Small DNA tumor viruses and human cancer: Preclinical models of virus infection and disease

Spurgeon, Megan E.

doi:10.1016/j.tvr.2022.200239

Cited by 11 publications

(11 citation statements)

References 298 publications

(397 reference statements)

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“…Polyomavirus LT also encodes a LxCxE motif to target pRb pocket proteins [ 34 , 35 ]. We extended our study to human tumorigenic polyomavirus MCV.…”

Section: Resultsmentioning

confidence: 99%

Methyltransferase-independent function of enhancer of zeste homologue 2 maintains tumorigenicity induced by human oncogenic papillomavirus and polyomavirus

Khattri,

Amako,

Gibbs

et al. 2023

Tumour Virus Research

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“…Polyomavirus LT also encodes a LxCxE motif to target pRb pocket proteins [ 34 , 35 ]. We extended our study to human tumorigenic polyomavirus MCV.…”

Section: Resultsmentioning

confidence: 99%

Methyltransferase-independent function of enhancer of zeste homologue 2 maintains tumorigenicity induced by human oncogenic papillomavirus and polyomavirus

Khattri,

Amako,

Gibbs

et al. 2023

Tumour Virus Research

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“…A number of animal papillomavirus have been used to mimic HPV infection, but there are clear differences between the different animal viral life cycles and HPV life cycles. 182,183 The development of a murine model of infection has transformed the HPV research field. [183][184][185][186][187][188] However, murine epithelia generally display fewer cell layers than human epithelia 188 and MmuPV1 does not express an E5 protein, which is important for late gene expression 44,45 meaning that late events in the MmuPV1 184 life cycle may exhibit significant differences to that of HPVs.…”

Section: Future Directionsmentioning

confidence: 99%

“…182,183 The development of a murine model of infection has transformed the HPV research field. [183][184][185][186][187][188] However, murine epithelia generally display fewer cell layers than human epithelia 188 and MmuPV1 does not express an E5 protein, which is important for late gene expression 44,45 meaning that late events in the MmuPV1 184 life cycle may exhibit significant differences to that of HPVs. Importantly, the tractability of a murine model offers an approach to lineage tracing of MmuPV1 infected cells, including observation of late events and spatial analysis of host-pathogen interactions, which could transform our understanding of HPV late gene expression.…”

Section: Future Directionsmentioning

confidence: 99%

“…That said, these are in vitro approaches, which may not recapitulate the in vivo environment. A number of animal papillomavirus have been used to mimic HPV infection, but there are clear differences between the different animal viral life cycles and HPV life cycles 182,183 . The development of a murine model of infection has transformed the HPV research field 183–188 .…”

Section: Introductionmentioning

confidence: 99%

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The human papillomavirus late life cycle and links to keratinocyte differentiation

Kirk,

Graham

2024

Journal of Medical Virology

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Regulation of human papillomavirus (HPV) gene expression is tightly linked to differentiation of the keratinocytes the virus infects. HPV late gene expression is confined to the cells in the upper layers of the epithelium where the virus capsid proteins are synthesized. As these proteins are highly immunogenic, and the upper epithelium is an immune‐privileged site, this spatial restriction aids immune evasion. Many decades of work have contributed to the current understanding of how this restriction occurs at a molecular level. This review will examine what is known about late gene expression in HPV‐infected lesions and will dissect the intricacies of late gene regulation. Future directions for novel antiviral approaches will be highlighted.

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“…Infectious agents play an important role as etiological factors in human disease, such as cancer [ 13 ] and autoimmune disorders [ 14 ]. In addition to their primary infections, the role of DNA viruses as causative agents in human disease development is not yet fully understood.…”

Section: Introductionmentioning

confidence: 99%

Viral DNA in submandibular gland tissue with an inflammatory disorder

Keski-Säntti,

Waltimo,

Mäkitie

et al. 2024

Journal of Oral Microbiology

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Background The etiology behind different types of chronic sialadenitis (CS), some of which exhibit IgG4 overexpression, is unknown. Further, IgG4-related disease (IgG4-RD) commonly affects the submandibular gland, but its relationship to IgG4-overexpressing CS, and the antigen triggering IgG4 overexpression, remain unknown. Materials and Methods By qPCR, we assessed the presence of 21 DNA-viruses causing IgG4 overexpression in submandibular gland tissue from patients with IgG4-positive and IgG4-negative CS. Healthy submandibular glands and glands with sialolithiasis without CS were used as controls. We examined the distribution of HHV-7, HHV-6B and B19V DNA, within virus PCR-positive tissues with RNAscope in-situ hybridization (RISH). Results We detected DNA from seven viruses in 48/61 samples. EBV DNA was more prevalent within the IgG4-positive samples (6/29; 21%) than the IgG4-negative ones (1/19; 5.3%). B19V DNA was more prevalent within the IgG4-negative samples (5/19; 26%) than the IgG4-positive ones (4/29; 14%). The differences in virus prevalence were not statistically significant. Of the IgG4-RD samples ( n = 3) one contained HHV-6B DNA. RISH only showed signals of HHV-7. Conclusions None of the studied viruses are implicated as triggering IgG4-overexpression in CS. Although our results do not confirm viral etiology in the examined conditions, they provide valuable information on the prevalence of viruses in both diseased and healthy submandibular gland tissue.

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Small DNA tumor viruses and human cancer: Preclinical models of virus infection and disease

Cited by 11 publications

References 298 publications

Methyltransferase-independent function of enhancer of zeste homologue 2 maintains tumorigenicity induced by human oncogenic papillomavirus and polyomavirus

Methyltransferase-independent function of enhancer of zeste homologue 2 maintains tumorigenicity induced by human oncogenic papillomavirus and polyomavirus

The human papillomavirus late life cycle and links to keratinocyte differentiation

Viral DNA in submandibular gland tissue with an inflammatory disorder

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