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Review
. 2024 Mar 8;16(3):416.
doi: 10.3390/v16030416.

Human Oncogenic Viruses: Characteristics and Prevention Strategies-Lessons Learned from Human Papillomaviruses

Affiliations
Review

Human Oncogenic Viruses: Characteristics and Prevention Strategies-Lessons Learned from Human Papillomaviruses

Luisa Galati et al. Viruses. .

Abstract

Approximately 12% of human cancers worldwide are associated with infectious agents, which are classified by the International Agency for Research on Cancer (IARC) as Group 1 within the agents that are carcinogenic to humans. Most of these agents are viruses. Group 1 oncogenic viruses include hepatitis C virus, hepatitis B virus (HBV), human T-cell lymphotropic virus type 1, Epstein-Barr virus, Kaposi sarcoma-associated herpesvirus, human immunodeficiency virus-1 and high-risk human papillomaviruses (HPVs). In addition, some human polyomaviruses are suspected of inducing cancer prevalently in hosts with impaired immune responses. Merkel cell polyomavirus has been associated with Merkel cell carcinoma and included by the IARC in Group 2A (i.e., probably carcinogenic to humans). Linking viruses to human cancers has allowed for the development of diagnostic, prophylactic and therapeutic measures. Vaccination significantly reduced tumours induced by two oncogenic viruses as follows: HBV and HPV. Herein, we focus on mucosal alpha HPVs, which are responsible for the highest number of cancer cases due to tumour viruses and against which effective prevention strategies have been developed to reduce the global burden of HPV-related cancers.

Keywords: Epstein-Barr virus (EBV; HHV-4); HHV-8); Kaposi sarcoma-associated herpesvirus (KSHV; hepatitis B virus (HBV); hepatitis C virus (HCV); human T-cell lymphotropic virus type 1 (HTLV-1); human immunodeficiency virus-1 (HIV); human papillomavirus (HPV); oncoviruses.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
“Cancer hallmarks” according to Hanahan and Weinberg. The oncoproteins of each virus are listed in the column of the corresponding cancer hallmarks. The information is summarised from [40,41,42,43].
Figure 2
Figure 2
Genome organization of the prototype HPV16 and the main functions of HPV’s early (E) and late (L) encoded proteins. The circular dsDNA genome is indicated by a blue circle in which the six early (E1 up to E7) and the two late (L1 and L2) ORFs are separated by bars. The long control region (LCR), which is also called the URR, contains the origin of replication (ori) and transcription including transcription enhancer sequences. The early (p97) and late (p670) promoters are indicated by light-blue arrows. The early (pAE) and late (pAL) polyadenylation signals are also indicated.
Figure 3
Figure 3
Natural History of HR HPV infection. (A) Schematic representation of the progression of HR HPV infection. The host immune system usually clears the infection within a couple of years, and the associated lesion can regress; however, less frequently, the HPV infection can persist and lead to the dysregulation of E6 and E7, which may favour the progression of a premalignant lesion to an invasive cancer. (B) Panel reports the spectrum of HPV-related histological premalignant lesions and cancer types occurring in women and men.
Figure 3
Figure 3
Natural History of HR HPV infection. (A) Schematic representation of the progression of HR HPV infection. The host immune system usually clears the infection within a couple of years, and the associated lesion can regress; however, less frequently, the HPV infection can persist and lead to the dysregulation of E6 and E7, which may favour the progression of a premalignant lesion to an invasive cancer. (B) Panel reports the spectrum of HPV-related histological premalignant lesions and cancer types occurring in women and men.
Figure 4
Figure 4
Prevention strategies to control cervical cancer involve both vaccination and screening.

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