Available Online Through: ISSN 2321 - 6328
Available Online Through: ISSN 2321 - 6328
Available Online Through: ISSN 2321 - 6328
2014
Review Article
HUMAN-PAPILLOMA VIRUS IN ORAL MUCOSA: AN OVERVIEW
Thukral Himanshu1*, Vohra Jayati1, Sarkar Aparna2
1
PG Scholar, Medical Physiology, Amity Institute of Physiology and Allied Sciences, Amity University, Noida,
Uttar Pradesh, India
2
Associate Professor and Coordinator, Amity Institute of Physiology and Allied Sciences, Amity University, Noida,
Uttar Pradesh, India
*Corresponding Author Email: [email protected]
ABSTRACT
Since 20 years there been an ever-increasing interest in human papillomaviruses HPV for the reason that of their impending character in the
pathogenesis of malignant tumors. HPV was undeniably confirmed as an independent risk factor which leads to oral carcinoma. Up to now, totally
more than 200 different strains and 170 types of HPV have been identified with their genomes and of them generally very less leads to the cancerous
stage. As in HPV type 16 is the most prevalent type in oral carcinomas. The benign oral lesions, related with HPV infection, include Oropharyngeal
squamous cell carcinoma, verrucca vulgaris and focal epithelial hyperplasia (FEH) and benign warts (genital, plantar and flat warts). These Oral
benign HPV lesions are mostly asymptomatic as they may persist or regress spontaneously.
Keywords: Human papilloma viruses, malignant tumors, oral carcinoma, HPV infection
INTRODUCTION Various scientists have identified that there are two major
Human papillomavirus (HPV) is a DNA virus from variants of HPV16, European HPV16-E and Non-
the papillomavirus family that is capable of infecting European HPV16-NE11. The casual link between human
humans1-2. The first visualization of papillomavirus papillomavirus HPV infection and the growth of head and
particles in human warts by electron microscopy was neck carcinomas (HNCs) particularly in the oropharynx
reported in 19493. The structure of papillomavirus are becoming more firmly established12-14. Still there are
genomes was unraveled by Crawford and Crawford in number of unanswered questions remain. Unlike cervical
1963. The unavailability of tissue culture systems and the cancer, with high risk HPVs in HNC are neither an
apparent benign nature of human warts led to few obligatory nor an adequate cause of cancer and only of
additional experimental approaches in subsequent years. these 20 % malignancies are associated with the
Gradually interest in papillomaviruses evolved in second transmission12. There is a need to conclude whether a test
part of the 1970s, evidenced by the first papillomavirus based on oral exfoliated cells can be used to provide a
workshops, commonly attended at that time by 15 to 30 sensitive method for predicting oncogenic mucosal HPV
participants. This developed in part from the hypothesis types in head and neck tissues15. This review tries to
that papillomavirus may play significant role in etiology summarize our present understanding of papillomavirus
of cancer of the cervix4,5. Meisels and Fortin proposed a infections by emphasizing their role in human cancers.
papillomavirus origin of koilocytotic atypias, separating
them from ‘true’ pre-neoplastic lesions. In the 1980s the The current review was conducted by means of a search
situation changed almost abruptly; the isolation of new of various articles and various websites associated with
HPV types HPV 6 and 11 from genital warts67 and the HPV. The search terms used were: ‘History
subsequently directly from cervical cancer biopsies HPV Associated with HPV,” ‘Structure of Human
type 16 and 188 resulted in a rapid expansion of Papillomavirus,’ ‘Types of HPV Has Been Identified Up
experimental work and also in early epidemiological to The Date,’ ‘Physiological Basis Of Human
approaches. HPVs establish productive infections only Papillomavirus,’ ‘Preventive Measures Associate With
in keratinocytes of the skin or mucous membranes. There Human Papillomavirus.’ Based on these review and
are two types of sexually transmitted HPV infections: considering only published information, this article is
1. Low risk viruses that can cause skin warts like constructed.
Condylomata acuminata
2. High risk or cancer producing viruses are Type 16 and Structure of Viral Particles
18. HPV 16 and 18 infections are a cause of a unique The diameter of HPV particles amounts to approx 55 nm.
type of oropharyngeal throat cancer 9,10. Full particles contain the double-stranded closed circular
DNA genome. The viral DNA is associated with histone-
like proteins16,17 and encapsulated by 72 capsomeres18. of these proteins in recombinant vectors19,20. Obviously
The major capsid protein is coded by the L1 open reading the L1 protein suffices for this particle formation. This
frame seems to contain reactive epitopes for type-specific protein has a molecular weight of approx 55000 and is
neutralization. The L2 open reading frame codes for an highly conserved among different papillomavirus types.
additional structural component of the viral capsid. The second structural protein, L2 is less conserved and
Antigenic domains of this protein appear to be responsible possesses a molecular weight of about 75000. The non-
for a group-specific reactivity of antisera. Virus like enveloped structure renders papillomaviruses relatively
particles containing the structural components of various resistant to heating and to organic solvents21.
types of HPV can however be obtained by the expression
Patho-physiology shows that virus can survive without host for long26.
HPV infects the basal cells of stratified squamous Studies have showed that HPV is a small DNA virus with
epithelium tissue, where they replicate25. They infect a genome of approximately 8000 base pairs27. The
epithelial tissues through expose segments (abrasions or development and history of the various strains of HPV
trauma) of the basement membrane or during human usually shows the relocation patterns of modern humans
sexual behavior25. The infection is having slow course of (Homo sapiens) and suggested that HPV may have
action, takes around 12–24 hours for initiation of become more varied among humans. It has been showed
transcription process. HPV lesions and infections arise in many studies that HPV evolved along the five major
from the proliferation of cells in the epidermis (Infected branches that would be a sign of the civilization of human
basal keratinocyte). HPVs are released as a result of hosts, and varied along with the human population28.
deterioration of desquamating cells. Individuals with
plantar warts spread virus by walking barefoot which
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04.004 Cite this article as:
26. Greer CE, Wheeler CM, Ladner MB, Beutner K, Coyne MY, Liang Thukral Himanshu, Vohra Jayati, Sarkar Aparna. Human-papilloma
H, Langenberg A, Yen TS, Ralston R. Human papillomavirus HPV virus in oral mucosa: An overview. J Biol Sci Opin 2014;2(6): 335-338
type distribution and serological response to HPV type 6 virus-like http://dx.doi.org/10.7897/2321-6328.02676