Human
parainfluenzaviruses (HPIV) is the type species of the
genus Pneumovirus. Along with other members of the family Paramyxoviridae, hRSV is an enveloped virus with a negative sense, single-stranded RNA genome. These viruses are 150-200nm in diameter with a helical nucleocapsid.
The viruses were first described in the 1950s and differentiated from the myxoviruses (myxo="mucous") such as influenzavirus . Hence tha name para-influenza was applied where para means against, counter or outside.
Other members of the family include mumps virus (MuV), human parainfluenzavirus 2 and 4 (HPIV-2 and HPIV-4; genus Rubulavirus), measles virus
(MeV; genus
Morbillivirus), Hendravirus and Nipahvirus (genus Henipavirus) and human metapneumovirus (hMPV; genus Metapneumovirus).
A distinguishing feature among genera is the possession (Paramyxovirus) or absence (e.g. Morbilliviruis and Pneumovirus) of neuraminidase (NA).
Figure
1.
Schematic representation of the human parainfluenzaviruses 1, 2 and 3 (HPIV-1, HPIV-2 & HPIV3) (-)ssRNA genome. Based on GenBank accession no. NC_003461, NC_003443, NC_001796.
Different diseases are associated with these viruses and they occur at different times of the year. Like other paramyxoviruses, HPIVs can repeatedly infect a person over the course of their life. Infection usually results in a cold (upper respiratory tract disease (URTD)) but can also affect the lower respiratory tract (LRT) especially among the very young, the elderly and the immunocompromised.
HPIV-1 and HPIV-2 frequently cause croup (laryngotracheobronchitis) in children;
HPIV-2 is more frequently associated with lower respiratory tract disease (LRTD) including bronchiolitis and pneumonia;
HPIV-4 is infrequently detected and therefore poorly linked to a specific disease.
Disease follows infection with HPIV by 1 to 7 days.
Direct identificaton of HPIV infection can be achieved by:
Isolating live virus from patient's respiratory secretions using cell culture. This classical approach identifies an active infection, demonstrating that infectious virus is present. The virus causes cytopathic changes to infecte cells and also cause haemadsorption via the HN product. Tgis approach can not discrimnate acute from persistent infections.
Detection of viral proteins within infected host cells collected from the patient's respiratory secretions, using immunoflurescence assays or enzyme immunoassays. This approach will prove recent or past infection but not active infection, nor is it always a specific tool.
Detection of viral genetic material (RNA for these viruses) using RT-PCR or another nucleic acid (NA) technique, collectively called molecular testing. These approaches will not prove active infection, only the presence of viral NA.
Indirect identificaton of HPIV infection can be achieved by:
Detection of host antibodies to viral antigens coated using a solid substrate such as in enzyme immunoassays. Where possible, the detection of a four-fould or greater rise in IgG antibodies between two sera collected four weeks apart, or the presence of IgM antibodies in a single serum.
Expansion of a cell population in response to the presence of a specific agent when using a cell-proliferation assay. Not used routinely.
No vaccine or specific antiviral is currently available.
