scholarly journals Complex Adenovirus-Mediated Expression of West Nile Virus C, PreM, E, and NS1 Proteins Induces both Humoral and Cellular Immune Responses

2007 ◽  
Vol 14 (9) ◽  
pp. 1117-1126 ◽  
Author(s):  
Jennifer Schepp-Berglind ◽  
Min Luo ◽  
Danher Wang ◽  
Jason A. Wicker ◽  
Nicholas U. Raja ◽  
...  
Keyword(s):  
West Nile Virus ◽  
North America ◽  
Immune Responses ◽  
Genetic Variants ◽  
De Novo ◽  
Clinical Manifestations ◽  
Effective Vaccine ◽  
West Nile ◽  
Cellular Immune Responses ◽  
Cellular Immune

ABSTRACT West Nile Virus (WNV), a member of the family Flaviviridae, was first identified in Africa in 1937. In recent years, it has spread into Europe and North America. The clinical manifestations of WNV infection range from mild febrile symptoms to fatal encephalitis. Two genetic lineages (lineages I and II) are recognized; lineage II is associated with mild disease, while lineage I has been associated with severe disease, including encephalitis. WNV has now spread across North America, significantly affecting both public and veterinary health. In the efforts to develop an effective vaccine against all genetic variants of WNV, we have studied the feasibility of inducing both neutralizing and cellular immune responses by de novo synthesis of WNV antigens using a complex adenoviral vaccine (CAdVax) vector. By expressing multiple WNV proteins from a single vaccine vector, we were able to induce both humoral and cellular immune responses in vaccinated mice. Neutralization assays demonstrated that the antibodies were broadly neutralizing against both lineages of WNV, with a significant preference for the homologous lineage II virus. The results from this study show that multiple antigens synthesized de novo from a CAdVax vector are capable of inducing both humoral and cellular immune responses against WNV and that a multiantigen approach may provide broad protection against multiple genetic variants of WNV.

A DNA-based West Nile virus replicon elicits humoral and cellular immune responses in mice

2011 ◽  
Vol 178 (1-2) ◽  
pp. 87-93 ◽  
Author(s):  
Fei Cao ◽  
Xiao-Feng Li ◽  
Xue-Dong Yu ◽  
Yong-Qiang Deng ◽  
Tao Jiang ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Immune Responses ◽  
West Nile ◽  
Cellular Immune Responses ◽  
Cellular Immune

scholarly journals A Combined Adjuvant TF–Al Consisting of TFPR1 and Aluminum Hydroxide Augments Strong Humoral and Cellular Immune Responses in Both C57BL/6 and BALB/c Mice

Vaccines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1408
Author(s):  
Qiao Li ◽  
Zhihua Liu ◽  
Yi Liu ◽  
Chen Liang ◽  
Jiayi Shu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Vaccine Development ◽  
Inbred Mouse ◽  
Effective Vaccine ◽  
Mouse Strains ◽  
Cellular Immune Responses ◽  
Recombinant Hbsag ◽  
Cellular Immune

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.

scholarly journals Immunogenicity analysis of conserved fragments in Plasmodium ovale species merozoite surface protein 4

2020 ◽  
Author(s):  
Uwase Juliette ◽  
Ruilin Chu ◽  
Kokouvi Kassegne ◽  
Yao Lei ◽  
Feihu Shen ◽  
...  
Keyword(s):  
Immune Responses ◽  
Plasmodium Species ◽  
Surface Protein ◽  
Merozoite Surface Protein ◽  
Effective Vaccine ◽  
Plasmodium Ovale ◽  
Tropical Regions ◽  
Cellular Immune Responses ◽  
Cellular Immune ◽  
Proliferation Assays

