HIV-1-Mediated Acceleration of Oncovirus-Related Non-AIDS-Defining Cancers

Proulx, Jessica; Ghaly, Maria; Park, In-Woo; Borgmann, Kathleen

doi:10.3390/biomedicines10040768

Cited by 8 publications

(13 citation statements)

References 297 publications

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“…HIV-induced immune deficiency was the most common risk factor for developing malignancies [ 70 ]. HIV infection targets CD4 T cells, and immune responses progressively decrease, which allows cancer cells to escape immune surveillance and grow rapidly.…”

Section: Hiv and Tcmentioning

confidence: 99%

The Potential Role of Virus Infection in the Progression of Thyroid Cancer

Wu,

Jiang,

et al. 2024

World J Oncol

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Multiple factors have engaged in the progression of thyroid cancer (TC). Recent studies have shown that viral infection can be a critical factor in the pathogenesis of TC. Viruses, such as Epstein-Barr virus (EBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may play an essential role in the occurrence, development, and even prognosis in TC. This review mainly explored the potential role of viral infection in the progress of TC. The possible mechanisms could be recognizing the host cell, binding to the receptors, affecting oncogenes levels, releasing viral products to shape a beneficial environment, interacting with immune cells to induce immune evasion, and altering the pituitary-thyroid axis. Thus, comprehensive knowledge may provide insights into finding molecular targets for diagnosing and treating virus-related TC.

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Section: Hiv and Tcmentioning

confidence: 99%

The Potential Role of Virus Infection in the Progression of Thyroid Cancer

Wu,

Jiang,

et al. 2024

World J Oncol

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“…Hallmarks of viral carcinogenesis from integration to malignant transformation for human oncoviruses i.e., HPV, HBV, and HIV-1* (accelerates oncovirus-mediated carcinogenesis). Viral entry into mammalian cells is host and surface receptor specific [4,11,12]. The modes of viral-host integration differ respectively among HPV, HBV, and HIV-1 to include faulty viral partitioning to daughter cells during mitosis, nonhomologous end joining (NHEJ) or micro-homology mediated end-joining (MMEJ) at double-strand DNA breaks, and provirus insertion [13][14][15][16][17][18][19].…”

Section: Figure 1 Viral Carcinogenesis Viral Entry and Viral-host Gen...mentioning

confidence: 99%

“…3 Chromosomal region and band recognized as an HPV integration hotspot (i.e., 2q22.3, 3p14.2, 3q28, 8q24.21, 8q24.22, 13q22.1, 14q24.1, 17p11.1, 17q23.1 and 17q23.2) [42]. 4 Disrupted oncogenic, tumor suppressor or cancer-associated gene(s) . 5 Nearby oncogenic, tumor suppressor or cancer-associated gene(s) .…”

Section: Figure 7 Viral Integration Site (Vis) Circular Plotsmentioning

confidence: 99%

“…The journey from viral infection to malignant transformation of the host cell is complicated and disparate for HPV, HBV, and HIV-1 (Figure 1). Typically, these three viruses display host cell specificity, requiring binding to specific cell surface proteins for entry [4,11,12]. After traversing the cytoplasm, the viral genomes enter the nucleus for replication (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

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HPV, HBV, and HIV-1 Viral Integration Site Mapping: A Streamlined Workflow from NGS to Genomic Insights of Carcinogenesis

Shen-Gunther,

Easley

2024

Preprint

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Viral integration within the host genome plays a pivotal role in carcinogenesis. Various disruptive mechanisms are involved, leading to genomic instability, mutations, and DNA damage. With next-generation sequencing (NGS), we can now precisely identify viral and host genomic breakpoints and chimeric sequences, which are useful for integration site analysis. In this study, we evaluated a commercial hybrid-capture NGS panel specifically designed for detecting three key viruses: HPV, HBV, and HIV-1. We also tested workflows for Viral Hybrid Capture (VHC) and Viral Integration Site (VIS) analysis, leveraging customized viral databases in CLC Microbial Ge-nomics. By analyzing sequenced data from virally infected cancer cell lines (including SiHa, HeLa, CaSki, C-33A, DoTc2, 2A3, SCC154 for HPV; 3B2, SNU-182 for HBV; and ACH-2 for HIV-1), we precisely pinpointed viral integration sites. The workflow also highlighted disrupted and neigh-boring human genes that may play a crucial role in tumor development. Our results included in-formative virus-host read mappings, genomic breakpoints, and integration circular plots. These visual representations enhance our understanding of the integration process. In conclusion, our seamless end-to-end workflow bridges the gap in understanding viral contributions to cancer development, paving the way for improved diagnostics and treatment strategies.

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“…Regarding the Human Immunodeficiency Virus-1 (HIV-1), the introduction of the antiretroviral combined therapy reduced the incidence of AIDS-associated cancers, in particular, Kaposi sarcoma and non-Hodgkin lymphoma. On the contrary, some others cancers, the so-called non-AIDS-defining cancers, have increased significantly (49). Among these, head and neck squamous cell cancers.…”

Section: Infections As Prognostic Factors In Oral Squamous Cell Carci...mentioning

confidence: 99%

Oral infections in oral cancer survivors: A mini-review

Pispero

Lombardi²,

Manfrēdi³

et al. 2022

Front. Oral. Health

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The oral cancer survivors are a group of special individuals whose disease affect anatomical structures with a key role in identity and communication and a fundamental role in basic human functions such as speaking, eating, swallowing and breathing. Thus, quality of life of these individuals can be impaired by the consequences of disease and treatments, in particular surgery and radiotherapy. Among others, infectious conditions of any nature, bacterial, viral, fungal, are a frequent finding among oral cancer survivors. In fact, the peculiar systemic and local conditions of these subjects are known to significantly modify the microbiota, which, besides facilitating opportunistic infections, can affect the cancer microenvironment, as well as alter the effects of the anti-cancer therapies. Similarly, mouth infections can also affect the prognosis of oral cancer survivors. Among the opportunistic infections, fungal are the most common infections affecting these subjects, since neutropenia resulting from cancer, as well as chemotherapy and/or radiotherapy treatments, promote the shift from the carrier state of Candida species, to pathogen state. Treatment of oral candidiasis can be difficult in oral cancer survivors, and good evidence supports clotrimazole as the most effective for prevention, and fluconazole as the one with the best risk-benefit profile. Probiotics, although promising, need better evidence to be considered an effective treatment or preventive measure.

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HIV-1-Mediated Acceleration of Oncovirus-Related Non-AIDS-Defining Cancers

Cited by 8 publications

References 297 publications

The Potential Role of Virus Infection in the Progression of Thyroid Cancer

The Potential Role of Virus Infection in the Progression of Thyroid Cancer

HPV, HBV, and HIV-1 Viral Integration Site Mapping: A Streamlined Workflow from NGS to Genomic Insights of Carcinogenesis

Oral infections in oral cancer survivors: A mini-review

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