scholarly journals Induction of Humoral and Cellular Immune Responses to the Human Immunodeficiency Type 1 Virus in Nonhuman Primates by in Vivo DNA Inoculation

Virology ◽  
1995 ◽  
Vol 211 (1) ◽  
pp. 102-112 ◽  
Author(s):  
Bin Wang ◽  
Jean Boyer ◽  
Vasantha Srikantan ◽  
Kenneth Ugen ◽  
Lori Gilbert ◽  
...  
Vaccines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1408
Author(s):  
Qiao Li ◽  
Zhihua Liu ◽  
Yi Liu ◽  
Chen Liang ◽  
Jiayi Shu ◽  
...  

TFPR1 is a novel adjuvant for protein and peptide antigens, which has been demonstrated in BALB/c mice in our previous studies; however, its adjuvanticity in mice with different genetic backgrounds remains unknown, and its adjuvanticity needs to be improved to fit the requirements for various vaccines. In this study, we first compared the adjuvanticity of TFPR1 in two commonly used inbred mouse strains, BALB/c and C57BL/6 mice, in vitro and in vivo, and demonstrated that TFPR1 activated TLR2 to exert its immune activity in vivo. Next, to prove the feasibility of TFPR1 acting as a major component of combined adjuvants, we prepared a combined adjuvant, TF–Al, by formulating TFPR1 and alum at a certain ratio and compared its adjuvanticity with that of TFPR1 and alum alone using OVA and recombinant HBsAg as model antigens in both BALB/c and C57BL/6 mice. Results showed that TFPR1 acts as an effective vaccine adjuvant in both BALB/c mice and C57BL/6 mice, and further demonstrated the role of TLR2 in the adjuvanticity of TFPR1 in vivo. In addition, we obtained a novel combined adjuvant, TF–Al, based on TFPR1, which can augment antibody and cellular immune responses in mice with different genetic backgrounds, suggesting its promise for vaccine development in the future.


2004 ◽  
Vol 53 (9) ◽  
pp. 825-834 ◽  
Author(s):  
Jing Ye ◽  
Guang-Sheng Chen ◽  
Hong-Ping Song ◽  
Zeng-Shan Li ◽  
Ya-Yu Huang ◽  
...  

2001 ◽  
Vol 184 (4) ◽  
pp. 488-496 ◽  
Author(s):  
Pauline N. M. Mwinzi ◽  
Diana M. S. Karanja ◽  
Daniel G. Colley ◽  
Alloys S. S. Orago ◽  
W. Evan Secor

Vaccine ◽  
2007 ◽  
Vol 25 (36) ◽  
pp. 6635-6645 ◽  
Author(s):  
Carlota Dobaño ◽  
Georg Widera ◽  
Dietmar Rabussay ◽  
Denise L. Doolan

2002 ◽  
Vol 76 (6) ◽  
pp. 2817-2826 ◽  
Author(s):  
Georg M. Lauer ◽  
Tam N. Nguyen ◽  
Cheryl L. Day ◽  
Gregory K. Robbins ◽  
Theresa Flynn ◽  
...  

ABSTRACT Both human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) lead to chronic infection in a high percentage of persons, and an expanding epidemic of HIV-1-HCV coinfection has recently been identified. These individuals provide an opportunity for simultaneous assessment of immune responses to two viral infections associated with chronic plasma viremia. In this study we analyzed the breadth and magnitude of the CD8+- and CD4+-T-lymphocyte responses in 22 individuals infected with both HIV-1 and HCV. A CD8+-T-lymphocyte response against HIV-1 was readily detected in all subjects over a broad range of viral loads. In marked contrast, HCV-specific CD8+-T-lymphocyte responses were rarely detected, despite viral loads in plasma that were on average 1,000-fold higher. The few HCV-specific responses that were observed were relatively weak and limited in breadth. CD4-proliferative responses against HIV-1 were detected in about half of the coinfected subjects tested, but no proliferative response against any HCV protein was found in these coinfected persons. These data demonstrate a major discordance in immune responses to two persistent RNA viruses. In addition, they show a consistent and profound impairment in cellular immune responses to HCV compared to HIV-1 in HIV-1-HCV-coinfected persons.


2003 ◽  
Vol 19 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Parth Narendran ◽  
Alistair J. Williams ◽  
Kathryn Elsegood ◽  
Nicola J. Leech ◽  
Colin M. Dayan

1988 ◽  
pp. 185-196
Author(s):  
Anne Durandy ◽  
Alain Fischer ◽  
Edouard Drouhet ◽  
Claude Griscelli

1999 ◽  
Vol 15 (18) ◽  
pp. 1685-1689 ◽  
Author(s):  
Christopher P. Locher ◽  
Robert M. Grant ◽  
Eric A. Collisson ◽  
Gustavo Reyes-Teran ◽  
Tarek Elbeik ◽  
...  

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