In vivo depletion of CD8+ T lymphocytes abrogates protective immunity to African swine fever virus

J Gen Virol. 2005 Sep;86(Pt 9):2445-2450. doi: 10.1099/vir.0.81038-0.


To understand the mechanisms involved in protective immunity to African swine fever virus (ASFV) infection, the observation that infection with the avirulent Portuguese ASFV isolate OUR/T88/3 protects outbred pigs from challenge with the virulent Portuguese ASFV isolate OUR/T88/1 was exploited. It was demonstrated that pigs exposed to OUR/T88/3 and then depleted of CD8+ lymphocytes were no longer fully protected from OUR/T88/1 challenge. This indicated that CD8+ lymphocytes play an important role in the protective immune response to ASFV infection and that anti-ASFV antibody alone, from OUR/T88/3 infection, was not sufficient to protect pigs from OUR/T88/1 challenge. Inbred pigs of the cc haplotype infected with OUR/T88/3 were not always protected from OUR/T88/1 challenge and developed both viraemia and fever. Such viraemia was always correlated with increased numbers of circulating CD8beta+ lymphocytes, indicating a specific role for CD8beta+ lymphocytes in combating viraemia. These experiments indicate an important role for CD8+ lymphocytes, particularly CD8beta+ lymphocytes, in ASF protective immunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • African Swine Fever / immunology*
  • African Swine Fever / prevention & control*
  • African Swine Fever / virology
  • African Swine Fever Virus / immunology
  • African Swine Fever Virus / pathogenicity*
  • Animals
  • Animals, Outbred Strains
  • CD4-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / immunology*
  • Lymphocyte Count
  • Lymphocyte Depletion*
  • Swine
  • Viremia / immunology
  • Viremia / prevention & control
  • Viremia / virology