RABIES VIRUS INFECTS MOUSE AND HUMAN-LYMPHOCYTES AND INDUCES APOPTOSIS

Attenuated and highly neurovirulent rabies virus strains have distinct cellular tropisms, Highly neuroviru lent strains such as the challeng e virus standard (CVS) are highly neurotropic, whereas the attenuated strain ERA also infects nonneuronal cells, We report that both rabies virus strains infect activated murine lymphocytes and the human lympho blastoid Jurkat T-cell Line in vitro, The lymphocytes are more permiss ive to the attenuated ERA. rabies virus strain than to the CVS strain in both cases, We also report that in contrast to that of the CVS stra in, ERA viral replication induces apoptosis of infected Jurkat T cells , and cell death is con-comitant with viral glycoprotein expression, s uggesting that this protein has a role in the induction of apoptosis, Our data indicate that (i) rabies virus infects lymphocytes, iii) lymp hocyte infection with the attenuated rabies virus strain causes apopto sis, and (iii) apoptosis does not hinder rabies virus production, In c ontrast to CVS, ERA rabies virus and other attenuated rabies virus vac cines stimulate a strong immune response and are efficient live vaccin es, The paradoxical finding that a rabies virus triggers a strong immu ne response despite the fact that it infects lymphocytes and induces a poptosis is discussed in terms of the function of apoptosis in the imm une response.