In-Host Dynamics of the Human Papillomavirus (HPV) in the Presence of Immune Response

2021 ◽  
pp. 79-97
Author(s):  
Z. Chazuka ◽  
G. M. Moremedi ◽  
E. Rapoo
Keyword(s):  
Immune Response ◽  
Human Papillomavirus

scholarly journals Head-to-Head Comparison of Modular Vaccines Developed Using Different Capsid Virus-Like Particle Backbones and Antigen Conjugation Systems

Vaccines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 539
Author(s):  
Laurits Fredsgaard ◽  
Louise Goksøyr ◽  
Susan Thrane ◽  
Kara-Lee Aves ◽  
Thor G. Theander ◽  
...  
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Immune Responses ◽  
Capsid Protein ◽  
Major Capsid Protein ◽  
Molecular Scaffolds ◽  
Conjugation System ◽  
Virus Like Particles ◽  
Virus Like Particle ◽  
Specific Igg

Capsid virus-like particles (cVLPs) are used as molecular scaffolds to increase the immunogenicity of displayed antigens. Modular platforms have been developed whereby antigens are attached to the surface of pre-assembled cVLPs. However, it remains unknown to what extent the employed cVLP backbone and conjugation system may influence the immune response elicited against the displayed antigen. Here, we performed a head-to-head comparison of antigen-specific IgG responses elicited by modular cVLP-vaccines differing by their employed cVLP backbone or conjugation system, respectively. Covalent antigen conjugation (i.e., employing the SpyTag/SpyCatcher system) resulted in significantly higher antigen-specific IgG titers compared to when using affinity-based conjugation (i.e., using biotin/streptavidin). The cVLP backbone also influenced the antigen-specific IgG response. Specifically, vaccines based on the bacteriophage AP205 cVLP elicited significantly higher antigen-specific IgG compared to corresponding vaccines using the human papillomavirus major capsid protein (HPV L1) cVLP. In addition, the AP205 cVLP platform mediated induction of antigen-specific IgG with a different subclass profile (i.e., higher IgG2a and IgG2b) compared to HPV L1 cVLP. These results demonstrate that the cVLP backbone and conjugation system can individually affect the IgG response elicited against a displayed antigen. These data will aid the understanding and process of tailoring modular cVLP vaccines to achieve improved immune responses.

scholarly journals Mechanisms of virus immune evasion lead to development from chronic inflammation to cancer formation associated with human papillomavirus infection

2012 ◽  
Vol 6 (2) ◽  
pp. 17 ◽  
Author(s):  
Masachika Senba ◽  
Naoki Mori
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Immune System ◽  
Tumor Suppressor ◽  
Chronic Inflammation ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Latency Period ◽  
Class I ◽  
Presentation Pathway

Human papillomavirus (HPV) has developed strategies to escape eradication by innate and adaptive immunity. Immune response evasion has been considered an important aspect of HPV persistence, which is the main contributing factor leading to HPV-related cancers. HPV-induced cancers expressing viral oncogenes E6 and E7 are potentially recognized by the immune system. The major histocompatibility complex (MHC) class I molecules are patrolled by natural killer cells and CD8<sup>+</sup> cytotoxic T lymphocytes, respectively. This system of recognition is a main target for the strategies of immune evasion deployed by viruses. The viral immune evasion proteins constitute useful tools to block defined stages of the MHC class I presentation pathway, and in this way HPV avoids the host immune response. The long latency period from initial infection to persistence signifies that HPV evolves mechanisms to escape the immune response. It has now been established that there are oncogenic mechanisms by which E7 binds to and degrades tumor suppressor Rb, while E6 binds to and inactivates tumor suppressor p53. Therefore, interaction of p53 and pRb proteins can give rise to an increased immortalization and genomic instability. Overexpression of NF-kB in cervical and penile cancers suggests that NF-kB activation is a key modulator in driving chronic inflammation to cancer. HPV oncogene-mediated suppression of NF-kB activity contributes to HPV escape from the immune system. This review focuses on the diverse mechanisms of the virus immune evasion with HPV that leads to chronic inflammation and cancer.

