Protection of mice against virulent virus infection by a temperature-sensitive mutant derived from an HVJ (Sendai virus) carrier culture

Abstract

Experimental infection with HVJ (haemagglutinating virus of Japan-the Sendai strain of parainfluenza 1 virus) in mice was studied. Aerosol infection of newborn mice with the wild-type virus (HVJ-W) retarded the development of body weight and killed the animals within a few weeks. Large amounts of virus were isolated from both the lungs and the nasal turbinates of infected mice. In contrast, newborn mice exposed by inhalation to a temperature-sensitive (ts) mutant (HVJ-pB) derived from an HVJ carrier culture showed no clinical signs and grew equally well as mock-infected animals. No infectious virus could be recovered from the lungs although the ts mutant grew to moderate titre in the nasal turbinates. The prior inoculation of newborn mice with the ts mutant virus induced a state of significant resistance to subsequent challenge with the virulent wild-type virus. No replication of challenge virus in both lungs and nasal turbinates could be detected and the animals were protected a lethal infection. It is suggested that an avirulent temperature-sensitive mutant which has lost the capacity to replicate in the lower respiratory tract but is still capable of multiplying in the nasal turbinates may be a promising candidate for use in live vaccines especially against the infectious disease of the lower respiratory tract.

Sendai Virus Induces Persistent Olfactory Dysfunction in a Murine Model of PVOD via Effects on Apoptosis, Cell Proliferation, and Response to Odorants

“…In these experiments, the viral load of SeV peaked at day 10 after infection. These results differ from the work of others [ 10 , 29 – 30 ], which showed that virus growth peaked in nasal turbinates, tracheas, and lungs at 5 days p.i., but may be related to difference in protocol, assessment time, and location (we did not examine turbinates or the lower airway). We found that the peak of olfactory dysfunction in the mice appeared at day 15 p.i., a time point at which the immune responses against SeV had geared up for nearly 10 days.…”

Parainfluenza virus type 1 infects olfactory neurons and establishes long-term persistence in the nerve tissue

“…The primers used in this research were designed with reference to the published sequences of Sendai virus gene (Shioda et al, 1983). As reported previously (Kimura et al, 1979;Iwata et aI., 1990), virus growth peaked in nasal turbinates, tracheas, and lungs at 5 days post-infection (p.i.). Thereafter, the immune response against Sendai virus excluded progeny virus from the respiratory tracts within the subsequent 5 days.…”

Expression of the HN, F, NP and M proteins of Sendai virus by recombinant vaccinia viruses and their contribution to protective immunity against Sendai virus infections in mice

“…There are many reports about protection of mice from Sendai virus infections by the use of killed and live vaccines. These include inactivated virus (Fukumi & Takeuchi, 1975), a synthetic oligopeptide corresponding to the partial amino acid sequence of NP protein (Kast et al, 1991), F protein-cleavage mutants (Tashiro & Homma, 1985;Itoh et al, 1990) and a temperature-sensitive mutant possessing homologous interfering capacity (Kimura et al, 1979;Kiyotani et al, 1990).…”