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Viral Infections and Cancer: Recent Advances and Future Perspectives

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 2618

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Guest Editor
Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: interferons; cancer; innate immunity; adaptive immunity; skin; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Viral infections account for 15–20% of human cancers. They are the second most important cause of cancer and a matter of global concern. Viruses can target major cellular mechanisms and pathways in a direct or indirect manner to cause the development of cancer. The mechanism(s) by which viruses can cause cancer are complex and one or more viruses can contribute to the development of cancer. Viruses can cause cancer by alterations in protein expression, genomic modification, chronic inflammation and by causing immune suppression. Some commonly known examples of virus-induced cancers are cervical squamous cell carcinoma, head and neck squamous cell carcinoma, hepatocellular carcinoma, Kaposi’s sarcoma and Burkitt’s lymphoma. Studies on the role of viruses as a cause of cancer has led to the development of vaccines that can protect against oncogenic viral infections. This Special Issue is expanding the current knowledge on cancers caused by viral infections. Experimental studies on in vivo and in vitro models and review articles are all welcome for publication.

Dr. Nabiha Yusuf
Guest Editor

Manuscript Submission Information

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Keywords

  • virus
  • infection
  • cancer
  • immune response

Published Papers (2 papers)

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Research

15 pages, 3157 KiB  
Article
Epstein–Barr Virus Promotes Oral Squamous Cell Carcinoma Stemness through the Warburg Effect
by Chukkris Heawchaiyaphum, Hironori Yoshiyama, Hisashi Iizasa, Ati Burassakarn, Zolzaya Tumurgan, Tipaya Ekalaksananan and Chamsai Pientong
Int. J. Mol. Sci. 2023, 24(18), 14072; https://doi.org/10.3390/ijms241814072 - 14 Sep 2023
Cited by 1 | Viewed by 1232
Abstract
Epstein–Barr virus (EBV) is associated with various human malignancies. An association between EBV infection and oral squamous cell carcinoma (OSCC) has recently been reported. We established EBV-positive OSCC cells and demonstrated that EBV infection promoted OSCC progression. However, the mechanisms by which EBV [...] Read more.
Epstein–Barr virus (EBV) is associated with various human malignancies. An association between EBV infection and oral squamous cell carcinoma (OSCC) has recently been reported. We established EBV-positive OSCC cells and demonstrated that EBV infection promoted OSCC progression. However, the mechanisms by which EBV promotes OSCC progression remain poorly understood. Therefore, we performed metabolic analyses of EBV-positive OSCC cells and established a xenograft model to investigate the viral contribution to OSCC progression. Here, we demonstrated that EBV infection induced mitochondrial stress by reducing the number of mitochondrial DNA (mtDNA) copies. Microarray data from EBV-positive OSCC cells showed altered expression of glycolysis-related genes, particularly the upregulation of key genes involved in the Warburg effect, including LDHA, GLUT1, and PDK1. Furthermore, lactate production and LDH activity were elevated in EBV-positive OSCC cells. EBV infection significantly upregulated the expression levels of cancer stem cell (CSC) markers such as CD44 and CD133 in the xenograft model. In this model, tumor growth was significantly increased in EBV-positive SCC25 cells compared with that in uninfected cells. Furthermore, tumorigenicity increased after serial passages of EBV-positive SCC25 tumors. This study revealed the oncogenic role of EBV in OSCC progression by inducing the Warburg effect and cancer stemness. Full article
(This article belongs to the Special Issue Viral Infections and Cancer: Recent Advances and Future Perspectives)
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12 pages, 639 KiB  
Article
Preferential Tissue Sites of Different Cancer-Risk Groups of Human Papillomaviruses
by Mitsuaki Okodo, Kaori Okayama, Toshiyuki Sasagawa, Koji Teruya, Rei Settsu, Shuichi Mizuno, Yasuyoshi Ishii and Mizue Oda
Int. J. Mol. Sci. 2023, 24(17), 13151; https://doi.org/10.3390/ijms241713151 - 24 Aug 2023
Viewed by 929
Abstract
The oncogenic potential of human papillomavirus (HPV) may be used to determine the tissue tropism of each HPV type. Cervical cancer develops in the squamo-columar junction of the cervices, and most lesions are induced by high-risk (HR) HPV types. This suggests that HR [...] Read more.
The oncogenic potential of human papillomavirus (HPV) may be used to determine the tissue tropism of each HPV type. Cervical cancer develops in the squamo-columar junction of the cervices, and most lesions are induced by high-risk (HR) HPV types. This suggests that HR types preferentially infect the cervix, whereas the preferential infection site for low-risk (LR) types is not well defined. The determination of HPV tropism when using cytology samples can be uncertain since it is difficult to avoid contamination of cell samples between the cervix and the vagina. Herein, cell samples were carefully collected by independently scraping the cervix and vagina, after which the HPV types were determined. HPV tissue tropism was determined by considering what HPV types were positive at only one of the sites (the cervix or the vagina) as the viruses that preferentially infected that site. This method revealed that all LR types were only identified in vaginal samples, whereas 87% of HR types were identified in cervical sites. Thus, LR types may preferentially infect the vagina, whereas HR types infect the cervix. These findings suggest that preferential tissue tropism of certain HPV types is a probable factor for malignant progression. Full article
(This article belongs to the Special Issue Viral Infections and Cancer: Recent Advances and Future Perspectives)
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