The unexpectedly low efficacy of influenza vaccine during school outbreaks of influenza B virus in the spring of 1987 in Japan was probably attributable to a poor antibody response of vaccinees to the epidemic viruses. An antigenic analysis of the causative B viruses isolated in 1987 and 1988 showed much variation in hemagglutination inhibition patterns. The nucleotide sequences that code for the HAl domain of B/

Intranasal (i.n.) vs. subcutaneous (s.c.) administration of influenza hemagglutinin (HA) vaccine was systematically compared in BALB/c mice. Mice were immunized with different vaccines, together with cholera toxin B subunit as an adjuvant, and 4 weeks later were challenged with either a small (2 microliters) or a large (20 microliters) volume of mouse-adapted A/Guizhou-X (H3N2) virus, each of which gave virgin mice either a nasal or a lung predominant infection. Both i.n. and s.c. inoculations of A/Guizhou-X vaccine conferred almost complete protection against both challenges, i.n. inoculation of A/Fukuoka (H3N2) or A/Sichuan (H3N2) vaccine conferred almost complete cross-protection against 2-microliters challenge and a partial cross-protection against 20-microliters challenge, whereas the s.c. inoculation conferred no cross-protection against 2-microliters challenge with a partial cross-protection against 20-microliters challenge. Moreover, i.n. immunization of PR8 (H1N1) vaccine gave a slight cross-protection against 2-microliters challenge, while the s.c. inoculation did not. The degree of protection was easily improved by i.n. inoculation of higher doses of vaccine, but not by the s.c. inoculation. In parallel with the protection, the i.n. vaccination produced a high level of cross-reacting IgA and IgG antibody to A/Guizhou-X HA in nasal and broncho-alveolar washes, while the s.c. vaccination produced the cross-reacting IgG antibody alone. Thus, i.n. inoculation with inactivated vaccines, which induces cross-reacting anti-HA IgA antibody as well as IgG antibody, is more effective than s.c. vaccination for providing cross-protection against drift viruses.

SUMMARY: Twenty-three rat lung specimens collected in outbreaks of hemorrhagic fever with renal syndrome (HFRS) in three medical institutions were inoculated onto the VERO-E6 cell monolayers. After several blind passages, an agent growing serially in the cell cultures and reacting specifically with known HFRSpositive sera was isolated from two of these specimens. The two isolates were antigenically identical each other. The agent, named strain SR-11, was identified as the causative virus of HFRS by its antigenic identity with E6 cell-adapted HFRS virus, Hantaan 76-118 strain, and the specific reactions with sera from various HFRS cases.

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