PARAINFLUENZA viruses are mainly reported as causing respiratory-tract infections in children. Of the four types, parainfluenza type 4 is the least and type 3 is the most frequently reported. Parainfluenza type 3 (PI-3) is found more often in very young children. The lungs are the main site of infection and local immunity develops early (Smith , 1966; Kasel , 1969).

Reports on cell-mediated immune responses during experimental respiratory-virus infections are few (Waldman and Ganguly, 1974). Delayed hypersensitivity has been demonstrated after parenteral administration of inactivated respiratory syncytial virus (Forsyth, 1968; Tremonti and Jackson, 1969) and inactivated influenza virus (Feinstone, Beachey and Rytel, 1969). There are some conflicting reports of suppression of cell-mediated immunity (CMI) in respiratory viral infection (Kantzler , 1974; Kauffman , 1974). Even the reports on the development of delayed hypersensitivity after experimental inoculation of live PI-3 virus are contradictory. Tremonti and Jackson (1969) failed to induce a delayed hypersensitivity response by intranasal inoculation of live PI-3 virus whereas Wetherbee (1973) could induce it. We have produced PI-3 virus infection in the respiratory tract of guinea-pigs and have studied the development of systemic CMI for 70 days, using dermal reactivity, leucocyte-migration inhibition (LMI), macrophage-migration inhibition (MMI), macrophage aggregation (MA) and adoptive spleen-cell transfer as indicators.


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