Human Papillomavirus: Pathogenesis and Host Immune Response

2014 ◽  
pp. 167-197
Author(s):  
Jennifer M. Spangle ◽  
Alyce A. Chen ◽  
Karl Munger
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Host Immune Response

scholarly journals Human Papillomavirus Type 16 E7 Peptide-Directed CD8+ T Cells from Patients with Cervical Cancer Are Cross-Reactive with the Coronavirus NS2 Protein

2003 ◽  
Vol 77 (9) ◽  
pp. 5464-5474 ◽  
Author(s):  
Katja Nilges ◽  
Hanni Höhn ◽  
Henryk Pilch ◽  
Claudia Neukirch ◽  
Kirsten Freitag ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Immune Response ◽  
T Cells ◽  
Human Papillomavirus ◽  
T Cell ◽  
T Cell Responses ◽  
Cross Reactivity ◽  
Antiviral Immune Response ◽  
Human Papillomavirus Type 16 ◽  
Cell Responses

ABSTRACT Human papillomavirus type 16 (HPV16) E6 and E7 oncoproteins are required for cellular transformation and represent candidate targets for HPV-specific and major histocompatibility complex class I-restricted CD8+-T-cell responses in patients with cervical cancer. Recent evidence suggests that cross-reactivity represents the inherent nature of the T-cell repertoire. We identified HLA-A2 binding HPV16 E7 variant peptides from human, bacterial, or viral origin which are able to drive CD8+-T-cell responses directed against wild-type HPV16 E7 amino acid 11 to 19/20 (E711-19/20) epitope YMLDLQPET(T) in vitro. CD8+ T cells reacting to the HLA-A2-presented peptide from HPV16 E711-19(20) recognized also the HLA-A2 binding peptide TMLDIQPED (amino acids 52 to 60) from the human coronavirus OC43 NS2 gene product. Establishment of coronavirus NS2-specific, HLA-A2-restricted CD8+-T-cell clones and ex vivo analysis of HPV16 E7 specific T cells obtained by HLA-A2 tetramer-guided sorting from PBL or tumor-infiltrating lymphocytes obtained from patients with cervical cancer showed that cross-reactivity with HPV16 E711-19(20) and coronavirus NS252-60 represents a common feature of this antiviral immune response defined by cytokine production. Zero of 10 patients with carcinoma in situ neoplasia and 3 of 18 patients with cervical cancer showed ≥0.1% HPV16 E7-reactive T cells in CD8+ peripheral blood lymphocytes. In vivo priming with HPV16 was confirmed in patients with cervical cancer or preinvasive HPV16-positive lesions using HLA-A2 tetramer complexes loaded with the E6-derived epitope KLPQLCTEL. In contrast, we could not detect E6-reactive T cells in healthy individuals. These data imply that the measurement of the HPV16 E711-19(20) CD8+-T-cell response may reflect cross-reactivity with a common pathogen and that variant peptides may be employed to drive an effective cellular immune response against HPV.

scholarly journals Ex Vivo Analyses of Ano-genital Wart Lymphocytes to Study the Human Papillomavirus Immune Response

2009 ◽  
Vol 89 (3) ◽  
pp. 303-304
Author(s):  
A Heaps ◽  
N Hanna ◽  
M Stanley ◽  
P Goon
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Genital Wart ◽  
Ex Vivo

scholarly journals O16.3 Cytokine immune response against natural human papillomavirus infection among men in kisumu, kenya

2019 ◽  
Author(s):  
Raphael Ondondo ◽  
Elizabeth Bukusi ◽  
Zipporah Nganga ◽  
Michael Kiptoo ◽  
Solomon Mpoke
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Human Papillomavirus Infection ◽  
Papillomavirus Infection

scholarly journals Immune Response Following Quadrivalent Human Papillomavirus Vaccination in Women After Hematopoietic Allogeneic Stem Cell Transplant

JAMA Oncology ◽  
2020 ◽  
Vol 6 (5) ◽  
pp. 696 ◽  
Author(s):  
Pamela Stratton ◽  
Minoo Battiwalla ◽  
Xin Tian ◽  
Suzanne Abdelazim ◽  
Kristin Baird ◽  
...  
Keyword(s):  
Immune Response ◽  
Stem Cell ◽  
Human Papillomavirus ◽  
Stem Cell Transplant ◽  
Cell Transplant ◽  
Allogeneic Stem Cell Transplant ◽  
Human Papillomavirus Vaccination
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