Antibody Responses to Murine Cytomegalovirus in Genetically Resistant and Susceptible Strains of Mice

A flow cytometry-based method for detecting antibody responses to murine cytomegalovirus infection

“…This diminished antibody response in C57BL/6 mice is consistent with previous studies showing that other MCMV resistant mouse strains develop less antiviral antibody than susceptible mice (Lawson et al, 1988). C57BL/6 mice exhibit lower viral titers in tissues than BALB/c mice after primary infection (Chalmer et al, 1977;Grundy et al, 1981;Scalzo et al, 1990), and thus lower anti-viral antibody responses to wild type virus could simply reflect a lower viral antigen load.…”

“…Previous investigators have argued that if humoral responses are important for viral control, then higher antibody titers and earlier kinetics would be characteristic in that mouse strain (Lawson et al, 1988). Conversely, if humoral antiviral responses were not important to a particular strain, then antibody levels might be lower and slower to develop.…”

“…Polyclonal antibody responses to multiple viral proteins occur following MCMV infection, with production of virus specific antibodies of both IgG and IgM classes (Araullo-Cruz et al, 1978;Farrell and Shellam, 1989;Karupiah et al, 1998;Lawson et al, 1988;Selgrade et al, 1983). Adoptive transfer of anti-CMV antibody has been shown to be protective during acute infection (Araullo-Cruz et al, 1978;Farrell and Shellam, 1991;Lawson et al, 1988;Shanley et al, 1981), but does not prevent development of latent infection (Shanley et al, 1981).…”

“…Adoptive transfer of anti-CMV antibody has been shown to be protective during acute infection (Araullo-Cruz et al, 1978;Farrell and Shellam, 1991;Lawson et al, 1988;Shanley et al, 1981), but does not prevent development of latent infection (Shanley et al, 1981). Although preformed antibody does help protect from lethal primary infection, it is not required for viral control in non-lethal models, but does appear to be important in viral control after reactivation from latency (Jonjic et al, 1994).…”

“…Previous kinetic studies have shown that development of an MCMV specific IgG response begins 5-10 days after primary infection, and peaks ~45-90 days after primary infection (Araullo-Cruz et al, 1978;Classen et al, 1987;Gonczol et al, 1985;Lawson et al, 1988;Selgrade et al, 1983). Data from our study corroborate these previous findings, with BALB/c mice developing demonstrable IgG 1 antibody by 2 weeks after infection, increasing to maximum by 8 weeks then beginning to decline by 20 weeks after infection ( figure 6A).…”