HPV52 is one of the most commonly detected genotypes in women with cervical intraepithelial neoplasia (CIN). Some methods for genotyping HPV are, however, biased against detection of HPV52. Current literature on this topic primarily focuses on the earliest consensus primer sets MY09/11 and GP5+/6+, or derivatives thereof. There are now many more genotyping assays in use. Given the importance of HPV52 and CIN, and the recent approval of the nine-valent HPV vaccine including HPV52, we undertook an updated discussion and analysis of HPV52 detection in women with CIN2+ by assay type and geographical region from cohorts published between 2006 and 2016. Little difference in HPV52 prevalence was observed by assay type, except sequencing and restriction fragment length polymorphism methods. The most commonly used genotyping methods in the past decade appear to be consistent for detection of HPV52. However, in longitudinal studies the same assay system should be used where possible.
Human herpesvirus 8 (HHV-8) causes Kaposi sarcoma (KS) and is associated with B-cell malignancies. Intravascular large B-cell lymphoma is an uncommon B-cell lymphoma characterized by proliferation of neoplastic B cells within the lumina of blood vessels. Although the underlying cause of this lymphoma is unclear, a previous report has identified a single case of HHV-8–associated intravascular lymphomatosis (IVL). We analyzed 5 cases of IVL for the presence of HHV-8, finding the second case of HHV-8–associated IVL. Human herpesvirus 8 protein expression (latency-associated nuclear antigen 1 [LANA-1]), Epstein-Barr virus–encoded RNAs (EBERs), and the cellular markers CD20 and CD45 were determined by immunohistochemistry. Intravascular lymphoma cells from a subject with human immunodeficiency virus (HIV) were positive for HHV-8 LANA-1, EBV EBER, and CD20 and CD45 expression. The 4 non-HIV–infected IVL cases were negative for HHV-8 LANA-1 and EBER expression. Future studies are required to determine whether the association between HHV-8 and HIV with IVL is true.
Long noncoding RNAs (lncRNAs) play important roles in a wide range of oncogenic processes, including malignant transformation, epigenetic reprogramming, epithelial-to-mesenchymal transition, and metastasis development. LncRNAs induced by oncogenic viral proteins were shown to play critical roles in tumor initiation and progression. Despite this, little is known about Human papillomavirus (HPV)-induced modulation of host’s lncRNAs. In this review, we gathered published information about altered lncRNAs upon HPV status (infection/protein activity), making use of descriptive research works and published gene expression microarray experiments. A diversity of lncRNAs demonstrated to be altered, including metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), H19, and maternally expressed gene 3 (MEG3). Their functions in several cancers were reviewed, indicating that they may represent potential candidates for future research on HPV-induced oncogenesis.
While the process of inflammation is a normal biological process to protect the body from harmful stimuli, chronic inflammation has been linked to a number of human diseases, including cancer. A number of agents can stimulate a chronic inflammatory response, which in turn promotes carcinogenesis. Here, we will describe how chronic inflammation is established through changes in cytokine signaling, perturbations of the NF-κB pathway, DNA damage, and physiological changes within the microenvironment and how these changes also contribute to tumorigenesis. In addition, we will describe the direct and indirect mechanisms by which infection by six viruses—Epstein-Barr, human herpesvirus-8, hepatitis B and C, human papilloma, and human T-lymphotropic virus type 1—induces chronic inflammation leading to tumor formation.
The evidence is that infection with high-risk human papillomavirus (HRHPV), particularly HPV 16, is the cause of the increase in incidence over the past 2–3 decades, in economically developed countries, of oropharyngeal squamous cell carcinoma (OPSCC), a subset of head and neck squamous cell carcinomas (HNSCC). HRHPV DNA sequences are detected in HNSCC with tonsil and base of tongue, the sites with the highest prevalence of HPV+ve carcinomas. HRHPV E6/E7 mRNA oncogene expression and p16INK4A overexpression (a marker of HRHPVE7 overexpression) are detected in 50–80% of OPSCC depending on geographical locale. Evidence from in vitro studies with oral keratinocyte cell lines and E6/E7 transgenic mice shows that E6/E7 oncogene expression is required for initiation and maintenance of the malignant phenotype. Case–control and cohort studies show that risk for OPSCC is associated with HPV exposure prior to cancer diagnosis. The experimental and epidemiological data provide robust evidence for a causal role in OPSCC, but the evidence for association of HPV with other HNSCC such as oral cavity or larynx is weak.
