TY - JOUR
T1 - Immune protection against HSV-2 in B-cell-deficient mice
AU - Dudley, Kristen L.
AU - Bourne, Nigel
AU - Milligan, Gregg N.
N1 - Funding Information:
We thank Alisa Reece for excellent technical assistance and Dr. Lawrence Stanberry and Dr. Raphael Hirsch for critical review of the manuscript. This work was supported by Research Grant AI-42815 from the National Institutes of Health (to G.N.M.) and the Gamble Center for Infectious Diseases.
PY - 2000/5/10
Y1 - 2000/5/10
N2 - The role of antibody in protection of the vaginal mucosa and sensory ganglia against HSV-2 infection was examined using HSV- immune, B-cell- deficient μMT mice. Significantly higher virus titers were detected in the vaginal mucosae of immune μMT mice compared to immune C57BL/6J mice 24 h after HSV-2 rechallenge. However, virus was rapidly cleared in immune μMT mice, and the infection was resolved with only a 2-day delay. Passive transfer of immune serum to immune μMT mice prior to rechallenge resulted in HSV-specific vaginal IgG levels comparable to those of immune C57BL/6J mice. Although transferred antibody failed to prevent reinfection of the majority of recipients, vaginal virus titers at 24 h and clearance kinetics were similar to those of immune C57BL/6J controls. Following vaginal rechallenge, HSV-2 did not spread to the sensory ganglia of immune C57BL/6J mice nor was the rechallenge virus detected in the ganglia of the majority of immune μMT mice. However, protection was severely compromised by T-cell depletion of immune C57BL/6J mice. These results suggest that HSV-specific antibody limits, but does not prevent, infection of the genital epithelia. Further, prevention of virus spread to the sensory ganglia in immune animals requires vigorous T-cell immune responses. (C) 2000 Academic Press.
AB - The role of antibody in protection of the vaginal mucosa and sensory ganglia against HSV-2 infection was examined using HSV- immune, B-cell- deficient μMT mice. Significantly higher virus titers were detected in the vaginal mucosae of immune μMT mice compared to immune C57BL/6J mice 24 h after HSV-2 rechallenge. However, virus was rapidly cleared in immune μMT mice, and the infection was resolved with only a 2-day delay. Passive transfer of immune serum to immune μMT mice prior to rechallenge resulted in HSV-specific vaginal IgG levels comparable to those of immune C57BL/6J mice. Although transferred antibody failed to prevent reinfection of the majority of recipients, vaginal virus titers at 24 h and clearance kinetics were similar to those of immune C57BL/6J controls. Following vaginal rechallenge, HSV-2 did not spread to the sensory ganglia of immune C57BL/6J mice nor was the rechallenge virus detected in the ganglia of the majority of immune μMT mice. However, protection was severely compromised by T-cell depletion of immune C57BL/6J mice. These results suggest that HSV-specific antibody limits, but does not prevent, infection of the genital epithelia. Further, prevention of virus spread to the sensory ganglia in immune animals requires vigorous T-cell immune responses. (C) 2000 Academic Press.
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U2 - 10.1006/viro.2000.0298
DO - 10.1006/viro.2000.0298
M3 - Article
C2 - 10793004
AN - SCOPUS:0034630862
SN - 0042-6822
VL - 270
SP - 454
EP - 463
JO - Virology
JF - Virology
IS - 2
ER -