Inhibition of human herpes simplex virus type 2�by interferon ? and tumor necrosis factor ? is mediated by indoleamine 2,3-dioxygenase

2004 ◽  
Vol 6 (9) ◽  
pp. 806-812 ◽  
Author(s):  
O ADAMS ◽  
K BESKEN ◽  
C OBERDORFER ◽  
C MACKENZIE ◽  
D RUSING ◽  
...  
2002 ◽  
Vol 22 (6) ◽  
pp. 671-676 ◽  
Author(s):  
Masato Minami ◽  
Masakazu Kita ◽  
Xiao-Qun Yan ◽  
Toshiro Yamamoto ◽  
Tohko Iida ◽  
...  

2002 ◽  
Vol 13 (1_suppl) ◽  
pp. 38-41 ◽  
Author(s):  
Mark A Fletcher

Sexually transmitted diseases (STDs) are caused by organisms that infect the mucosal surfaces of the genitourinary tract. In spite of its public health importance, current STD vaccine research lags behind work against pathogens that target another mucosal region, the respiratory tract. In the latter case, live-attenuated viral vaccines, killed whole-cell bacterial vaccines, subunit/protein bacterial vaccines, and bacterial polysaccharide vaccines have been enormously successful. To move STD vaccine research forward, complex issues must be resolved. Those include selection of an appropriate antigen (e.g. scientific feasibility and intellectual property rights), the manufacture of the vaccine (e.g. delivery systems, formulation processes, and production steps), and the appropriate public health approach (e.g. medical indications and marketing aspects). Particular scientific problems have delayed STD vaccine development, like incomplete attenuation (human herpes simplex virus type 2), accentuated immunopathology (Chlamydia trachomatis), poor immunogenicity (Treponema pallidum), and broad antigenic heterogeneity (Neisseria gonorrhoeae). Nevertheless, efforts continue with the use of protein antigens: for example, the haemolysin toxoid of Haemophilus ducreyi; the major outer membrane protein(s) of N. gonorrhoeae and C. trachomatis; the glycoprotein D of human herpes simplex virus type 2; and the proteins E6 and E7 of human papilloma virus. It may be predicted that eventual STD vaccines (administered either for prophylaxis or for therapy) will use approaches that include (1) live-attenuated viruses, (2) subunit proteins or inactivated whole organisms given with mucosal adjuvants or with cellular immune response adjuvants, and (3) DNA plasmids expressing the vaccine antigen.


2000 ◽  
Vol 5 (3) ◽  
pp. 366-372
Author(s):  
Liu Jian-jun ◽  
Guo Guang-song ◽  
Xu Shun-xian ◽  
Yang zhan-qiu

2004 ◽  
Vol 74 (3) ◽  
pp. 467-472 ◽  
Author(s):  
A. Volpi ◽  
L. Sarmati ◽  
B. Suligoi ◽  
M. Montano ◽  
G. Rezza ◽  
...  

2008 ◽  
Vol 82 (20) ◽  
pp. 10295-10301 ◽  
Author(s):  
Manoj Thapa ◽  
Daniel J. J. Carr

ABSTRACT The role of tumor necrosis factor alpha (TNF-α) was evaluated for CXCL10-deficient (CXCL10−/−) mice which succumbed to genital herpes simplex virus type 2 (HSV-2) infection and possessed elevated levels of virus and TNF-α but not other cytokines in the central nervous system (CNS) and vaginal tissue within the first 7 days following virus exposure. Anti-TNF-α but not control antibody treatment offsets the elevated mortality rate of CXCL10−/− mice, despite increased CNS viral titers. In addition, TNF-α neutralization suppressed recruitment of leukocyte subpopulations into the CNS, which is associated with reduced CCL2 and CXCL9 expression. Collectively, the results implicate TNF-α as the principal mediator of mortality in response to genital HSV-2 infection.


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