ORIGINAL ARTICLE: Estradiol Limits Viral Replication Following Intravaginal Immunization Leading to Diminished Mucosal IgG Response and Non-sterile Protection Against Genital Herpes Challenge
Article first published online: 11 JAN 2010
© 2010 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 63, Issue 4, pages 299–309, April 2010
How to Cite
Gillgrass, A., Chege, D., Bhavanam, S. and Kaushic, C. (2010), ORIGINAL ARTICLE: Estradiol Limits Viral Replication Following Intravaginal Immunization Leading to Diminished Mucosal IgG Response and Non-sterile Protection Against Genital Herpes Challenge. American Journal of Reproductive Immunology, 63: 299–309. doi: 10.1111/j.1600-0897.2009.00796.x
- Issue published online: 10 MAR 2010
- Article first published online: 11 JAN 2010
- Submitted November 7, 2009; accepted November 11, 2009.
- humoral immunity;
- mucosal immunity;
- sex hormone
Citation Gillgrass A, Chege D, Bhavanam S, Kaushic C. Estradiol limits viral replication following intravaginal immunization leading to diminished mucosal IgG response and non-sterile protection against genital herpes challenge. Am J Reprod Immunol 2010; 63: 299–309
Problem Previously we reported that ovariectomized (OVX) mice receiving estradiol (E) prior to immunization with an attenuated strain of HSV-2 (TK-HSV-2) were not protected. Lack of protection in the E group was because of the inability of TK-HSV-2 to penetrate the thick keratinized epithelium. In this study, we determined the outcome of immunization after the thickening of vaginal epithelium following E-treatment waned. OVX, C57BL/6 mice were given Progesterone (P), E or saline (S) for 3 days and immunized with IVAG TK-HSV-2.
Method of study To determine the time point at which E-treated mice could be successfully immunized, the mice were inoculated with TK-HSV-2 between days 1 and 7 (ED1–ED7) post-E-treatment and challenged with IVAG HSV-2 three weeks later.
Results The level of infection post-immunization correlated with HSV-2-specific IgG antibody level, which correlated with sterile protection. No viral infection was observed in ED1–ED3 groups and no specific antibodies were detected, resulting in no protection. Moderate infection was seen in ED5 group, resulting in low antibody production and non-sterile protection in 87.5% of mice. High antibody titers and sterile protection were observed in all groups that experienced robust infection post-immunization.
Conclusion The results show that estradiol leads to limited viral replication and diminished mucosal IgG response, resulting in non-sterile immune protection against genital herpes infection.