T-cell-independent antiviral antibody responses.

Recent work has shown that viruses can act in vivo as T-cell-independent antigens, eliciting protective, isotype-switched antibodies in the absence of conventional TCR alpha beta+ T cell help. Inactivated virus or virus-like particles can stimulate IgM production, but factors induced during live virus infection appear to be required to induce the isotype switch that leads to IgG or IgA responses.