Human parainfluenza virus infection is limited to respiratory tract. Respiratory epithelium appears to be the important site of virus binding and subsequent infection.
The virus adsorbs to the respiratory epithelial cells by spe-cifically combining with neuraminic acid receptors in the cell through its hemagglutinin. Subsequently, the virus enters the cells following fusion with the cell membrane, mediated by F1 and F2 receptors. The virus replicates more rapidly than mumps and measles viruses in the cell cytoplasm and causes formation of multinucleated giant cells. These giant cells, each of which contains two to seven nuclei, usually develop late in the infection. The virus also causes the formation of single and multilocular cytoplasmic vacuoles and basophilic or eosino-philic inclusions.
The virus causes inflammation of the respiratory tract, lead-ing to secretions of high level of inflammatory cytokines, usu-ally 7–10 days after initial exposure. Airways inflammation, necrosis, and sloughing of respiratory epithelium, edema, and excessive mucus production are the noted pathological features associated with HPIV infections
Humoral immunity plays a major role in defense against HPIVs. The antibodies are produced against both surface glycoproteins (HN and F) of the virus. Neutralizing antibodies to all the five types of the viruses are seen in most of the children at the time of birth; but the titer falls rapidly after 6 months. Most children and adults develop detectable level of neutralizing antibodies in the serum following natural infection with the virus.
Secretory IgA antibodies also appear to play an important role. The CMI appears to play some role in containing the dis-ease, as HPIV infection tends to be more severe in persons with defective CMI.
Immunity to HPIV is long-lasting, but reinfection may occur many times throughout the life, most probably due to the pres-ence of multiple serotypes of HPIV.