the appearance of inflammatory infiltrates. Like many other respiratory viruses, the host immune response, including innate immune system responses, antibody responses, and T cell responses, is a significant contributor to the pathogenesis of PIV infection. Inflammatory infiltrates develop and the host immune response is thought to contribute to disease pathogenesis.

Epidemiology

The prevalence of each serotype attributed to infection varies over time, but most studies have documented PIV-3 as the most common cause of clinically significant infection. The four different serotypes of PIV also show remarkably different seasonal patterns. PIV-1 follows a biennial pattern, while outbreaks of PIV-3 infections occur yearly, primarily from April to June. PIV-2 occurs on an annual basis. PIV-4 is infrequently tested for and isolated. Seasonal PIV virus epidemics result in a significant burden of disease in children and the highest attack rates occur in children under 3 years old. PIV infections are typically transient, mild, and self-limited. However, in immunocompromised or elderly adults, the infection may progress to the lower respiratory tract and cause severe and life-threatening pneumonia.

Fig.2 Seasonal circulation of PIV. (Steffens, 2016)

Symptoms

PIV infections have a wide range of clinical manifestations including colds, croup, bronchiolitis, and pneumonia. The extent of infection correlates with location, that is, cold symptoms are associated with infection in the upper airways, infection of the larynx and trachea results in croup and bronchiolitis, and pneumonia occurs with replication in the distal airways. The classic signs of croup include hoarseness, cough, and stridor which are due to obstruction from inflammation of the subglottic region of the trachea.

Prophylaxis and Treatment

Presently there are no licensed antiviral agents for the treatment and vaccine for the prevention of PIV infection. Treatment is primarily symptomatic; aerosolized or systemic ribavirin in combination with intravenous gamma globulin has been reported in small, uncontrolled series, and case reports. New effective antiviral agents (such as HN inhibitors) for human PIV are ongoing and several new agents show promise in vitro and in vivo. Antibody to the two surface glycoproteins, F and HN are neutralizing and serum and nasal antibody to either protein protects against human PIV infection and ameliorates disease.

Research demonstrated that antibodies specific target the HPIV or surface HN protein and F protein can be used for neutralizing viral particles. Equipped with world-leading technology platforms and professional scientific staff, Creative Biolabs has successfully developed a platform for anti-virus antibody generation. Our services are built to meet the customer’s projects and tailored demands. Please feel free to contact us.

References

1. Falsey, A.R. Current management of parainfluenza pneumonitis in immunocompromised patients: a review. Infect Drug Resist, 2012, 5: 121-127.
2. Steffens, A.; et al. Population-based surveillance for medically attended human parainfluenza viruses from the influenza incidence surveillance project, 2010-2014. Pediatr Infect Dis J, 2016, 35(7): 717-722.

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