Protection from herpes simplex virus type 2 is associated with T cells involved in delayed type hypersensitivity that recognize glycosylation-related epitopes on glycoprotein D

Vaccine ◽  
1992 ◽  
Vol 10 (7) ◽  
pp. 447-454 ◽  
Author(s):  
M. Wachsman ◽  
J.H. Luo ◽  
L. Aurelian ◽  
E. Paoletti
1992 ◽  
Vol 73 (9) ◽  
pp. 2357-2366 ◽  
Author(s):  
M. D. Drew ◽  
A. Estrada-Correa ◽  
B. J. Underdown ◽  
M. R. McDermott

2010 ◽  
Vol 84 (6) ◽  
pp. 3116-3120 ◽  
Author(s):  
Michael J. Vanden Oever ◽  
Jin-Young Han

ABSTRACT Herpes simplex virus type 2 (HSV-2) induces apoptosis in T cells by a caspase-dependent mechanism. Apoptosis can occur via extrinsic (death receptor) and/or intrinsic (mitochondrial) pathways. Here, we show that the initiator caspase for the intrinsic pathway is activated in T cells following HSV-2 exposure. To determine the respective contributions of intrinsic and extrinsic pathways, we assessed apoptosis in Jurkat cells that are deficient in caspase 8 or Fas-associating protein with death domain (FADD) for the extrinsic pathway and in cells deficient in caspase 9 for the intrinsic pathway. Our results indicate HSV-2-induced apoptosis in T cells occurs via the intrinsic pathway.


Vaccine ◽  
1993 ◽  
Vol 11 (4) ◽  
pp. 407-414 ◽  
Author(s):  
V. Landolfi ◽  
C.D. Zarley ◽  
A.S. Abramovitz ◽  
N. Figueroa ◽  
S.L. Wu ◽  
...  

2006 ◽  
Vol 80 (11) ◽  
pp. 5509-5515 ◽  
Author(s):  
Nancy Hosken ◽  
Patrick McGowan ◽  
Amalia Meier ◽  
David M. Koelle ◽  
Paul Sleath ◽  
...  

ABSTRACT Cytolytic T cells play a major role in controlling herpes simplex virus type 2 (HSV-2) infections in humans. In an effort to more thoroughly evaluate the response to HSV-2 directly, ex vivo, we developed an enzyme-linked immunospot (ELISPOT) assay that utilized pools of overlapping synthetic peptides presented by autologous dendritic cells to purified CD8+ T cells. Donor response rates to individual open reading frames (ORFs) ranged from fewer than 5% responding to as many as 70% responding, with the greatest frequency of responses (by ORF) being directed against UL39, UL25, UL27, ICP0, UL46, and UL47 in descending order of frequency. HSV-2-seropositive subjects responded to as few as 3 or as many as 46 of the 48 ORFs tested, with a median of 11 ORFs recognized. HLA-B*07 expression correlated with stronger responses overall that were directed primarily against UL49 and UL46. Cumulative precursor frequencies in the blood ranged from 500 to almost 6,000 HSV-2 spot-forming units/106 CD8+ T cells. The magnitude and breadth of the response in the infected population were greater than previously appreciated. Whether this variability in the CD8+ T-cell response within individuals is associated with the frequency of viral reactivation warrants further study.


2001 ◽  
Vol 82 (4) ◽  
pp. 845-853 ◽  
Author(s):  
Ali M. Harandi ◽  
Bo Svennerholm ◽  
Jan Holmgren ◽  
Kristina Eriksson

The role of B, CD4+ T and CD8+ T cells in both primary genital infection with attenuated herpes simplex virus type 2 (HSV-2) and development of protective immunity to a later challenge with virulent HSV-2 using lymphocyte-deficient mice has been elucidated. Following primary inoculation with attenuated thymidine kinase-deficient (TK−) HSV-2, B cell-deficient (μMT) mice developed a local viraemia and transient genital inflammation, suggesting a role for B cells in the innate control of local infection and inflammation. Natural antibodies are implicated in this process, as passive transfer of normal serum into μMT mice significantly reduced HSV-2 TK− shedding in the vaginal lumen, although it did not affect subsequent inflammation. Protection against lethal HSV-2 challenge was noted in HSV-2-vaccinated wild-type, CD8+ T cell-deficient and μMT mice and was characterized by strong virus-specific IFN-γ responses in vitro and delayed type hypersensitivity (DTH) responses in vivo. In contrast, CD4+ T cell-deficient (CD4−/−) mice had impaired HSV-2-specific IFN-γ production and DTH responses and succumbed rapidly to genital HSV-2 challenge. However, protective responses to HSV-2 could be induced in HSV-2-vaccinated CD4−/− mice by treatment with recombinant IFN-γ. Taken together, these results suggest that CD4+ T cells secreting IFN-γ are critical for immune protection against lethal genital HSV-2 re-infection, whereas B cells/natural antibodies have anti-viral and -inflammatory effects in the innate control of a primary infection.


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