       Document 0527
 DOCN  M9630527
 TI    Role of B cells and cytotoxic T lymphocytes in clearance of and immunity
       to rotavirus infection in mice.
 DT    9603
 AU    Franco MA; Greenberg HB; Department of Medicine, Microbiology and
       Immunology, Stanford; University School of Medicine, California 94305,
       USA.
 SO    J Virol. 1995 Dec;69(12):7800-6. Unique Identifier : AIDSLINE
       MED/96079028
 AB    The immune mechanisms involved in clearance of and immunity to rotavirus
       infection are poorly understood. Although mice with severe combined
       immunodeficiency (SCID mice) become chronically infected, nude mice have
       been reported to clear rotavirus infection similarly to immunocompetent
       controls. To better characterize the role of cytotoxic T lymphocytes
       (CTLs) in clearance of and immunity to rotavirus infection, we infected
       naive or previously infected beta 2-microglobulin (beta 2m) knockout
       mice with murine rotavirus. Naive beta 2m knockout mice shed rotavirus
       antigen 2 days longer than did normal control mice but completely
       resolved primary infection. beta 2m knockout naive mice treated with
       depleting doses of an anti-CD8 monoclonal antibody before infection shed
       viral antigen for an additional day. Upon rechallenge, beta 2m knockout
       mice, either treated with the anti-CD8 antibody or not treated, were
       completely resistant to reinfection. Clearance of rotavirus infection in
       naive beta 2m knockout mice correlated with the development of
       intestinal rotavirus-specific immunoglobulin A. Before rechallenge, beta
       2m knockout mice had high levels of intestinal rotavirus-specific
       immunoglobulin A. These findings suggest that CTLs mediate rotavirus
       clearance but are not required for this function and that CTLs are not
       necessary for development of immunity to rotavirus reinfection. To
       further characterize the effector mechanisms involved in clearance and
       prevention of rotavirus infection, similar studies were performed with
       B-cell-deficient JHD knockout mice. After primary infection, most naive
       JHD mice had similar virus-shedding clearance curves as did control mice
       and completely resolved primary infection. However, 2 of 29 became
       chronically infected. All JHD mice treated with anti-CD8 antibody became
       chronically infected with murine rotavirus. Upon rechallenge, JHD mice
       which had cleared primary infection were all susceptible to reinfection.
       These findings suggest that B cells also play a role in clearance of
       primary infection but are absolutely necessary for development of
       immunity against rotavirus reinfection.
 DE    beta 2-Microglobulin/DEFICIENCY/GENETICS  Animal  Antibodies,
       Viral/ANALYSIS/BLOOD  Antigens, Viral/ANALYSIS
       B-Lymphocytes/*IMMUNOLOGY  Cell Line  Comparative Study  Cytotoxicity,
       Immunologic  CD8-Positive T-Lymphocytes/IMMUNOLOGY  Feces/VIROLOGY  Flow
       Cytometry  IgA/ANALYSIS/BLOOD  Mice  Mice, Inbred C57BL  Mice, Inbred
       Strains  Mice, Knockout  Mice, SCID  Receptors, Antigen, T-Cell,
       alpha-beta/ANALYSIS  Receptors, Antigen, T-Cell, gamma-delta/ANALYSIS
       Rotavirus/*ISOLATION & PURIF  Rotavirus Infections/*IMMUNOLOGY  Species
       Specificity  Support, Non-U.S. Gov't  Support, U.S. Gov't, Non-P.H.S.
       Support, U.S. Gov't, P.H.S.  T-Lymphocytes, Cytotoxic/*IMMUNOLOGY  Time
       Factors  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

