H. Minagawa et Y. Yanagi, Latent herpes simplex virus-1 infection in SCID mice transferred with immune CD4+T cells: a new model for latency, ARCH VIROL, 145(11), 2000, pp. 2259-2272
In C.B-17 severe combined immunodeficiency (SCID) mice, corneal challenge w
ith herpes simplex virus-1 (HSV-1) KOS strain usually leads to fatal enceph
alitis. With the transfer of T cells from immunized BALB/c mice, these SCID
mice developed a latent HSV-1 infection. In order to determine the respons
ible T cell subset, fractionated immune T cells were transferred. Those SCI
D mice transferred with immune CD4+T cell-enriched fraction developed laten
t HSV-I infection in their trigeminal ganglia. Their splenocytes had an inc
reased percentage of CD4+T cells and showed a proliferative response agains
t HSV-1. The transfer of CD8+T cells increased survival in the acute infect
ion, but their engraftment seemed less needed for latency than that of CD-4
+T cells. Mice that received immune serum survived without developing laten
t HSV-1 infection. Some latently infected SCID mice had anti-HSV antibodies
while others did not, indicating that the engraftment of antibody-producin
g B cells was not required for latency. Thus, immune CD4+T cells were impor
tant for the survival of SCID mice with latent HSV-1 infection. This animal
model should be useful for investigation of latency/reactivation of HSV-1.