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J Gen Virol 70 (1989), 819-825; DOI 10.1099/0022-1317-70-4-819
© 1989 Society for General Microbiology

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Cross-reactive Immunity among Different Serotypes of Virus Causing Haemorrhagic Fever with Renal Syndrome

Hideo Asada1, Kruavon Balachandra2, Manabu Tamura1, Kazuhiro Kondo1 and Koichi Yamanishi1

1 Department of Virology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565 Japan
and2 Department of Immunology, National Institute of Health, Ministry of Public Health, 88/7 Gp.4 Soi Bamrasnaradura Hospital, Trad Khuan District, Amphur Muang, Nonthaburi, Thailand

Spleen cells primed by Prospect Hill (PH) or Puumala (Pu) virus could cross-react with Hantaan virus (HV) 76-118 strain-infected target cells after in vitro stimulation with HV-infected cells, although anti-PH or anti-Pu immune serum showed no cross-reactive neutralizing (NT) activity to HV without complement. These results and our previous findings with cross-reactive cytotoxic T lymphocytes (CTLs) suggest that some epitopes recognized by CTLs might be common among the hantavirus genus, while the epitopes related to NT activity were mainly specific to each virus of this genus. Next, to evaluate the cross-reactive immunities demonstrated by in vitro study, we investigated the effect of transferring T lymphocytes and sera from BALB/c mice immunized with PH or Pu virus into nude mice before HV inoculation. Transferring T lymphocytes primed by PH or Pu virus reduced HV titres in lungs and spleens of nude mice, corresponding with the results of the in vitro CTL assays. Transferring anti-Pu immune serum also decreased HV titres in nude mice, which seemed to reflect complement-dependent NT activity. Moreover ICR mice previously immunized with PH or Pu virus showed resistance to challenge with a lethal dose of the HV KHF strain, indicating that cross-reactive immunity induced by PH or Pu virus could protect ICR mice against pathogenic HV infection.

Keywords: hantavirus, HV, cross-reactivity

Received 18 October 1988; accepted 22 December 1988.


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