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H‐2 linked genetic control of immune responsiveness to hepatitis B surface antigen (HBsAg) in mice
Author(s) -
Neurath A. Robert,
Stark Dennis,
Strick Nathan,
Sproul Phyllis
Publication year - 1983
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1890120402
Subject(s) - congenic , hbsag , biology , inbred strain , major histocompatibility complex , immune system , histocompatibility , gene , virology , immunology , haplotype , antigen , genetics , allele , human leukocyte antigen , hepatitis b virus , virus
Recent data suggest that genes involved in the control of (1) immune responses of humans to HBsAg and (2) the susceptibility to the development of chronic hepatitis B are linked to the major HLA histocompatibility complex. Studies on the genetic regulation of anti‐HBs responses and on the possible abrogation of nonresponsiveness to HBsAg in humans are difficult. In an attempt to develop a relevant animal model system, the anti‐HBs response of inbred and congenic strains of mice was investigated. A great variation in anti‐HBs responses among individual mice belonging to the same strains was observed. Nevertheless, it was possible to rank the inbred mouse strains studied according to their decreasing anti‐HBs responses as follows: BALB/c[d] ∽ SWR/J[q] > C57BL/6J[b] ∽ DBA/2J[a] > AKR/J[k] > A/J[a] > CBA/CaJ[k] > SJL/J[s]. (Letters in brackets indicate H‐2 haplotype). Only a small proportion of SJL mice had an anti‐HBs response. Therefore, this strain may serve as a model for human nonresponders. Studies with the congenic strains B10.D2[d] and B10.S[s] indicated that genes conferring responsiveness to HBsAg are linked to the H‐2 histocompatibility complex. However, genes not linked to H‐2 also probably play a role in regulating anti‐Hbs responses.