From HPV infection to oncogenesis: A brief review of the complex immunobiological events

Peter L. Stern, Mark H. Einstein

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

This article reviews the natural history of HPV infection covering key aspects of cell biology, virology and immunology. The oncogenic HPV lifecycle is characterised by infection in basal cells of anogenital epithelia with virus production dependent on epithelial differentiation and virions produced only in terminally differentiated cells. Natural control of an oncogenic type HPV infection depends on appropriate activation of innate immune mechanisms leading to stimulation of adaptive immunity in the form of specific T cells against viral proteins such as E2, E6 and E7 which can ef- fect clearance of the virally infected cells. Neutralising antibodies are detected in about 50% of women who have cleared such infections but are not necessarily protective against future infection by the same HPV type and are never therapeutic. In addition, the stealthy lifecycle of the virus which causes little or damage and no viraemia as well as various viral im- mune evasion strategies sometimes allows the virus to avoid immune detection providing for persistent infection which is the major risk factor for development of intraepithelial neoplasia. Oncogenic HPV infection is necessary but insufficient for development of a cervical cancer and additional genetic changes are acquired over time through selection including those that allow for immune escape from immune surveillance.

Original languageEnglish (US)
Pages (from-to)110-116
Number of pages7
JournalCurrent Cancer Therapy Reviews
Volume6
Issue number2
DOIs
StatePublished - 2010

Fingerprint

Carcinogenesis
Infection
Viruses
Immune Evasion
Virology
Viremia
Adaptive Immunity
Viral Proteins
Allergy and Immunology
Neutralizing Antibodies
Natural History
Uterine Cervical Neoplasms
Virion
Cell Biology
Epithelium
T-Lymphocytes
Neoplasms

Keywords

  • Antigen presenting cells (APC)
  • Cytotoxic T lymphocytes (CTL)
  • Human leucocyte antigen (HLA)
  • Immune escape
  • Interferon
  • Neutralising antibodies
  • T regulatory cells

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Molecular Medicine

Cite this

From HPV infection to oncogenesis : A brief review of the complex immunobiological events. / Stern, Peter L.; Einstein, Mark H.

In: Current Cancer Therapy Reviews, Vol. 6, No. 2, 2010, p. 110-116.

Research output: Contribution to journalArticle

Stern, Peter L. ; Einstein, Mark H. / From HPV infection to oncogenesis : A brief review of the complex immunobiological events. In: Current Cancer Therapy Reviews. 2010 ; Vol. 6, No. 2. pp. 110-116.
@article{0d22d02794e14242b9d1803611c3c5b9,
title = "From HPV infection to oncogenesis: A brief review of the complex immunobiological events",
abstract = "This article reviews the natural history of HPV infection covering key aspects of cell biology, virology and immunology. The oncogenic HPV lifecycle is characterised by infection in basal cells of anogenital epithelia with virus production dependent on epithelial differentiation and virions produced only in terminally differentiated cells. Natural control of an oncogenic type HPV infection depends on appropriate activation of innate immune mechanisms leading to stimulation of adaptive immunity in the form of specific T cells against viral proteins such as E2, E6 and E7 which can ef- fect clearance of the virally infected cells. Neutralising antibodies are detected in about 50{\%} of women who have cleared such infections but are not necessarily protective against future infection by the same HPV type and are never therapeutic. In addition, the stealthy lifecycle of the virus which causes little or damage and no viraemia as well as various viral im- mune evasion strategies sometimes allows the virus to avoid immune detection providing for persistent infection which is the major risk factor for development of intraepithelial neoplasia. Oncogenic HPV infection is necessary but insufficient for development of a cervical cancer and additional genetic changes are acquired over time through selection including those that allow for immune escape from immune surveillance.",
keywords = "Antigen presenting cells (APC), Cytotoxic T lymphocytes (CTL), Human leucocyte antigen (HLA), Immune escape, Interferon, Neutralising antibodies, T regulatory cells",
author = "Stern, {Peter L.} and Einstein, {Mark H.}",
year = "2010",
doi = "10.2174/157339410791202565",
language = "English (US)",
volume = "6",
pages = "110--116",
journal = "Current Cardiology Reviews",
issn = "1573-3947",
publisher = "Bentham Science Publishers B.V.",
number = "2",

}

TY - JOUR

T1 - From HPV infection to oncogenesis

T2 - A brief review of the complex immunobiological events

AU - Stern, Peter L.

AU - Einstein, Mark H.

PY - 2010

Y1 - 2010

N2 - This article reviews the natural history of HPV infection covering key aspects of cell biology, virology and immunology. The oncogenic HPV lifecycle is characterised by infection in basal cells of anogenital epithelia with virus production dependent on epithelial differentiation and virions produced only in terminally differentiated cells. Natural control of an oncogenic type HPV infection depends on appropriate activation of innate immune mechanisms leading to stimulation of adaptive immunity in the form of specific T cells against viral proteins such as E2, E6 and E7 which can ef- fect clearance of the virally infected cells. Neutralising antibodies are detected in about 50% of women who have cleared such infections but are not necessarily protective against future infection by the same HPV type and are never therapeutic. In addition, the stealthy lifecycle of the virus which causes little or damage and no viraemia as well as various viral im- mune evasion strategies sometimes allows the virus to avoid immune detection providing for persistent infection which is the major risk factor for development of intraepithelial neoplasia. Oncogenic HPV infection is necessary but insufficient for development of a cervical cancer and additional genetic changes are acquired over time through selection including those that allow for immune escape from immune surveillance.

AB - This article reviews the natural history of HPV infection covering key aspects of cell biology, virology and immunology. The oncogenic HPV lifecycle is characterised by infection in basal cells of anogenital epithelia with virus production dependent on epithelial differentiation and virions produced only in terminally differentiated cells. Natural control of an oncogenic type HPV infection depends on appropriate activation of innate immune mechanisms leading to stimulation of adaptive immunity in the form of specific T cells against viral proteins such as E2, E6 and E7 which can ef- fect clearance of the virally infected cells. Neutralising antibodies are detected in about 50% of women who have cleared such infections but are not necessarily protective against future infection by the same HPV type and are never therapeutic. In addition, the stealthy lifecycle of the virus which causes little or damage and no viraemia as well as various viral im- mune evasion strategies sometimes allows the virus to avoid immune detection providing for persistent infection which is the major risk factor for development of intraepithelial neoplasia. Oncogenic HPV infection is necessary but insufficient for development of a cervical cancer and additional genetic changes are acquired over time through selection including those that allow for immune escape from immune surveillance.

KW - Antigen presenting cells (APC)

KW - Cytotoxic T lymphocytes (CTL)

KW - Human leucocyte antigen (HLA)

KW - Immune escape

KW - Interferon

KW - Neutralising antibodies

KW - T regulatory cells

UR - http://www.scopus.com/inward/record.url?scp=77952950068&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77952950068&partnerID=8YFLogxK

U2 - 10.2174/157339410791202565

DO - 10.2174/157339410791202565

M3 - Article

AN - SCOPUS:77952950068

VL - 6

SP - 110

EP - 116

JO - Current Cardiology Reviews

JF - Current Cardiology Reviews

SN - 1573-3947

IS - 2

ER -