Abstract Background: There is an urgent need for an effective vaccine to control and eradicate malaria, one of the most serious global infectious diseases. Plasmodium merozoite surface protein 4 (MSP4) has been listed as a blood-stage subunit vaccine candidate for malaria. Plasmodium ovale species (spp.) infection is also a source of malaria burden in tropical regions where it is sometimes mixed with other Plasmodium species. However, little is known about P. ovale spp. MSP4. Methods: The msp4 gene was amplified through polymerase chain reaction using genomic DNA extracted from blood samples of 46 patients infected with P. ovale spp. and amplified products were sequenced. Open reading frames predicted as immunogenic peptides consisting of 119 and 97 amino acids of P. ovale curtisi MSP4 (PocMSP4) and P. ovale wallikeri MSP4 (PowMSP4), respectively, were selected for protein expression. Recombinant proteins (rPoMSP4) were expressed in Escherichia coli, purified, analyzed, and immunized in BALB/c mice. The specificity of anti-MSP4-immunoglubulin (Ig) G antibodies was evaluated by Western blot and enzyme-linked immunosorbent assays, and cellular immune responses were analyzed via lymphocyte proliferation assays. Results: Full peptide sequences of PocMSP4 and PowMSP4 were completely conserved in all clinical isolates, except in the epidermal growth factor-like domain at the carboxyl terminus where only one mutation was observed in one P. ovale wallikeri isolate. Furthermore, we successfully expressed the truncated pocmsp4 and powmsp4 and purified as ~32 kDa proteins. Our results showed that PocMSP4 and PowMSP4 induced high antibody responses with end-point titers ranging from 1:10,000 to 1:2,560,000 in all immunized mouse groups and with high IgG avidity to PocMSP4 (80.5%) and PowMSP4 (92.3%). Furthermore, rPocMSP4 and rPowMSP4 cross-reacted with anti-PowMSP4-specific or anti-PocMSP4-specific antibodies. Additionally, anti-PoMSP4 IgG antibodies showed broad immuno-specificity in reacting against rPoMSP1 and rPoAMA1. Lastly, PocMSP4- and PowMSP4-immunized mice induced cellular immune responses with PocMSP4 (36%) and PowMSP4 cells (15.8%) as observed through splenocyte proliferation assays. Conclusion: Our study suggested conservation in PoMSP4 protein sequences and high immunogenicity was observed in rPoMSP4. Furthermore, PocMSP4- and PowMSP4-immunized mice induced cellular immune responses, suggesting that both humoral and cellular immune responses play crucial roles in the protection against any antigen.

scholarly journals The host cellular immune response to infection by Campylobacter spp. and its role in disease

2021 ◽  
Author(s):  
Sean M. Callahan ◽  
Carolina G. Dolislager ◽  
Jeremiah G. Johnson
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Gastrointestinal Disease ◽  
Clinical Manifestations ◽  
Host Immune Response ◽  
Secretion Systems ◽  
Cellular Immune Responses ◽  
Gastrointestinal Pathology ◽  
Cellular Immune ◽  
Post Infectious

Campylobacter spp. are the leading cause of bacterial-derived gastroenteritis worldwide, impacting ninety-six million individuals annually. Unlike other bacterial pathogens of the gastrointestinal tract, Campylobacter spp. lack many of the classical virulence factors that are often associated with the ability to induce disease in humans, including an array of canonical secretion systems and toxins. As such, the clinical manifestations of human campylobacteriosis and its resulting gastrointestinal pathology are believed to be primarily due to the host immune response toward the bacterium. Further, while gastrointestinal infection is usually self-limiting, numerous post-infectious disorders can occur, including the development of Guillan-Barré syndrome, reactive arthritis, and irritable bowel syndrome. Because gastrointestinal disease likely results from the host immune response, the development of these post-infectious disorders may be due to dysregulation or misdirection of the same inflammatory response. As a result, it is becoming increasingly important to the Campylobacter field, and human health, that the cellular immune responses toward Campylobacter be better understood, including which immunological events are critical to the development of disease and the post-infectious disorders mentioned above. In this review, we will collectively cover the cellular immune responses across susceptible hosts to C. jejuni infection, along with the tissue pathology and post-infectious disorders which may develop.

De novo syntheses of Marburg virus antigens from adenovirus vectors induce potent humoral and cellular immune responses

Vaccine ◽  
2006 ◽  
Vol 24 (15) ◽  
pp. 2975-2986 ◽  
Author(s):  
Danher Wang ◽  
Alan L. Schmaljohn ◽  
Nicholas U. Raja ◽  
Charles M. Trubey ◽  
Laure Y. Juompan ◽  
...  
Keyword(s):  
Immune Responses ◽  
De Novo ◽  
Marburg Virus ◽  
Cellular Immune Responses ◽  
Adenovirus Vectors ◽  
Virus Antigens ◽  
Cellular Immune

scholarly journals Current Understanding of West Nile Virus Clinical Manifestations, Immune Responses, Neuroinvasion, and Immunotherapeutic Implications

Pathogens ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 193 ◽  
Author(s):  
Fengwei Bai ◽  
E. Ashley Thompson ◽  
Parminder J. S. Vig ◽  
A. Arturo Leis
Keyword(s):  
New York ◽  
West Nile Virus ◽  
Immune Responses ◽  
Clinical Manifestations ◽  
The United States ◽  
Current Understanding ◽  
Therapeutic Interventions ◽  
Clinical Practices ◽  
West Nile ◽  
Neuroinvasive Disease

West Nile virus (WNV) is the most common mosquito-borne virus in North America. WNV-associated neuroinvasive disease affects all ages, although elderly and immunocompromised individuals are particularly at risk. WNV neuroinvasive disease has killed over 2300 Americans since WNV entered into the United States in the New York City outbreak of 1999. Despite 20 years of intensive laboratory and clinical research, there are still no approved vaccines or antivirals available for human use. However, rapid progress has been made in both understanding the pathogenesis of WNV and treatment in clinical practices. This review summarizes our current understanding of WNV infection in terms of human clinical manifestations, host immune responses, neuroinvasion, and therapeutic interventions.

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